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Primary Prevention Trial

While the trial is limited to members of families with genetic mutations that all but guarantee they will develop Alzheimer’s at a young age, typically in their 30s, 40s or 50s, the researchers expect that the study’s results will inform prevention and treatment efforts for all forms of Alzheimer’s disease.

Called the Primary Prevention Trial, the new study investigates whether remternetug — an investigational antibody being developed by Eli Lilly and Company — can remove plaques of a key Alzheimer’s protein called amyloid beta from the brain or block them from accumulating in the first place. Both genetic and nongenetic forms of Alzheimer’s disease start with amyloid slowly collecting in the brain two decades before memory and thinking problems arise. By clearing out low levels of amyloid beta plaques or preventing them from accumulating during the early, asymptomatic phase of the disease, or both, the researchers hope to interrupt the disease process at the earliest stage and spare people from ever developing symptoms.

“We have seen tremendous progress in the treatment of Alzheimer disease in the past few years,” said Eric McDade, DO, a professor of neurology and the trial’s principal investigator. “Two amyloid-targeting drugs were shown to slow symptoms of the disease and have now been approved by the Food and Drug Administration (FDA) as treatments for people with mild cognitive impairment or mild dementia due to Alzheimer’s disease. This provides strong support for our hypothesis that intervening when amyloid beta plaques are at the very earliest stage, long before symptoms arise, could prevent symptoms from emerging in the first place.”

The trial is part of the Knight Family Dominantly Inherited Alzheimer Network-Trials Unit (Knight Family DIAN-TU), a clinical trials platform designed to find medicines to prevent or treat Alzheimer’s disease. It is closely associated with DIAN, a National Institutes of Health (NIH)-funded international research network led by WashU Medicine that involves research institutes in North America, Australia, Europe, Asia and South America. DIAN follows families with mutations in any of three genes that cause Alzheimer’s at a young age. A child born into such a family has a 50% chance of inheriting such a mutation, and those who do so typically develop signs of dementia near the same age his or her parent did. All the participants in the Primary Prevention Trial come from such families.

“My grandfather passed away from Alzheimer’s, and so did his mother and all but one of his brothers,” said Hannah Richardson, 24, a participant in the Primary Prevention Trial. “My mom and my uncle have been participating in DIAN trials since I was about 10 years old. My mom was always very open about her diagnosis and how it spurred her advocacy for Alzheimer’s research, and I’ve always known I wanted to follow in her footsteps. I am happy to be involved in the Primary Prevention Trial and be involved in research because I know how important it is.”


Cancer’s ripple effect may promote blood clot formation in the lungs

Blood clots form in response to signals from the lungs of cancer patients—not from other organ sites, as previously thought—according to a preclinical study by Weill Cornell Medicine, Memorial Sloan Kettering Cancer Center and University of California San Diego Health. Clots are the second-leading cause of death among cancer patients with advanced disease or aggressive tumors.

While blood clots usually form to stop a wound from bleeding, cancer patients can form clots without injury, plugging up vessels and cutting off circulation to organs. The study, published in Cell, shows that tumors drive clot formation (thrombosis) by releasing chemokines, secreted proteins which then circulate to the lung. Once there, the chemokines prompt immune cells called macrophages to release small vesicles that attach to cell fragments (platelets), forming life-threatening clots.

The findings may lead to to determine blood clotting risk and safer therapies that target the root of the problem to prevent blood clots.

Medical Breakthroughs May Mean That More People Will Live To Be Over 100

Medical breakthroughs could mean that more of us will live to be 100 or even more, according to longevity medicine expert Dr. Edouard Debonneuil co-founder of the London-based Longevity Clinic who says that modern technology, new medicine, additional medical breakthroughs, and healthy living could help more of us reach that mammoth milestone.

“If the current trend continues, we could see individuals living to 140 or 150 in good health. While that might sound sensational, it’s grounded in science and the longevity field is booming because of these breakthroughs,” said Dr. Debonneuil after a first-of-its-kind study, Rejuvenation Olympics, which produced promising anti-aging results.

“One of the guys taking part is in his 60’s but biologically he resembles someone in their later 30’s. Some participants halved their biological age within two to three years and have reduced their ageing rate by 40 percent. This is a significant leap in human history, we now have the tools to age slowly,” continued Debonneuil.

