alzheimer's research news

Alzheimer's Research News

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• Early Alzheimer's Diagnostics
• Protecting Brain Cells With Cannabinol
• HIV Treatments May Aid Alzheimer's Patients
• Tiny Brain Bubbles Carry Complete Codes
• How to Protect the Brain After Traumatic Injury
• Immunotherapy for Alzheimer's Disease
• Treatments for No. 1 Dementia in Under-60s
• Antioxidant Supplement May Improve Cognition
• What Drives Protein Build-Up in Parkinson's?
• Illuminating Oxygen's Journey in the Brain

Earlier Headlines

Thursday, march 28, 2024.

• Familial Alzheimer's Disease Transferred Via Bone Marrow Transplant in Mice

Wednesday, March 27, 2024

• Making Long-Term Memories Requires Nerve-Cell Damage
• Risk Factors for Faster Aging in the Brain Revealed in New Study
• Memory Self-Test Via Smartphone Can Identify Early Signs of Alzheimer's Disease

Tuesday, March 26, 2024

• New Treatment Target Identified for Alzheimer's Disease
• Common Degenerative Brain Disease May Begin to Develop in Middle Age
• Large-Scale Animal Study Links Brain pH Changes to Wide-Ranging Cognitive Issues

Monday, March 25, 2024

• Human Brains Are Getting Larger: That May Be Good News for Dementia Risk

Friday, March 22, 2024

• Physicists Develop Modeling Software to Diagnose Serious Diseases
• Movement Disorder ALS and Cognitive Disorder FTLD Show Strong Molecular Overlaps, New Study Shows

Thursday, March 21, 2024

• Novel Genetic Variants Associated With Alzheimer's Disease
• Immune Cells Identified as Key Players in Brain Health

Wednesday, March 20, 2024

• Rural and Minority Dementia Patients Face Disparities in Access to Neurologists
• Keto Diet Prevents Early Memory Decline in Mice

Tuesday, March 19, 2024

• Biomarkers of the Middle-Aged Brain Predict Cognitive Health in Old Age

Thursday, March 14, 2024

• A Healthier Diet Is Linked With a Slower Pace of Aging, Reduced Dementia Risk, Study Shows
• Alzheimer's Drug Fermented With Help from AI and Bacteria Moves Closer to Reality

Wednesday, March 13, 2024

• Blast-Related Concussions Linked to Higher Alzheimer's Risk
• Genetic Condition Haemochromatosis Linked to Higher Levels of Disease in Older People
• Integrity of Blood-Brain Barrier Depends on Protein That Is Altered in Some Neurodegenerative Diseases
• Recreational Activities Such as Golfing, Gardening May Be Associated With Increased ALS Risk Among Men

Tuesday, March 12, 2024

• 'Curved' Walking and a Depth Camera: New Tool Detects Early Cognitive Decline

Monday, March 11, 2024

• Researchers Identify Gene Involved in Neuronal Vulnerability in Alzheimer's Disease
• Wrist Device That Monitors Activity Could Help Provide Early Warning of Alzheimer's

Wednesday, March 6, 2024

• Earliest-Yet Alzheimer's Biomarker Found in Mouse Model Could Point to New Targets
• A Noninvasive Treatment for 'chemo Brain'
• Amyloid Blood Levels Associated With Brain Changes in Alzheimer's Study

Thursday, February 29, 2024

• Tiny Magnetic Particles in Air Pollution Linked to Development of Alzheimer's
• How Cognition Changes Before Dementia Hits
• Mutations in Hereditary Alzheimer's Disease Damage Neurons Without 'usual Suspect' Amyloid Plaques
• Poor Spatial Navigation Could Predict Alzheimer's Disease Years Before the Onset of Symptoms

Wednesday, February 28, 2024

• More Than Just Neurons: A New Model for Studying Human Brain Inflammation
• How 40Hz Sensory Gamma Rhythm Stimulation Clears Amyloid in Alzheimer's Mice

Monday, February 26, 2024

• Yoga Provides Unique Cognitive Benefits to Older Women at Risk of Alzheimer's Disease

Wednesday, February 21, 2024

• Air Pollution Linked to More Signs of Alzheimer's in Brain
• How AI Can Help Spot Early Risk Factors for Alzheimer's Disease

Tuesday, February 20, 2024

• Fixing Rogue Brain Cells May Hold Key to Preventing Neurodegeneration
• Blocking Key Protein May Halt Progression of Alzheimer's Disease

Friday, February 16, 2024

• New Genetic Therapy Holds Promise for ALS and Frontotemporal Dementia

Thursday, February 15, 2024

• Helping Caregivers Help People With Dementia Eat at Home

Wednesday, February 14, 2024

• Double Risk of Dementia After Mouth Ulcer Virus
• Exposure to Agent Orange Damages Brain Tissue in Ways Similar to Alzheimer's Disease
• Team Creates Novel Rabies Viral Vectors for Neural Circuit Mapping
• Gargling Away the 'bad' Bacteria in Type 2 Diabetes

Tuesday, February 13, 2024

• Are Stressed-out Brain Cells the Root Cause of Neurodegenerative Disease?

Monday, February 12, 2024

• Protein Modifications Key Influencers in Neurodegenerative Diseases

Friday, February 9, 2024

• Immune Genes Are Altered in Alzheimer's Patients' Blood
• Protein Accumulation on Fat Droplets Implicated in Late-Onset Alzheimer's Disease
• Language Barriers Could Contribute to Higher Aggression in People With Dementia

Thursday, February 8, 2024

• Analysis of Biological Networks Helps Explain the Complexity of Multiple Sclerosis
• Illuminating the Invisible: Detecting Proteins Linked to Diseases

Wednesday, February 7, 2024

• Erectile Dysfunction Drugs May Be Linked to Reduced Risk of Alzheimer's Disease
• New Direct Links Discovered Between the Brain and Its Surrounding Environment

Tuesday, February 6, 2024

• Study Finds Strongest Evidence to Date of Brain's Ability to Compensate for Age-Related Cognitive Decline

Monday, February 5, 2024

• Lighting Up Alzheimer's-Related Proteins to Allow for Earlier Disease Detection

Thursday, February 1, 2024

• Researchers 3D-Print Functional Human Brain Tissue
• Scientists Discover a Potential Way to Repair Synapses Damaged in Alzheimer's Disease
• Understanding Rapid Weight Loss in Older Women: Message from the Heart

Wednesday, January 31, 2024

• A New Way to Visualize Brain Cancer
• Did Dementia Exist in Ancient Greek and Rome?
• Researchers Find Enzyme Plays Much Larger Role in Preventing Neurodegenerative Diseases

Tuesday, January 30, 2024

• How Fasting May Protect Against Inflammation

Monday, January 29, 2024

• Re-Energizing Mitochondria to Treat Alzheimer's Disease
• Alzheimer's Disease Acquired from Historic Medical Treatments

Friday, January 26, 2024

• New Tool Helps Predict Progression of Alzheimer's
• Brain Drain: Nasopharyngeal Lymphatics Found to Be Crucial for Cerebrospinal Fluid Outflow

Tuesday, January 23, 2024

• Bioengineers on the Brink of Breaching Blood-Brain Barrier
• Could Bizarre Visual Symptoms Be a Telltale Sign of Alzheimer's?

Monday, January 22, 2024

• Liquid Laundry Detergent Packet Exposure Burden
• Thinning of Brain Region May Signal Dementia Risk 5-10 Years Before Symptoms

Friday, January 19, 2024

• Research Into the Nature of Memory Reveals How Cells That Store Information Are Stabilized Over Time

Thursday, January 18, 2024

• Wireless Drug Patch Shows Promise as Chronic Disease Treatment Delivery System
• Using Magnetized Neurons to Treat Parkinson's Disease Symptoms
• Don't Look Back: The Aftermath of a Distressing Event Is More Memorable Than the Lead-Up
• New Cause of Neuron Death in Alzheimer's Discovered
• Third Major Study Finds Evidence That Daily Multivitamin Supplements Improve Memory and Slow Cognitive Aging in Older Adults

Sunday, January 14, 2024

• Study Reveals Function of Little-Understood Synapse in the Brain

Wednesday, January 10, 2024

• ALS: Blocking Inflammation to Reduce Symptoms

Friday, January 5, 2024

• Hearing Loss Increases the Risk of Dementia

Thursday, January 4, 2024

• Even in Midlife, Disrupted Sleep Tied to Memory, Thinking Problems Later on

Wednesday, January 3, 2024

• Researchers Identify Path to Prevent Cognitive Decline After Radiation

Tuesday, January 2, 2024

• New Method Illuminates Druggable Sites on Proteins
• Healthy Omega-3 Fats May Slow Deadly Pulmonary Fibrosis

Wednesday, December 27, 2023

• Risk of Young-Onset Dementia Could Be Reduced Through Targeting Health and Lifestyle Factors

Sunday, December 24, 2023

• Predicting Alzheimer's Dementia in Oldest of the Old

Thursday, December 21, 2023

• Alzheimer's Discovery Reveals Dire Effect of Toxic Tau Protein on Brain Cells
• Integrating Research and Clinical Care to Uncover Secrets of Brain Development
• Evidence Early, but Emerging, That Gamma Rhythm Stimulation Can Treat Neurological Disorders
• Brain Lesions in Former Football Players Linked to Vascular, Brain Changes

Wednesday, December 20, 2023

• Finding That Statins Could Slow Dementia Stimulates Further Research

Tuesday, December 19, 2023

• Protein-Protein Interaction Discovery Unveils Down Syndrome's Molecular Mechanism Potential

Wednesday, December 13, 2023

• Very Irregular Sleep Linked to Higher Risk of Dementia
• Exercise Can Boost Brain Health
• Infection With Stomach Bacteria May Increase Risk of Alzheimer's Disease

Tuesday, December 12, 2023

• Smoking Causes Brain Shrinkage, Study Finds
• Saliva: A Means to Detect Pain in People With Dementia

Monday, December 11, 2023

• Clues to Preventing Alzheimer's Come from Patient Who, Despite Genetics, Evaded Disease
• Nanoparticle-Delivered RNA Reduces Neuroinflammation in Lab Tests

Friday, December 8, 2023

• New Cause of Diabetes Discovered, Offering Potential Target for New Classes of Drugs to Treat the Disease

Thursday, December 7, 2023

• Alzheimer's: Researchers Determine the Structural Basis for Interactions Between Apolipoprotein E and Amyloid Beta
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Shots - Health News

Alzheimer's researchers are looking beyond plaques and tangles for new treatments.

