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Alzheimer’s trial to test drug on people without symptoms to see if it can be prevented

Healthy middle-aged people deemed to be at higher risk of developing condition among those eligible to participate People without memory loss will be offered an experimental Alzheimer’s drug that could stop the development of the condition before dementia symptoms emerge. Healthy middle-aged people deemed to have a higher risk of developing the condition will be eligible to participate in the trial, which is being run by an NHS trust as part of an international clinical trial aiming to prevent dementia. Continue reading...

Early mitochondrial stress reveals potential mechanism for lasting heart protection

Mitochondria are popularly known as the "powerhouse of the cell," but these cellular structures do much more—including acting as signaling hubs. Some signals that mitochondria send can reprogram the activity of the entire cell by switching "on" or "off" different genes through epigenetic changes. Mitochondria's signals can be so effective that, in yeast, fruit flies and worms, mild stress in mitochondria early in life can make the entire organism more resilient and live longer through a process called mitohormesis.

Targeted Reduction of PTBP1 Reverses Cognitive Impairment in a Mouse Model of Alzheimer's Disease

Many of the more sophisticated forms of medicine, including gene therapies and immunotherapies, are challenging to deliver to the brain. At the very least there are far fewer practical options for delivery, and it is possible that none of that that exist fit a given desired use case. The blood-brain barrier stands in the way of intravenous injection as a path for most approaches, blocking passage of most cells and molecules from circulation to brain tissue. While direct injection into the brain or into reservoirs of cerebrospinal fluid can be achieved, they are sufficiently invasive and challenging to rule out commonplace use. The brain is made up of many different cell types, and more sophisticated approaches will want specificity to regions or cell types. Small […]

Stanford scientists discover a seafood that can reverse signs of aging

A substance found in edible sea squirts appeared to reverse several signs of aging in older mice. Plasmalogen supplements improved memory and learning, strengthened connections between brain cells, reduced inflammation, and even helped the mice grow thicker, darker hair. Researchers believe the compounds may encourage brain regeneration and protect aging synapses.

Scribe Therapeutics starts first human trial for cholesterol-lowering gene therapy

Scribe Therapeutics reported second-quarter 2026 financial results and pipeline progress. The company initiated a first-in-human phase 1 clinical trial of STX-1150 in Australia in mid-2026, according to the company, and presented late-breaking non-human primate data at the European Atherosclerosis Society showing up to 90% PCSK9 silencing and LDL-C reductions up to 68%, with a 0.75 […] The post Scribe Therapeutics starts first human trial for cholesterol-lowering gene therapy appeared first on Longevity.Technology.

Suggesting ERBB4 Overexpression as an Important Mechanism in Alzheimer's Disease

Researchers here suggest that increased ERBB4 expression in neurons is an important driving mechanism in the onset and progression of Alzheimer's disease. One has to be cautious with such findings, even given the effort made by the researchers to show that human data is compatible with the hypothesis, because the mouse models of Alzheimer's disease in which these sorts of discovery are made are very artificial. Mice do not normal exhibit anything like Alzheimer's disease, so the models induce forms of dysfunction that result in something resembling Alzheimer's in humans. The model embodies assumptions about relevant mechanisms that may not be correct, and this is one of the reasons why progress towards therapies has been slow and painful. Single-nucleus RNA-sequencing analysis identified the emergence of […]

Senescent Microglia Secrete DLK1, Which Causes Dysfunction in the Aging Brain

Senescent cells accumulate with age in tissues throughout the body, disrupting tissue structure and function with inflammatory secretions. The growing burden of senescent cells is an important contributing cause of degenerative aging. A cell becomes senescent in response to damage induced by some form of stress, or more often when a somatic cell reaches the Hayflick limit on cellular replication. In youth senescent cells are efficiently cleared by the immune system, but immune system aging allows senescent cells to linger and grow in number. Immune cells themselves are prone to reaching the Hayflick limit and entering replicative senescence because they respond to a variety of issues with greater replication to multiply their efforts. Research into neurodegenerative conditions and the state of the aging brain has […]

One immune switch may help drive aging across the body

Aging may be partly fueled by immune cells losing their ability to clear away damaged, inflammation-promoting cells. Blocking a single receptor restored that cleanup process in mice, reducing inflammation and helping their organs, muscles, and memory remain remarkably youthful.