Brain-computer interface study wins 2025 Top Ten Clinical Research Achievement Award

UC Davis Health is pleased to announce that Neurosurgeon David Brandman and his team at UC Davis Neuroprosthetics Lab were selected for a 2025 Top Ten Clinical Research Achievement Award. The Clinical Research Forum presents this award to honor 10 outstanding clinical research studies published in peer-reviewed journals in the previous year. This year’s Top 10 Awards ceremony will be held on April 14 in Washington, D.C.

Brandman and his team are recognized for their groundbreaking work in developing a new brain-computer interface (BCI) that translates brain signals into speech with up to 97% accuracy — the most accurate system of its kind. Their work was published in the New England Journal of Medicine.

“Our team is very honored that our study was selected among the nation’s best published clinical research studies. Our work demonstrates the most accurate speech neuroprosthesis (device) ever reported,” said Brandman, co-director of the Neuroprosthetics Lab. He is an assistant professor in the UC Davis Department of Neurological Surgery.

Vitamin K supplement slows prostate cancer in mice

This is probably a repost, but cool anyways.

CSHL Professor Lloyd Trotman and his team have discovered that menadione kills prostate cancer cells in mice by depleting a lipid known as PIP. Their findings set the stage for pilot studies in human prostate cancer patients and point to a potential treatment target for myotubular myopathy, a rare and fatal disease diagnosed in infant boys.


Prostate cancer is a quiet killer. In most men, it’s treatable. However, in some cases, it resists all known therapies and turns extremely deadly. A new discovery at Cold Spring Harbor Laboratory (CSHL) points to a potentially groundbreaking solution. CSHL Professor Lloyd Trotman’s lab has found that the pro-oxidant supplement menadione slows prostate cancer progression in mice. The supplement is a precursor to vitamin K, commonly found in leafy greens. The story begins more than two decades ago.

Breakthrough Drug Reverses Aging in Skin, Speeds Up Healing

Topical ABT-263 effectively reduced several senescence markers in aged skin, preparing it for improved wound healing. Researchers from Boston University’s School of Medicine have identified a promising treatment that could improve wound healing in aging skin. Their study, published in the journal Aging, reveals that the drug ABT-263 can significantly accelerate skin repair by eliminating old, damaged cells known as senescent cells.

Cyclarity Therapeutics Secures Approval for First-in-Human Clinical Trial

From the press release.

Cyclarity Therapeutics is pleased to announce regulatory approval to begin its first-in-human clinical trial. The trial will be conducted at CMAX, one of Australia’s leading clinical research centers, in partnership with Monash University. This effort will be led by Dr. Stephen Nicholls of the Victorian Heart Institute (VHI), a distinguished leader in cardiovascular medicine. In addition to a traditional SAD/MAD phase 1 trial, the authorization includes an allowance to enroll 12 patients with Acute Coronary Syndrome (ACS) to assess the safety of UDP-003 in individuals with plaque buildup, as well as to explore anecdotal evidence of efficacy. This represents a critical first step in evaluating the potential impact of our therapy in a population with high unmet need.

Pancreatic blood vessel cell map reveals potential diabetes treatment pathways

The distinct population of endothelial cells that line blood vessels in the insulin-producing “islets” of the human pancreas have been notoriously difficult to study, but Weill Cornell Medicine investigators have now succeeded in comprehensively detailing the unique characteristics of these cells.

The resulting atlas advances basic research on the biology of the pancreas and could lead to new treatment strategies for diabetes and other pancreatic diseases.

In the study, published in Nature Communications, the researchers devised a set of methods for rapidly isolating and profiling endothelial cells called ISECs (islet-specific endothelial cells) from donor pancreases.

Disruption of a single amino acid in a cellular protein makes breast cancer cells behave like stem cells

Vimentin is a type III intermediate filament (IF) protein normally expressed in cells that develop into connective tissue, blood vessels, and lymphatic tissue (mesenchymal cells). Despite being widely studied, its role in tumor growth and progression remains unexplored.

A team of researchers at Queen Mary University of London have discovered how a small change in the vimentin protein can make more aggressive. The work is published in the journal eLife.

By modifying a specific amino acid cysteine to serine residue at position 328 in vimentin, they discovered that this mutation disrupted the protein’s interaction with the cell’s structural network. Remarkably, the mutated vimentin induced aggressive cancer-like behavior in breast cancer cells, including faster cell growth, migration, and invasion accompanied by reduced .

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