Jon Hamilton

Scientists say research into Alzheimer's needs to take a broader view of how the disease affects the brain — whether that's changes in the cortex or the role of inflammation. Matt York/AP hide caption

Scientists say research into Alzheimer's needs to take a broader view of how the disease affects the brain — whether that's changes in the cortex or the role of inflammation.

The field of Alzheimer's research is branching out.

After decades of focusing on the sticky amyloid plaques and tangled tau fibers associated with the disease, brain researchers are searching for other potential causes of impaired memory and thinking.

That search is on full display this week at the Alzheimer's Association International Conference in San Diego, where sessions are exploring factors including genes, brain injury, clogged arteries and inflammation.

A group of researchers from Seattle even unveiled a highly detailed atlas showing how different types of brain cells change in Alzheimer's. The goal is to help scientists identify new approaches to treatment.

"Certainly, plaques and tangles are a hallmark," says Maria Carrillo , chief science officer of the Alzheimer's Association. "It doesn't mean plaques are the cause of cell death."

Plaques are clumps of a protein called beta-amyloid that appear in the spaces between neurons. Tangles are made up of a protein called tau that appears inside a neuron.

Both proteins tend to accumulate in the brains of people with Alzheimer's. But their role in killing brain cells is still unclear.

Carrillo says the Alzheimer's field needs to look to cancer research where a deeper understanding of the disease has led to better treatments.

The shift comes after a series of experimental drugs have succeeded in removing amyloid plaques and tau tangles from the brain, but failed to halt the disease.

The Food and Drug Administration has approved one amyloid drug, Aduhelm, but is still evaluating whether it actually helps patients.

An Alzheimer's Atlas

The study that produced the atlas is emblematic of how researchers are recalibrating.

"What we're trying to do with this study is to look at cell vulnerability early on in disease, before [people] have plaques and tangles, before they have cognitive impairment," says Dr. C. Dirk Keene , a neuropathologist at the University of Washington.

To create the atlas, Keene and a team of researches analyzed more than a million cells from 84 brains donated by people who'd signed up for Alzheimer's research projects run by the University of Washington and Kaiser Permanente Washington Research Institute.

The brains came from donors "at all different stages of disease" Keene says, "so we can pinpoint what's happening from the earliest levels all the way through to people with advanced disease."

The effort is funded by the National Institute on Aging and grew out of the federal BRAIN initiative launched by President Obama in 2013.

The atlas came from the realization that "If we want to treat diseases of an extremely complex cellular organ, you need to understand that organ much better than we do," says Ed Lein , a senior investigator at the Allen Institute for Brain Science, which played a key role in analyzing the brain tissue.

So the team spent years studying cells in healthy brains before looking at brains affected by Alzheimer's.

"We've defined what a normal adult brain looks like," Lein says, "and now we can use that knowledge and look for changes that are happening in specific kinds of cells."

Future Alzheimer's Treatments Aim To Do More Than Clear Plaques From The Brain

Finding vulnerable brain cells.

At the Alzheimer's meeting, the team described changes they saw in more than 100 types of cells taken from the cortex — an area of the brain which is important to memory and thinking.

One finding was that neurons that make connections within the cortex itself were much more likely to die than those that connect to distant areas of the brain.

"What we're seeing is a profound effect on cortical circuitry that very plausibly is the reason we have cognitive decline," Lein says.

If so, a treatment designed to protect those vulnerable neurons might prevent declines in memory and thinking linked to Alzheimer's.

The team also found a proliferation of brain cells that contribute to inflammation. These included certain immune cells and a type of cell that responds to injury.

"So while the neurons are lost, the non-neuronal cells are actually increasing and changing" Lein says.

The finding supports the idea that inflammation plays an important role in Alzheimer's, and that anti-inflammatory drugs might help protect the brain.

The Seattle team hopes other scientists will use the brain cell atlas to come up with new treatments for Alzheimer's.

"We've created an open-access resource where the whole community can come and look at this data," Lein says. "They can mine it to speed up progress in the field as a whole."

Speeding up progress is one reason Kyle Travaglini , a researcher at the Allen Institute, jumped at the chance to work on the Alzheimer's project.

"My grandmother started developing Alzheimer's disease when I was just going off to college," says Travaglini, who received his PhD in 2021.

Travaglini says the atlas project is appealing because it isn't based on a preconceived idea about what causes Alzheimer's.

"It's like looking at the same disease that everyone has been looking at but in an entirely different way," he says.

A substance found in young spinal fluid helps old mice remember

Scientists look to people with Down syndrome to test Alzheimer's drugs

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• NEWS AND VIEWS
• 13 February 2023

Drug trial for Alzheimer’s disease is a game changer

• Eric M. Reiman 0

Eric M. Reiman is at the Banner Alzheimer’s Institute, Phoenix, Arizona 85006, USA.

You can also search for this author in PubMed   Google Scholar

Researchers have long sought a treatment for Alzheimer’s disease that could target the biological underpinnings of the condition and slow cognitive decline and its disabling consequences in definitive clinical trials. Writing in the New England Journal of Medicine , van Dyck et al. 1 provide compelling evidence that an antibody treatment called lecanemab can drastically reduce measurements of a characteristic Alzheimer’s brain abnormality called amyloid plaques, alter other biomarkers of the disease and reduce the clinical decline in people with the condition. Although lecanemab did not stop clinical decline completely, the trial results promise to have a profound effect on Alzheimer’s research, patient care and the successful development of therapies that could modify or even prevent the disease.

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Nature 615 , 42-43 (2023)

doi: https://doi.org/10.1038/d41586-023-00393-7

van Dyck, C. H. et al. N. Engl. J. Med. 388 , 9–21 (2023).

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Selkoe, D. J. & Hardy, J. EMBO Mol. Med. 8 , 595–608 (2016).

Decourt, B. et al. Neurol. Neurosci. Rep. 21 , 39 (2021).

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Sevigny, J. et al. Nature 537 , 50–56 (2016).

Reiman, E. M. Nature 537 , 36–37 (2016).

Haeberlein, S. B. et al. J. Prev. Alzheimers Dis. 9 , 197–210 (2022).

Zhu, H. et al. Clin. Pharmacol Ther. 111 , 728–731 (2022).

Swanson, C. J. et al. Alzheimers Res. Ther. 13 , 80 (2021).

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Pontecorvo, M. J. et al. JAMA Neurol. 79 , 1250–1259 (2022).

Emanuel, E. J. JAMA 326 , 1367–1368 (2021).

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Start of new era for alzheimer’s treatment.

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Harvard Staff Writer

Expert discusses recent lecanemab trial, why it appears to offer hope for those with deadly disease

Researchers say we appear to be at the start of a new era for Alzheimer’s treatment. Trial results published in January showed that for the first time a drug has been able to slow the cognitive decline characteristic of the disease. The drug, lecanemab, is a monoclonal antibody that works by binding to a key protein linked to the malady, called amyloid-beta, and removing it from the body. Experts say the results offer hope that the slow, inexorable loss of memory and eventual death brought by Alzheimer’s may one day be a thing of the past.

The Gazette spoke with Scott McGinnis , an assistant professor of neurology at Harvard Medical School and Alzheimer’s disease expert at Brigham and Women’s Hospital , about the results and a new clinical trial testing whether the same drug given even earlier can prevent its progression.

Scott McGinnis

GAZETTE: The results of the Clarity AD trial have some saying we’ve entered a new era in Alzheimer’s treatment. Do you agree?

McGINNIS: It’s appropriate to consider it a new era in Alzheimer’s treatment. Until we obtained the results of this study, trials suggested that the only mode of treatment was what we would call a “symptomatic therapeutic.” That might give a modest boost to cognitive performance — to memory and thinking and performance in usual daily activities. But a symptomatic drug does not act on the fundamental pathophysiology, the mechanisms, of the disease. The Clarity AD study was the first that unambiguously suggested a disease-modifying effect with clear clinical benefit. A couple of weeks ago, we also learned a study with a second drug, donanemab, yielded similar results.

GAZETTE: Hasn’t amyloid beta, which forms Alzheimer’s characteristic plaques in the brain and which was the target in this study, been a target in previous trials that have not been effective?

McGINNIS: That’s true. Amyloid beta removal has been the most widely studied mechanism in the field. Over the last 15 to 20 years, we’ve been trying to lower beta amyloid, and we’ve been uncertain about the benefits until this point. Unfavorable results in study after study contributed to a debate in the field about how important beta amyloid is in the disease process. To be fair, this debate is not completely settled, and the results of Clarity AD do not suggest that lecanemab is a cure for the disease. The results do, however, provide enough evidence to support the hypothesis that there is a disease-modifying effect via amyloid removal.

GAZETTE: Do we know how much of the decline in Alzheimer’s is due to beta amyloid?

McGINNIS: There are two proteins that define Alzheimer’s disease. The gold standard for diagnosing Alzheimer’s disease is identifying amyloid beta plaques and tau neurofibrillary tangles. We know that amyloid beta plaques form in the brain early, prior to accumulation of tau and prior to changes in memory and thinking. In fact, the levels and locations of tau accumulation correlate much better with symptoms than the levels and locations of amyloid. But amyloid might directly “fuel the fire” to accelerated changes in tau and other downstream mechanisms, a hypothesis supported by basic science research and the findings in Clarity AD that treatment with lecanemab lowered levels of not just amyloid beta but also levels of tau and neurodegeneration in the blood and cerebrospinal fluid.

GAZETTE: In the Clarity AD trial, what’s the magnitude of the effect they saw?

McGINNIS: The relevant standards in the trial — set by the FDA and others — were to see two clinical benefits for the drug to be considered effective. One was a benefit on tests of memory and thinking, a cognitive benefit. The other was a benefit in terms of the performance in usual daily activities, a functional benefit. Lecanemab met both of these standards by slowing the rate of decline by approximately 25 to 35 percent compared to placebo on measures of cognitive and functional decline over the 18-month studies.

“In a perfect world, we’d have treatments that completely stop decline and even restore function. We’re not there yet, but this represents an important step toward that goal.”

Steven M. Smith

GAZETTE: What are the key questions that remain?

McGINNIS: An important question relates to the stages at which the interventions were done. The study was done in subjects with mild cognitive impairment and mild Alzheimer dementia. People who have mild cognitive impairment have retained their independence in instrumental activities of daily living — for example, driving, taking medications, managing finances, errands, chores — but have cognitive and memory changes beyond what we would attribute to normal aging. When people transition to mild dementia, they’re a bit further along. The study was for people within that spectrum but there’s some reason to believe that intervening even earlier might be more effective, as is the case with many other medical conditions.

We’re doing a study here called the AHEAD study that is investigating the effects of lecanemab when administered earlier, in cognitively normal individuals who have elevated brain amyloid, to see whether we see a preventative benefit. The hope is that we would at least see a delay to onset of cognitive impairment and a favorable effect not only on amyloid biomarkers, but other biomarkers that might capture progression of the disease.

GAZETTE: Is anybody in that study treatment yet or are you still enrolling?

McGINNIS: There’s a rolling enrollment, so there are people who are in the double-blind phase of treatment, receiving either the drug or the placebo. But the enrollment target hasn’t been reached yet so we’re still accepting new participants.

GAZETTE: Is it likely that we may see drug cocktails that go after tau and amyloid? Is that a future approach?

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McGINNIS: It has not yet been tried, but those of us in the field are very excited at the prospect of these studies. There’s been a lot of work in recent years on developing therapeutics that target tau, and I think we’re on the cusp of some important breakthroughs. This is key, considering evidence that spreading of tau from cell to cell might contribute to progression of the disease. Additionally, for some time, we’ve had a suspicion that we will likely have to target multiple different aspects of the disease process, as is the case with most types of cancer treatment. Many in our field believe that we will obtain the most success when we identify the most pertinent mechanisms for subgroups of people with Alzheimer’s disease and then specifically target those mechanisms. Examples might include metabolic dysfunction, inflammation, and problems with elements of cellular processing, including mitochondrial functioning and processing old or damaged proteins. Multi-drug trials represent a natural next step.

GAZETTE: What about side effects from this drug?

McGINNIS: We’ve known for a long time that drugs in this class, antibodies that harness the power of the immune system to remove amyloid, carry a risk of causing swelling in the brain. In most cases, it’s asymptomatic and just detected by MRI scan. In Clarity AD, while 12 to 13 percent of participants receiving lecanemab had some level of swelling detected by MRI, it was symptomatic in only about 3 percent of participants and mild in most of those cases.

Another potential side effect is bleeding in the brain or on the surface of the brain. When we see bleeding, it’s usually very small, pinpoint areas of bleeding in the brain that are also asymptomatic. A subset of people with Alzheimer’s disease who don’t receive any treatment are going to have these because they have amyloid in their blood vessels, and it’s important that we screen for this with an MRI scan before a person receives treatment. In Clarity AD, we saw a rate of 9 percent in the placebo group and about 17 percent in the treatment group, many of those cases in conjunction with swelling and mostly asymptomatic.

The scenario that everybody worries about is a hemorrhagic stroke, a larger area of bleeding. That was much less common in this study, less than 1 percent of people. Unlike similar studies, this study allowed subjects to be on anticoagulation medications, which thin the blood to prevent or treat clots. The rate of macro hemorrhage — larger bleeds — was between 2 and 3 percent in the anticoagulated participants. There were some highly publicized cases including a patient who had a stroke, presented for treatment, received a medication to dissolve clots, then had a pretty bad hemorrhage. If the drug gets full FDA approval, is covered by insurance, and becomes clinically available, most physicians are probably not going to give it to people who are on anticoagulation. These are questions that we’ll have to work out as we learn more about the drug from ongoing research.

GAZETTE: Has this study, and these recent developments in the field, had an effect on patients?

McGINNIS: It has had a considerable impact. There’s a lot of interest in the possibility of receiving this drug or a similar drug, but our patients and their family members understand that this is not a cure. They understand that we’re talking about slowing down a rate of decline. In a perfect world, we’d have treatments that completely stop decline and even restore function. We’re not there yet, but this represents an important step toward that goal. So there’s hope. There’s optimism. Our patients, particularly patients who are at earlier stages of the disease, have their lives to live and are really interested in living life fully. Anything that can help them do that for a longer period of time is welcome.

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A new peptide may hold potential as an Alzheimer’s treatment

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MIT neuroscientists have found a way to reverse neurodegeneration and other symptoms of Alzheimer’s disease by interfering with an enzyme that is typically overactive in the brains of Alzheimer’s patients.

When the researchers treated mice with a peptide that blocks the hyperactive version of an enzyme called CDK5, they found dramatic reductions in neurodegeneration and DNA damage in the brain. These mice also showed improvements in their ability to perform tasks such as learning to navigate a water maze.

“We found that the effect of this peptide is just remarkable,” says Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory and the senior author of the study. “We saw wonderful effects in terms of reducing neurodegeneration and neuroinflammatory responses, and even rescuing behavior deficits.”

With further testing, the researchers hope that the peptide could eventually be used as a treatment for patients with Alzheimer’s disease and other forms of dementia that have CDK5 overactivation. The peptide does not interfere with CDK1, an essential enzyme that is structurally similar to CDK5, and it is similar in size to other peptide drugs that are used in clinical applications.

Picower Institute Research Scientist Ping-Chieh Pao is the lead author of the paper , which appears this week in the Proceedings of the National Academy of Sciences .

Targeting CDK5

Tsai has been studying CDK5’s role in Alzheimer’s disease and other neurodegenerative diseases since early in her career. As a postdoc, she identified and cloned the CDK5 gene, which encodes a type of enzyme known as a cyclin-dependent kinase. Most of the other cyclin-dependent kinases are involved in controlling cell division, but CDK5 is not. Instead, it plays important roles in the development of the central nervous system, and also helps to regulate synaptic function.

CDK5 is activated by a smaller protein that it interacts with, known as P35. When P35 binds to CDK5, the enzyme’s structure changes, allowing it to phosphorylate — add a phosphate molecule to — its targets. However, in Alzheimer’s and other neurodegenerative diseases, P35 is cleaved into a smaller protein called P25, which can also bind to CDK5 but has a longer half-life than P35.

When bound to P25, CDK5 becomes more active in cells. P25 also allows CDK5 to phosphorylate molecules other than its usual targets, including the Tau protein. Hyperphosphorylated Tau proteins form the neurofibrillary tangles that are one of the characteristic features of Alzheimer’s disease.

In previous work, Tsai’s lab has shown that transgenic mice engineered to express P25 develop severe neurodegeneration. In humans, P25 has been linked to several diseases, including not only Alzheimer’s but also Parkinson’s disease and frontotemporal dementia.

Pharmaceutical companies have tried to target P25 with small-molecule drugs, but these drugs tend to cause side effects because they also interfere with other cyclin-dependent kinases, so none of them have been tested in patients.

The MIT team decided to take a different approach to targeting P25, by using a peptide instead of a small molecule. They designed their peptide with a sequence identical to that of a segment of CDK5 known as the T loop, which is a structure critical to the binding of CDK5 to P25. The entire peptide is only 12 amino acids long — slightly longer than most existing peptide drugs, which are five to 10 amino acids long.

“From a peptide drug point of view, usually smaller is better,” Tsai says. “Our peptide is almost within that ideal molecular size.”

Dramatic effects

In tests in neurons grown in a lab dish, the researchers found that treatment with the peptide led to a moderate reduction in CDK5 activity. Those tests also showed that the peptide does not inhibit the normal CDK5-P35 complex, nor does it affect other cyclin-dependent kinases.

When the researchers tested the peptide in a mouse model of Alzheimer’s disease that has hyperactive CDK5, they saw a myriad of beneficial effects, including reductions in DNA damage, neural inflammation, and neuron loss. These effects were much more pronounced in the mouse studies than in tests in cultured cells.

The peptide treatment also produced dramatic improvements in a different mouse model of Alzheimer’s, which has a mutant form of the Tau protein that leads to neurofibrillary tangles. After treatment, those mice showed reductions in both Tau pathologies and neuron loss. Along with those effects in the brain, the researchers also observed behavioral improvements. Mice treated with the peptide performed much better in a task that required learning to navigate a water maze, which relies on spatial memory, than mice that were treated with a control peptide (a scrambled version of the peptide used to inhibit CDK5-P25).

In those mouse studies, the researchers injected the peptide and found that it was able to cross the blood-brain barrier and reach neurons of the hippocampus and other parts of the brain.

The researchers also analyzed the changes in gene expression that occur in mouse neurons following treatment with the peptide. Among the changes they observed was an increase in expression of about 20 genes that are typically activated by a family of gene regulators called MEF2. Tsai’s lab has previously shown that MEF2 activation of these genes can confer resilience to cognitive impairment in the brains of people with Tau tangles, and she hypothesizes that the peptide treatment may have similar effects.

“Further development of such peptide inhibitors toward a lead therapeutic candidate, if proven to be selective for the target and relatively free of clinical side effects, may eventually lead to novel treatments for neurodegenerative disorders ranging from Alzheimer’s disease to Frontotemporal dementia to Parkinson’s disease,” says Stuart Lipton, a professor of neuroscience at Scripps Research, who was not involved in the study.

Tsai now plans to do further studies in other mouse models of diseases that involve P25-associated neurodegeneration, such as frontotemporal dementia, HIV-induced dementia, and diabetes-linked cognitive impairment.

“It’s very hard to say precisely which disease will most benefit, so I think a lot more work is needed,” she says.

The research was funded by the National Institutes of Health.

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In a new study, researchers at MIT showed that they “were able to interfere with an enzyme typically found to be overactive in the brains of Alzheimer’s patients,” reports Alex Mitchell for The New York Post . After using a peptide to treat the overactive enzyme, they found that “the peptide shows protective effects against loss of neurons and also appears to be able to rescue some of the behavior deficits,” says Prof. Li-Huei Tsai.

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Alzheimer's drug development pipeline: Positive results, new insight on biomarkers position 2024 as 'learning year'

by Steven Slivka, John Domol, University of Nevada, Las Vegas

The world of Alzheimer's treatments is at an inflection point as more potential drugs make their way out of clinical trials.

On the heels of newly FDA-approved drugs Aduhelm (aducanumab) in 2021 and Leqembi (lecanemab) in 2023, a UNLV researcher says that 2024 is a "learning year" for Alzheimer's drug development.

"There are a large number of drugs in the pipeline that have very diverse actions on the brain," said Dr. Jeffrey Cummings, a leading Alzheimer's clinician-scientist and research professor in UNLV's School of Integrated Health Sciences.

Cummings leads the Alzheimer's drug development observatory within UNLV's Department of Brain Health, a robust database of all clinical trials results he began in 2016. It is the only observatory of its kind in the world.

While nearly 7 million Americans are living with Alzheimer's disease and are in need of better treatments, Cummings remains encouraged by the results of this year's pipeline developments—including the recent inclusion of biomarkers, which are often found in blood and signal normal or abnormal processes, or a condition or disease. Alzheimer's biomarkers can now be measured in the blood.

"Most of our biomarkers for Alzheimer's and dementia have been discovered only within the past three years. They provide information on the drug's impact," he said. "Biomarkers will be featured in nearly all clinical trials moving forward to guide the process."

Biomarker studies highlight current treatment pipeline

Cummings's annual report is featured in Alzheimer's & Dementia: Translational Research & Clinical Interventions . According to this year's data, there are 164 active trials and 127 unique treatments, a roughly 10% decrease from the previous year that saw a record-high 187 active trials and 141 unique treatments.

Some of this year's results include:

• 76% are disease-modifying treatments that aim to slow the decline of memory
• 34% are biological therapies given intravenously or through some other injection
• 12% are cognitive enhancing agents that are intended to improve memory
• 13% are drugs for behavioral symptoms, such as agitation
• 31% are repurposed agents approved for other diseases, such as cancer or Parkinson's disease

"One prediction we can make with confidence is that we should be prepared for more complex biological therapies that require intravenous infusion and vigilant monitoring for side effects; more like cancer therapies," Cummings said.

Cummings attributes the decrease in overall clinical trials and unique treatments to a lack of funding on the federal level and from less private investment from the biopharmaceutical industry.

"Simply put, we need more investments from the government and from the pharmaceutical companies to fight this trend of declining clinical trials," Cummings said, adding that the purpose of his annual Alzheimer's drug development pipeline report is to keep policymakers, health care systems, and patients apprised of the updates taking place among Alzheimer's clinical trials.

A lack of participants for clinical trials has also inhibited results, as nearly 51,400 participants are needed for all active trials. Still, Cummings said the newest Alzheimer's treatments in the pipeline, including results from 35 phase 2 trials and 12 from phase 3—the final phase before FDA review—will offer critical information as newer drugs continue to be developed.

"Eight of the drugs with reported data from phase 2 for this year are all anti-inflammatory drugs and the biomarkers included in the trials will allow us to dissect the importance of the individual aspects of inflammation," he added. He said that mounting results from multiple drugs focusing on one target will lead to new and potentially helpful information that could advance multiple related trials.

"The pipeline of potential new Alzheimer's treatments is diverse, offering a future with new, safe, and effective treatments and powerful combination therapies," said Maria C. Carrillo, Ph.D., Alzheimer's Association chief science officer. "The recent FDA approvals for Alzheimer's, and the diversity of the pipeline, provide hope to those impacted by this devastating disease."

"The Alzheimer's Association has long been committed to advancing all evidence-based potential treatment avenues, and to combining diverse approaches," Carrillo said.

Hopeful for the future

In addition to the FDA-approved Aduhelm and Leqembi, Cummings is confident that the FDA will approve the use of donanemab, which yielded positive results in its clinical trials before FDA review was halted for further evaluation.

"Development successes are emerging, which is why I think we are experiencing such a breakthrough in the world of Alzheimer's treatment," he said. "It takes a decade to advance a drug from phase 1 to phase 3 and then nearly two more years for FDA review, so these processes take time. We know that most drugs fail, but not all of them. Even drugs that fail in the clinical trial can still tell us a lot."

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Recent breakthroughs in Alzheimer’s research provide hope for patients

While there is no cure, researchers say a newly approved drug, advanced testing, and increasing knowledge about the disease may improve patients’ lives..

A few years ago, Lori Weiss, a high school math and engineering teacher, noticed it was taking her longer to do her lesson plans and grading. She also repeatedly needed to ask for help using spreadsheets she’d once mastered and she struggled to answer her students’ questions.

The symptoms were all too familiar to Weiss. Not only had she cared for her grandfather with Alzheimer’s disease when she was a teenager, she’d also watched her mother slowly lose her memory to the disease for nearly two decades. She had aunts, uncles, and a cousin as well who were diagnosed with the neurological disorder, which gradually steals a person’s memory and cognitive abilities.

“It’s rampant in my family,” Weiss says.

Weiss decided to speak with her primary care physician, who referred her to a neurologist for testing. In 2020, at the age of 62, Weiss was diagnosed with mild cognitive impairment. Two years after that, a PET scan revealed amyloid plaques, a buildup of toxic proteins in the brain that disrupt neural function and are a hallmark of Alzheimer’s disease.

Soon, Weiss began to lose her sense of direction, which prompted fears that she might be forced into a full-time care facility at a young age.

“Losing my freedom was just more than I could handle,” she says. Around that time, a friend saw a TV advertisement for a clinical trial for a drug that would attempt to slow progression of the disease using manmade monoclonal antibodies to attack and remove the amyloid plaques in the brain.

“I don’t even think that I thought twice about” enrolling in the trial, says Weiss, who has been receiving monthly infusions of the drug, called donanemab , near her home in Portland, Oregon, for about a year. “I just said, ‘Yeah, sign me up!’”

Although donanemab is not approved by the Food and Drug Administration (FDA), it uses a similar approach to the drug lecanemab, which received accelerated FDA approval on Jan. 6, and which showed biological and clinical benefits for patients in trials. In November, drugmaker Eli Lilly and Company announced promising results for donanemab, but last week, the FDA denied the company’s request for accelerated approval, saying it needed more data for participants receiving the drug for at least 12 months.

Nonetheless, this recent progress has given people like Weiss hope that previous generations have not had.

“Alzheimer’s research is getting to a place where cancer research was maybe 30, 40 years ago.” Anton Porsteinsson, MD, University of Rochester Medical Center in New York

Participating in the clinical trial “has had a huge impact,” Weiss says. “It’s given me the drive to do things while I can; it’s given me the desire to talk to more people about getting treatment, getting diagnosed early, and getting in drug trials.”

Weiss says that since she’s begun taking donanemab, she’s regained her sense of direction and has not noticed significant cognitive decline. For her, even the hope that the trial has given her has made all the difference.

“For my husband and I, it’s totally changed our lives. Instead of living in fear … we treat each day like it’s Valentine’s Day,” Weiss says. Getting diagnosed early has “given me so much more life. [I thought] getting the disease was a death sentence for me, but I’m taking a water painting class, I’m in a walking group and a music group. I thrive on my relationships with my Alzheimer’s friends and other friends, and I’m connected with my family. I feel like I’m living my life. It’s so much better than I imagined.”

And while Alzheimer’s researchers are careful to emphasize that they are still a long way from a cure, many say the hope is not a false one. The field has had several breakthroughs in recent years, from identifying easier and cheaper ways to diagnose the disease early to better understanding how individuals with the disease might require a variety of interventions.

“Alzheimer’s research is getting to a place where cancer research was maybe 30, 40 years ago,” says Anton Porsteinsson, MD, director of the Alzheimer’s Disease Care, Research and Education Program at the University of Rochester Medical Center in New York. “I think we’re at a point where we’re going to see a logarithmic increase in discovery.”

Fighting a complex disease

Alzheimer’s disease, which was discovered in 1906 and is now the seventh leading cause of death in the United States, has long boggled the scientific community. Though research over the decades has identified characteristics of the disease — such as the presence of amyloid plaques between neurons and the buildup, known as tangles, of another toxic protein, tau, inside neurons — questions remain about what causes the disease and how best to treat it in a clinically meaningful way.

“It’s a complex disease. It’s not just a single molecule that’s gone awry. It’s not an infection that has a viral particle,” says Ronald C. Petersen, MD, PhD, director of the Mayo Clinic Alzheimer’s Disease Research Center in Rochester, Minnesota. “We’ve defined it by the presence of amyloid , neuritic plaques , and neurofibrillary tangles , but that’s just the tip of the iceberg.”

Many researchers now believe that the precursors to developing Alzheimer’s begin to accumulate in the brain 10 or more years before symptoms begin to show.

Alzheimer’s disease progression affects the brain much like a forest fire, with many factors affecting how it spreads, says Rudolph E. Tanzi, PhD, director of the Genetics and Aging Research Unit at Massachusetts General Hospital in Boston.

Amyloid plaques and tau tangles can build up over years, at some point triggering an inflammatory response that can quickly destroy brain cells. These conditions can be influenced by a range of factors, from genetic predisposition to environmental exposures to lifestyle, he explains.

That’s why the solution to treating — or ideally, preventing — Alzheimer’s disease will likely require a combination of interventions, Petersen says.

One important part of the puzzle — and a part that has been the focus of much pharmaceutical development — is targeting the amyloid plaques.

This approach has been controversial. In 2021, the FDA granted accelerated approval to the anti-amyloid drug aducanumab, sold as Aduhelm, despite objections from an advisory committee and outcry from the scientific community that the lack of clinical benefit made the drug’s high cost, initially set at $56,000 a year and later reduced to $28,000 a year, unjustifiable. A Congressional investigation found numerous flaws and irregularities in the process the FDA used when approving the drug.

Lecanemab, on the other hand, has been met with more optimism in the Alzheimer’s research community because its clinical trials demonstrated an actual clinical benefit to patients early in the disease progression.

“The field is feeling that, finally, we have a drug that didn’t have the controversy aducanumab had,” Petersen says. “It looks like it does what it’s supposed to do biologically [and] this looks like it could be meaningful for patients.”

In clinical trials , lecanemab showed a modest but tangible decrease in cognitive decline (of 27%) over 18 months in Alzheimer’s patients who were early in the disease’s progression, compared with patients who were given a placebo. Though it’s far from a cure, experts say it could give patients months of retaining memory and cognition that they might otherwise lose, a prospect that could be meaningful for patients and their families who have no other options.

But this drug, too, has stirred some controversy because of its high price tag and potentially deadly side effects, including swelling and bleeding in the brain. The pharmaceutical company Eisai has priced lecanemab, sold as Leqembi, at $26,000 a year, and the Centers for Medicare and Medicaid Services has yet to decide if it will cover the drug.

“It’s very expensive,” Tanzi says, explaining that patients who take the drug will also need several MRIs to check for brain bleeds on top of the cost of the infusions. “There is a health care disparity this could create; those who want to remove amyloid can pay out of pocket [but] the average person can’t afford that. The wealthy can protect themselves.”

Equity starting in research

The high costs of treatment could also exacerbate existing racial disparities when it comes to Alzheimer’s outcomes. Although Black Americans are about twice as likely as White Americans to have Alzheimer’s, and Hispanics are about 1.5 times as likely to have it, White people make up a disproportionate majority of clinical trial participants and non-White people report greater barriers to diagnosis and access to care, according to the Alzheimer’s Association .

“Most of the research operations are either based at large academic institutions or private professional research sites,” Porsteinsson explains about pharmaceutical company trials. “The temptation [for researchers] is to go where the treatment is ‘easiest’; where you’ve recruited before.”

In its clinical trial recruitment for lecanemab, the University of Rochester succeeded in increasing the representation of Hispanic participants, but struggled to include a representative number of Black patients.

“We can’t just wait until the brain deteriorates.” Rudolph E. Tanzi, PhD, Massachusetts General Hospital in Boston

“If we want to go after historically underrepresented groups in research, first we need to recognize they’re underrepresented for a reason,” Porsteinsson says. “There might have been a poor experience with researchers coming [into their community], doing a study [the researchers] needed, and then basically leaving. There isn’t an ongoing commitment.”

He says that if Alzheimer’s treatments are going to be meaningful to all people affected by the disease, it will take a concerted effort to include more diversity in clinical trial participants, not only in race and ethnicity, but in health status and inclusion of people with comorbidities. Often, trials tend to select for the healthiest patients possible, he explains.

“[We must] secure making our research more representative of the American population,” Porsteinsson says. “It’s going to take an investment in infrastructure and it’s going to take an investment of time.”

A stage set for discovery

Alzheimer’s disease already affects more than six million people living in the United States, and that number is projected to grow to 13 million by 2050. It’s also an incredibly financially costly disease, with an economic impact of $321 billion in health care costs in 2022, expected to rise to $1 trillion by 2050, according to the Alzheimer’s Association. That prospect prompted the U.S. Congress to approve an additional $226 million to the National Institutes of Health for Alzheimer’s research in December, bringing the annual federal funding outlay to more than $3.7 billion .

Experts say it is not in vain. Research efforts, particularly those at teaching hospitals, have helped unlock mysteries about the genetic underpinnings of the disease, ways to identify biomarkers in the blood that can more easily diagnose the disease in its earliest states, and complex treatment approaches that use lifestyle interventions and a combination of drug therapies.

Tanzi believes that the future of Alzheimer’s treatment and prevention will be similar to current management of heart disease and diabetes. It could mean more regular screenings and early interventions, such as taking anti-amyloid drugs and incorporating lifestyle and diet changes before the disease gets out of control. And for those already diagnosed, it means using a combination of therapies that target different aspects of the disease, such as neuroinflammation and plaque buildup.

“We can’t just wait until the brain deteriorates,” he says.

With the current momentum, Porsteinsson hopes that young and aspiring physician-scientists will be inspired to join the field and continue the research for generations to come.

“What many medical students and young doctors have historically been hesitant about is that dementia is very nebulous, there is a lot of gray there. … They felt things were pretty bleak, too uncertain, and there was too little you could offer,” he says. “Now, I think we are at the dawn of a very different era.”

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Make an Impact in the Fight to End Alzheimer's

Today's dementia research investments are tomorrow's breakthroughs., that's why we invested $100 million in research in 2023 — the most the alzheimer’s association has devoted to dementia research in a single year. help us speed scientific progress toward a world without alzheimer's and all other dementia while providing care and support to those facing alzheimer's today..

Donate Today

In 2023, the Alzheimer's Association invested a record-breaking $100 million in research initiatives.

This unparalleled commitment to dementia science is our biggest single-year investment since the Alzheimer's Association was founded in 1980. And we have the momentum to keep going.

As the world's largest nonprofit funder of Alzheimer's research, the Alzheimer's Association has played a vital role in nearly every significant development in dementia research. Our strategic investments go toward advancing understanding of the disease, identifying new treatment strategies, improving care for people with dementia and furthering our knowledge of brain health.

As the world's largest nonprofit funder of Alzheimer's research, the Alzheimer's Association has played a vital role in nearly every significant development in dementia research. Our strategic investments go toward advancing understanding of the disease, identifying new treatment strategies, improving care for people with dementia and furthering our knowledge of brain health.  

Join the worldwide movement to fight Alzheimer’s and all other dementia when you support the Alzheimer’s Association.

"This opens a new door for Alzheimer’s research. And through that door are new opportunities for treatments."

– Yakeel T. Quiroz, Ph.D., whose work is partially funded by an Alzheimer's Association grant. Quiroz studies how a rare gene variant — the Christchurch variant — may be a key to slowing the progression of Alzheimer's. Learn more about Quiroz's research .

"My focus on the Black community in this grant is due to the underrepresentation of Black people in research, but overrepresentation in poor health outcomes."

– Antoine Trammell, M.D., MPH, Alzheimer's Association Research Grant recipient. Trammell examines whether a blood pressure medication could decrease the incidence of cognitive impairment and dementia in Black people. Learn more about Trammell's research .

"As we continue to move research forward and give patients access to novel therapies, I look forward to the opportunities to slow disease progression in the future."

– Ross Paterson, Ph.D., Part the Cloud grant recipient. Paterson's study aims to identify a novel drug therapy to reduce dementia-related tau production in people with Alzheimer’s. Learn more about Paterson's research .

From funding high-impact, best-in-class research projects…

The International Research Grant Program supports investigators at every professional stage and includes categories designed to address gaps in research efforts.

Part the Cloud funds novel research ideas to accelerate them from the laboratory, through clinical trials and into practice.

…to connecting people with trials and treatments…

TrialMatch ® is a free service that connects individuals living with Alzheimer's, caregivers and healthy volunteers to clinical trials that may advance Alzheimer's research.

Alzheimer's Network for Treatment and Diagnostics (ALZ-NET) connects clinical data from Alzheimer’s patients to medical professionals and researchers, promoting information sharing and education.

A study for people from diverse backgrounds, New IDEAS uses medical brain imaging to inform more accurate diagnoses and care for people with memory concerns.

The clinical trial U.S. POINTER evaluated the impact of lifestyle interventions on cognitive function — the first such study to be conducted in a large group of Americans across the U.S.

…to bringing the research community together…

Alzheimer's Association International Conference ® is the largest international meeting dedicated to advancing dementia science. AAIC convenes researchers, clinicians and dementia professionals from all career stages.

Alzheimer's & Dementia is the top-ranking peer-reviewed journal of dementia science and the parent of two companion journals.

An inclusive global network of scientists, clinicians and dementia professionals, ISTAART has more than 10,000 members in over 120 countries.

…the Alzheimer's Association is the organization that keeps the momentum going.

We are dedicated to accelerating the global effort to eliminate Alzheimer's and all other dementia. Learn more about projects the Association funds, conferences we convene, our advocacy efforts and other initiatives that show our commitment to research .

A world without Alzheimer's and all other dementia is within reach. But we can't lose momentum now.

Not only is the Alzheimer's Association the largest nonprofit funder of Alzheimer's research, but we are also one of the most trustworthy nonprofits. We've earned four stars from Charity Navigator and Platinum from Candid — the highest possible ratings. When you support the Alzheimer's Association, you can be confident you're helping to further the fight against Alzheimer's and all other dementia.

New Diffusion Basis Spectrum Imaging and Brain PET Identify Neuroinflammation and AD In Overweight and Obese Persons

Rsna research scholar grant recipient establishes nih-funded laboratory during covid-19 pandemic.

The risk of Alzheimer’s disease (AD) is increasingly recognized as modifiable by disorders arising from lifestyle, such as lack of exercise that can lead to unhealthy weight and obesity. Recently the Alzheimer’s Association and National Institute on Aging issued a new research framework for AD, focusing on biomarkers for amyloid (A), tau (T), and neurodegeneration (N).

Inclusion of obesity measures and metabolism into studies of AD based on the A-T-N framework allows for the expansion of the paradigm which could potentially lead to more personalized therapeutic interventions in the future.

Abnormally high body tissue adiposity is recognized as an attributable risk for dementia; in the U.S., midlife obesity increases the lifetime risk of dementia by 7.3%. Being overweight or obese in late life has been correlated with reduced brain volumes on MRI in regions important for memory and affected by AD pathology such as the hippocampus and posterior cingulate. However, evidence is emerging that differences exist between those who are overweight/obese and metabolically normal, and those who are metabolically abnormal.

In his 2019 RSNA Research Scholar Grant, “Diffusion Basis Spectrum Imaging for Quantifying Neuroinflammation in Metabolically Abnormal Overweight and Obese Persons at Risk for Alzheimer's Disease,” Cyrus A. Raji, MD, PhD, associate professor of radiology and director, Neuromagnetic Resonance Imaging at Mallinckrodt Institute of Radiology at Washington University School of Medicine, St. Louis, and his team hypothesized that metabolically abnormal overweight/obese individuals will have advanced A, T, and N pathology and increased neuroinflammation compared to metabolically normal overweight/obese and non-overweight individuals.

“The insulin resistance related to metabolically abnormal overweight and obese states can promote impaired clearance of amyloid, a key protein linked to the pathogenesis of Alzheimer's disease,” Dr. Raji said. “Additionally, metabolically abnormal overweight/obese states promote a pro-inflammatory state that can specifically increase neuroinflammation in the brain and consequently cerebral atrophy—a key feature of neurodegeneration in Alzheimer's disease.” 

Combined Imaging Focused on Brain Atrophy and Tau Deposition

Dr. Raji and his team evaluated brain atrophy on MR imaging to assess whether differences in neurodegeneration existed between metabolically abnormal and metabolically normal overweight and obese controls. All were cognitively normal. The cross-sectional study defined the metabolically abnormal overweight and obese categories using a combination of body mass index (BMI) greater than or equal to 25, which encompassed the overweight and obese groups, and a hemoglobin A1c of greater than or equal to 5.7.  They compared this group to metabolically normal overweight and obese participants and metabolically normal non-overweight participants.

They also evaluated neuroinflammation using a new type of diffusion MR imaging called diffusion basis spectrum imaging (DBSI), and AD pathology as characterized by amyloid and tau PET imaging.

“Diffusion basis spectrum imaging is a high-resolution diffusion MR imaging technique that can model the amount of extracellular water and cellular infiltration at the microstructural level in the white matter as imaging correlates of neuroinflammation. Neuroinflammation in turn has been linked to increased neurodegeneration as evidenced by increased brain atrophy,” Dr. Raji said.

The research compared the groups’ DBSI, atrophy, and amyloid and available tau imaging metrics. The preliminary data suggested a comparatively higher amount of brain atrophy and tau deposition in metabolically abnormal overweight and obese participants. 

Study Looked at Mid-Life and Younger Patients

A separate study in younger cognitively normal participants, 40-60 years old further refined the researchers’ understanding of obesity by going beyond BMI and measuring visceral and subcutaneous fat on abdominal MRI obtained at the same time as brain MRI with DBSI. The study correlated these measures along with cerebral volumetric analysis and the amyloid and tau PET markers for AD.

The researchers then statistically modeled the relationship between visceral fat and amyloid PET as well as brain atrophy metrics along with tau PET. They repeated the same analysis using subcutaneous fat as the predictor variable. They also performed these analyses evaluating these fat metrics against DBSI neuroinflammation imaging and MRI atrophy. 

“In our initial study of our midlife participants, we show that visceral fat is correlated with metabolically abnormal overweight and obese states, which makes sense given its tight link with insulin resistance. By contrast, subcutaneous fat was not found to have such a relationship, and this is important because 85% of BMI variance is due to subcutaneous fat and not visceral fat,” Dr. Raji said. “This is why visceral fat is called ‘hidden fat.’ It is considered to be a less healthy type of fat, related to its strong connection to metabolic abnormalities in pre-diabetes and diabetic states.”

The researchers found that in the midlife research participants, increased visceral fat predicts increased amyloid deposition on brain PET as well as a higher burden of entorhinal atrophy. By contrast, they did not find such a relationship between subcutaneous fat and the brain imaging metrics. This initial work was published in Aging and Disease with subsequent research on visceral fat predicting a higher burden of white matter neuroinflammation on DBSI being presented at RSNA 2023 .

For patients who struggle with their weight, Dr. Raji and his team found that mid-life obesity, occurring primarily between age 40-60 years, is the strongest predictor of future AD.

“Weight management during this time is especially crucial for reducing the risk of Alzheimer's. While behavioral steps towards healthier diets, calorie restriction and physical activity can certainly help in controlling weight, there is also increased interest in using recently innovated drugs, such as semaglutide and tirzepatide, for weight loss as well,” Dr. Raji said. “However, a pharmacological approach that uses midlife weight control towards future Alzheimer's prevention requires additional and separate research investigations.”

R&E Foundation Grant Leads to NIH Funding

Dr. Raji’s research was challenged during the COVID-19 pandemic, particularly in obtaining preliminary data due to the shutdown of human participant research in the initial months of the crisis.

“However, with the progress I had already made from the RSNA R&E Research Scholar Grant, I was able to obtain preliminary data. That in combination with the RSNA Advanced Course in Grant Writing resulted in a successful grant application to the NIH in 2020 that was funded in the amount of $2.3 million in 2021,” Dr. Raji said.

As the pandemic abated and studies of research participants were permitted to resume, Dr. Raji and his team were able to move the study forward with NIH support.

“This success led to the creation of my independent laboratory, the Raji Brain Health Imaging Lab and I have since been promoted to associate professor with tenure in the Washington University in St. Louis Mallinckrodt Institute of Radiology with a secondary appointment in the Department of Neurology,” Dr. Raji said. “Such outcomes would not have been possible without the supportive resources of RSNA overall and the R&E Foundation in particular.”

For More Information

Learn more about R&E Foundation grants at  RSNA.org/Research/Funding-Opportunities .

Read previous  RSNA News  stories about R&E Foundation grants:

• Toward More Minimally Invasive Therapy for Mesial Temporal Lobe Epilepsy
• Intensive Blood Pressure Lowering Safe, Beneficial for Brain Health
• Researching the Effects of Brain Tumor Removal on Language

Allegations of fabricated research undermine key Alzheimer’s theory

Allegations that part of a key 2006 study of Alzheimer's disease may have been fabricated have rocked the research community, calling into question the validity of the study's influential results.

Science magazine said Thursday that it uncovered evidence that images in the much-cited study, published 16 years ago in the journal Nature, may have been doctored.

The findings have thrown skepticism on the work of Sylvain Lesné, a neuroscientist and associate professor at the University of Minnesota, and his research, which fueled interest in a specific assembly of proteins as a promising target for treatment of Alzheimer's disease. Lesné didn’t respond to NBC News’ requests for comment, nor did he provide comment to Science magazine.

Science said it found more than 20 "suspect" papers by Lesné and identified more than 70 instances of possible image tampering in his studies. A whistleblower, Dr. Matthew Schrag, a neuroscientist at Vanderbilt University, raised concerns last year about the possible manipulation of images in multiple papers.

Karl Herrup, a professor of neurobiology at the University of Pittsburgh Brain Institute who wasn’t involved in the investigation, said the findings are "really bad for science."

"It's never shameful to be wrong in science," said Herrup, who also works at the school's Alzheimer's Disease Research Center. "A lot of the best science was done by people being wrong and proving first if they were wrong and then why they were wrong. What is completely toxic to science is to be fraudulent."

For decades, a leading theory stated that the amyloid beta protein formed sticky plaques in the brain that were the main cause of Alzheimer’s.

The 2006 study in Nature identified a subtype of the protein — Aβ*56, or "amyloid beta star 56" — as the cause of memory loss in rats.

The paper caused "a big splash at the time," said Donna Wilcock, the assistant dean of biomedicine at the University of Kentucky.

But Science magazine said it found evidence that the paper's images — and images in other studies on Aβ*56 by Lesné — had been doctored to inflate the protein's role in the progression to Alzheimer’s, according to experts like Wilcock who reviewed the images for Science.

Other researchers expressed concern that Lesné's results couldn’t be replicated, a key part of the scientific process to confirm the validity of certain findings.

"In my own work, [Aβ*56] was not a species ... that we had ever observed," said Dr. Thomas Wisniewski, a professor of neurology at the New York University Alzheimer’s Disease Center.

Wisniewski, who wasn’t involved in the investigation, said he looked at the images Monday and saw "evidence of what looks like copy and paste" to make a composite picture.

Wilcock said she also noticed small areas of the images that appeared to have been "selectively enhanced."

Dr. Karen Ashe, a neuroscientist and professor at the University of Minnesota who co-authored the 2006 paper, said her wish is to retract the study in its entirety, citing that confidence in it has been undermined — but she also maintained that a retraction "does not call the amyloid-beta hypothesis into question."

"Having worked for decades to understand the cause of Alzheimer disease, so that better treatments can be found for patients, it is devastating to discover that a co-worker may have misled me and the scientific community through the doctoring of images," she said in an emailed statement.

Kat Dodge, a spokesperson for the University of Minnesota Medical School, said the institution is aware of questions surrounding studies published by Lesné and Ashe.

"The University will follow its processes to review the questions any claims have raised," she said Monday in a statement provided to NBC News.

Nature issued a publisher's note July 14 saying that it was investigating the concerns about the 2006 paper and that "a further editorial response will follow as soon as possible."

More than $1 billion of government funding, through the National Institutes of Health, has been directed to amyloid-related Alzheimer's research. While the investigation suggests that studies of Aβ*56 should be opened up to new scrutiny, experts said the entire theory shouldn’t be discredited.

"Further work needs to be done by other groups to specifically try to reproduce this work in other experimental models," Wisniewski said.

Herrup said it wasn't just Lesné's work that influenced the direction of Alzheimer's research over the past two decades.

"There were so many other forces driving that conceptualization of the disease," he said.

But such incidents can be enormously damaging to scientists and the broader research community, experts said.

"It really hurts and erodes the public trust in the scientific process," Wilcock said. "That's what is the most disturbing and upsetting to me as a scientist."

Aria Bendix is the breaking health reporter for NBC News Digital.

Denise Chow is a reporter for NBC News Science focused on general science and climate change.

Alzheimer's Drug Adoption in US Slowed by Doctors' Skepticism

Alzheimer's Drug Adoption in US Slowed by Doctors' Skepticism

Lyn Castellano receives infusions of Eisai and Biogen's Alzheimer's drug Leqembi, alongside her service dog Jazmin at the Missouri Baptist Medical Center Infusion Center in St. Louis, Missouri, U.S. October 30, 2023. Joe Castellano/Handout via REUTERS

CHICAGO (Reuters) - Nine months into the U.S. launch of the first drug proven to slow the advance of Alzheimer's, Eisai and Biogen's Leqembi is facing an unexpected hurdle to widespread use: an entrenched belief among some doctors that treating the memory-robbing disease is futile.

Alzheimer's experts had anticipated bottlenecks due to Leqembi's requirements, which include additional diagnostic tests, twice-monthly infusions and regular brain scans to guard against potentially lethal side effects.

And those issues have played a role in slow adoption since the drug was approved by the U.S. Food and Drug Administration, according to interviews with 20 neurologists and geriatricians from rural, urban, academic and community practices in 19 states.

In interviews with Reuters, seven doctors treating patients for Alzheimer's attributed their own reluctance to prescribe Leqembi to concerns about the drug's efficacy, cost and risks. 

"I don't think it's a good Alzheimer's drug. I think that's the problem," said Dr. James Burke, a neurologist at the Ohio State University who has been an outspoken critic of Leqembi. "It's certainly nothing like the home run that we're looking for."

Another six scientists, all leaders in the field, said "therapeutic nihilism" – the belief that Alzheimer's is a hopelessly intractable disease – was playing a bigger role than anticipated in suppressing demand from primary care doctors, geriatricians and neurologists who could be sending patients to memory specialists for treatment.

Dr. Reisa Sperling, a neurologist and Alzheimer's researcher at Mass General Brigham in Boston, likens some doctors' skepticism to Leqembi to fatalistic attitudes about cancer treatment 30 years ago: "You can't really do anything about it, so why would you even want to get tested?"

Alex Scott, Eisai's chief administrative officer, acknowledged that skepticism has weighed on the launch along with slower-than-expected adoption by large health systems.

He suggested that some of the doctors' hesitancy could be a holdover from the decades-long journey to prove that removing the Alzheimer's protein beta amyloid from the brain could slow the course of the disease. Before Esai released the promising results of its Leqembi trial, some thought that area of research "a fool's errand," Scott said.

"We are beginning to make more and more progress every single month. So we're still quite encouraged," Scott said. "This is a new journey, and I think it takes some time for providers to figure it out."

'SIGNIFICANT RISKS, MARGINAL BENEFIT'

Leqembi was the first amyloid-targeting drug granted full FDA approval after it slowed the decline in cognition in people in the early stages of Alzheimer's by 27% in a clinical trial.

Of the 10,000 Americans the companies hoped to treat by the end of March, Eisai announced only a couple thousand had begun treatment as of the end of January. An Eisai spokeswoman declined to provide updated numbers.

Even for treatments that do not require dramatic changes to medical practice, adoption of new drugs is notoriously slow. Several studies have estimated that it can take 17 years on average for clinical research to be translated into routine practice.

The disease is estimated to affect more than 6 million Americans, according to the Alzheimer's Association.

Fewer than half of U.S. neurologists recommend Leqembi to patients, according to a January survey by life sciences market researcher Spherix Global Insights.

Dr. Michael Greicius, a professor at Stanford University's Center for Memory Disorders, said there is little evidence that Leqembi benefits patients in a meaningful way.

"If we take the trial result at face value, the differences between placebo and treatment are likely small enough as to be undetectable by patients and family members or physicians," said Greicius, who does not recommend Leqembi to patients.

He said the long wait for an Alzheimer's drug has put doctors in the position of feeling obligated to offer a treatment "even if the evidence for it is very slim."

Other doctors have raised concerns about the risk of brain swelling and bleeding associated with Leqembi as well as the costs associated with the $26,500 annual drug, frequent MRIs and twice-monthly infusions.

"There are significant risks associated with these drugs, there are significant costs, and I would say there is marginal benefit," said Dr. Eric Widera, a geriatrician and professor at University of California San Francisco, referring to amyloid-lowering treatments.

In an editorial published in November in the Journal of Gerontological Nursing, Donna Fick, president of the American Geriatrics Society, advised doctors that the group recommends caution in the use of lecanemab, which is sold under the brand name of Leqembi. 

"It is not yet clear whether treatments such as lecanemab that remove amyloid from the brain produce clinically important slowing of cognitive decline in Alzheimer's disease."

'YOUR ENEMY IS NIHILISM'

Dr. Jonathan Liss, a neurologist from Columbus, Georgia, who serves on Eisai's scientific advisory board and has tested Leqembi in clinical trials, said he first warned about nihilism at a November 2022 conference following a presentation of Leqembi's breakthrough study.

Eisai had asked its scientific advisors how the drug might fare against future rivals. Liss cautioned that rivals were not the enemy; "your enemy is nihilism,'" he recalled. "All of the neurologists around the table started applauding."

Dr. Nathaniel Chin, a geriatrician with the University of Wisconsin's Alzheimer's Disease Research Center, said he was the target of negative comments on social media after he urged geriatricians to embrace such treatments in the Journal of the American Geriatrics Society.

Geriatricians, geriatric social workers and nurses objected, arguing that the drug's statistically significant benefit was not clinically meaningful to patients, especially given the risks, he said.

"I would ask the question, 'Is it ethical to withhold a medication that is FDA-approved and covered by insurance from someone who knows the risk and is willing to take it?'" Chin said.

Dr. Priya Singhal, executive vice president and head of development at Biogen, acknowledged some apathy among physicians about the treatment but said that infrastructure and lack of access to neurologists have been bigger issues.

Singhal said the companies are working with physician and patient advocacy groups and developing educational programs and materials aimed at diagnosing early-stage patients, managing side effects and understanding the drug's benefits.

The companies said they intend to increase their salesforce by 30% as they aim for 100,000 patients by 2026.

For the moment, Leqembi is the only Alzheimer's drug on the market designed to slow the course of the disease. A decision on Lilly's donanemab has been delayed until the FDA convenes an advisory panel.

Lilly neuroscience president Anne White said in an interview that she sees doctor hesitancy as an issue that the company hopes to address by making clear which patients benefit from such treatments.

In the early stages of Alzheimer's, many patients are still independent, and to be able to remain so for longer is very meaningful, she said.

'PEACE AND QUIET'

Lyn Castellano, 64, who founded and ran a St. Louis breast cancer charity for 20 years and trained therapy dogs, started taking Leqembi last September, nearly a year after she found herself struggling with keeping track of appointments and was diagnosed with mild cognitive impairment.

Castellano said the prospect of bleeding in the brain – a possible side effect of the drug - was her biggest concern, but her family believed the drug may offer a chance at slowing the disease.

She is one of more than 140 patients being treated by physicians from Washington University in St. Louis, and has had 13 infusions and two MRIs without incident.

Dr. Suzanne Schindler, an Alzheimer's researcher who is treating Castellano, said Leqembi "forces clinicians to completely change the way they have practiced medicine for many years."

She said she is candid about Leqembi's modest benefit as well as the risks. About 80% of those she believes are good candidates have opted for the treatment, she said.

While Castellano can't tell if Leqembi is helping, she says the treatment has given her hope, and she doesn't mind the twice monthly infusions.

"I get to go, sit back in a nice chair, have my dog with me and read a book for a couple hours. It's about the only place I get some peace and quiet."

(Reporting by Julie Steenhuysen in Chicago; editing by Caroline Humer and Suzanne Goldenberg)

Copyright 2024 Thomson Reuters .

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Alzheimer's Association unveils research for risk reduction and treatment in Chico

by Hannah Gutierrez

CHICO, Calif. — On Wednesday evening, the Alzheimer's Association, in partnership with North Valley Indian Health and Butte County Public Health's Healthy Brain Initiative, hosted an event in Chico to unveil the latest research on Alzheimer's and Dementia. The event aimed to educate the community on treatments, lifestyle changes and new research findings that can help reduce the risks of Alzheimer's and dementia.

“Alzheimer’s is not just impacting people over the age of 65, and so there is some research being done that is really trying to understand some of the younger onset, those people are diagnosed earlier than the age of 65," said Claire Day, Chief Program Officer with the Alzheimer's Association Northern California-Northern Nevada chapter.

Dementia is a term used to describe a decline in cognitive abilities, such as memory loss, thinking skills, and problem-solving. Alzheimer's is a specific type of Dementia that accounts for a significant percentage of Dementia cases, ranging from 60% to 80%, according to the Alzheimer's Association.

“There is a difference between normal aging memory loss, which we all experience, and cognitive loss because of a dementia, or memory loss because of a dementia," said Day.

The Alzheimer's Association outlines 10 early signs of Alzheimer's and Dementia , including:

• Life disruptions caused by memory loss.
• Problem solving/planning challenges.
• Difficulty completing routine tasks.
• Confusing the time or place.
• Difficulty understanding images and space.
• New problems speaking or writing words.
• Misplacing items/difficulty recalling steps.
• Changes in decision making.
• Work and social withdrawals.
• Mood and personality changes.

The Butte County 2023 Community Health Assessment found that the rate of deaths associated with Alzheimer's in the county is higher than the state average, standing at 44.6% per 100,000 people.

“In California, more than 700,000 people are living with Alzheimer’s disease, we know that age is our biggest risk factor: One in three over the age of 85 and one in nine over the age of 65," explained Day.

The Alzheimer's Association provides information on various treatments and methods of mitigating the risk of Alzheimer's later in life. They emphasize that it's never too early or late to learn more about the risks and ways to decrease them, including maintaining a healthy diet, exercising regularly, and getting sufficient sleep.

“There’s been some recent FDA approvals of something that we call a Monoclonal Antibody. These are interventions that are actually designed to address the underlying biology of the disease," Day said.

The event allowed community members to learn the latest findings on Alzheimer's and Dementia, ask questions, and gain insights into how to reduce the risks of these cognitive diseases.

“It doesn’t mean if you do all these things you won’t get Alzheimer’s and Dementia, unfortunately we know that’s not the case, but we do think that it is a big step in decreasing your risk of getting Dementia," Day concluded.

For resources from the Alzheimer's Association, click here or call their 24-hour hotline at (800) 272-3900. For assistance in Butte County specifically, click here .

To report errors or issues with this article please email the editorial team.

Childhood dementia research gets funding boost from SA government and Little Heroes Foundation

Renee Staska's seven-year-old daughter Holly dreams of one day captaining the Port Adelaide women's football team.

But time is not on the side of the avid AFL fan, who alongside her five-and nine-year-old brothers, lives with a terminal illness.

"They think they're the fastest, the strongest, they have huge dreams," Ms Staska said.

"I don't want to be the one that takes the wind out of their sails and tells them that something is really wrong here.

"I just think they have every right to fulfil their dreams as much as they can."

The Adelaide siblings have all been diagnosed with Niemann-Pick Type C, which is one of more than 100 genetic conditions under the umbrella of childhood dementia.

According to the Australian Niemann-Pick Type C Disease Foundation, the disease causes an accumulation of cholesterol and other fatty acids in the body's cells, leading to progressive intellectual decline, loss of motor skills, seizures and dementia.

Most children with the illness die before turning 18.

Ms Staska said her children are already displaying symptoms.

"They are really struggling to keep up with their peers, they're struggling to participate in school, reading, writing, concentration," she said.

"They get sick quite a lot and it takes them quite a long time to rebound.

"But these symptoms are nothing compared to what they have on the horizon."

Calls for funding answered

The State of Childhood Dementia 2022 report states that about 90 children die in Australia every year from childhood dementia – a similar number of deaths as from childhood cancer.

Despite the high fatality rate, a report released by the Childhood Dementia Initiative last month found the condition received more than four times less government research funding than childhood cancer per patient.

After years of campaigning, researchers in South Australia have received $500,000 from the state government and Little Heroes Foundation charity, to grow childhood dementia research at Flinders University.

"It will allow our research group to grow what we do from single disorder research to multiple childhood dementia research," Flinders University professor Kim Hemsley said.

"The investment is also going to develop the next generation of childhood dementia researchers, which is incredibly important.

"We all hope that these disorders will be treated in our lifetime, I sincerely hope that's so, but we need more researchers in this field to help us make that happen."

SA government stepping in

SA Health Minister Chris Picton said the $250,000 contribution from the state government was a "one-off", but he was "open to having ongoing discussions with both Flinders University and Little Heroes Foundation".

"[The] state government generally doesn't provide research funding, that's generally done through the NHMRC (National Health and Medical Research Council), but… there's a relatively narrow amount of money that's been coming through the NHMRC grant process for childhood dementia compared to other conditions," he said.

"I think that's an appropriate reason for us to step in on this occasion."

The SA Premier Peter Malinauskas said around 150 South Australian children have childhood dementia.

He said the funding contribution from the state government was made following advocacy from One Nation upper house MP, Sarah Game.

"I can't think of anything more harrowing for a parent than the idea of having a child with dementia," he said during an at-times emotional press conference.

Little Heroes Foundation CEO Chris McDermott said only about 10 per cent of people know about childhood dementia and more community education was needed.

'We spend a lot of time hugging'

Ms Staska, who first spoke to the ABC about her children's condition in 2022 , described the funding announcement as "life-changing". 

She said the years ahead were "frightening", but her family tried to make the most of every day.

"That means saying 'yes' to a lot of things and exposing them [the children] to as many life experiences as I can," she said.

"We spend a lot more time hugging and we spend a lot more time having fun and making memories.

"There are families all over the country just like mine with children who are rapidly regressing and time is not on our side."

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• Alzheimer's and Dementia
• Child Health and Behaviour
• Diseases and Disorders
• Family and Relationships
• Genetic disorders
• Health Policy
• Infant Health
• State and Territory Government