GLP-1 receptor agonism extends median lifespan in mice

A consensus roadmap from the SENESCENCE2030 network towards precision senescence medicine

Senescent Cells in Metabolic Disorders

The most common metabolic diseases, such as type 2 diabetes or fatty liver disease leading to metabolic dysfunction-associated steatohepatitis (MASH), a fibrotic condition of the liver, are consequences of the dysfunctional state of metabolism that results from being overweight and sedentary. These conditions are rare in thin, fit people, even in later life when the damage of aging makes metabolism more vulnerable and inflammatory. Excess visceral fat tissue is known to promote the accumulation of senescent cells. While cells become senescent throughout life, in youth they are promptly cleared by the immune system. That clearance falters with age, allowing senescent cells to linger and accumulate. The metabolic dysfunction produced as a consequence of being overweight accelerates this process. In today's open access paper researchers review […]

GLP-1 treatment late in life extends lifespan in animal model

A study published in Nature has shown that the GLP-1 drug semaglutide extended the lifespan of older, healthy mice by tempering the detrimental effects of aging. Researchers at the University of California, Berkeley, directly compared the effects of the treatment with those of reduced food intake. They found that the drug mimicked the anti-aging benefits of calorie restriction, conferring even greater benefits in some areas.

Different Parts of the Brain Exhibit Different Vulnerability to Synucleinopathy

Parkinson's disease and Lewy body dementia are synucleinopathies, characterized by the spread of misfolded α-synuclein through the central nervous system. The presence of misfolded α-synuclein provokes harmful changes in cell behavior and ultimately cell death in important populations of neurons. Researchers here explore differences in the vulnerability of different parts of the brain to the pathology produced by misfolded α-synuclein. They conclude that more complex parts of the brain, characterized by increased mitochondrial activity and greater connectivity between neurons, are more fragile in the face of the pathological mechanisms of syncleinopathy. A total of 89 patients with dementia with Lewy bodies and 89 matched controls underwent T1-weighted brain MRI. Scans were processed to generate surface-based cortical thickness maps. Regional cortical thickness estimates, after slice-by-

Weight-loss drug slows ageing in female mice

Can GLP-1 drugs slow ageing? Mouse study shows promise

Late-life semaglutide treatment slows ageing and extends lifespan in female mice

Who decides what counts as longevity medicine?

Longevity is becoming big business, but the science, standards and clinical practices needed to guide the field are still catching up. Longevity medicine is having a moment. Biological age tests, epigenetic clocks, peptide protocols, microbiome panels and increasingly elaborate health packages are no longer confined to the fringes of medicine. They are showing up in […] The post Who decides what counts as longevity medicine? appeared first on Longevity.Technology.

Advances in the treatment of age-related hearing loss: from molecular mechanisms to targeted interventions

Age-related hearing loss (ARHL) is the most common sensory disorder in older adults. Current hearing interventions, including hearing aids and cochlear implants, face limitations in accessibility and adherence. Therefore, efforts have been devoted to elucidating the molecular mechanisms underlying cochlear aging and identifying effective therapeutic targets for ARHL. This review summarizes several molecular mechanisms implicated in cochlear aging and ARHL, including autophagy dysregulation, oxidative stress, stereocilia degeneration, and dysregulation of mitochondrial dynamics. We further discuss recent advances in potential therapeutic targets and intervention strategies associated with these pathways, and provide theoretical support for targeted interventions for ARHL.

A Mechanistic Explanation for SIRT1’s Effects

Researchers have found that the sirtuin SIRT1 stabilizes the human genome by suppressing retrotransposition, which occurs when parts of the genome transcribe themselves onto other parts. When […]

Greenstone bets on human cells to fix DMD hearts

Fresh NIH funding backs an iPSC-and-AI push to find drugs for Duchenne cardiomyopathy without relying on mouse models that rarely translate. By the numbers, the translational gap is expensive. Roughly nine in ten drug candidates that succeed in animal models still fail once they reach human trials, and cardiology has one of the worst records […] The post Greenstone bets on human cells to fix DMD hearts appeared first on Longevity.Technology.

Short-term environmental enrichment modulates brain region-specific redox responses in adolescent female mice

BackgroundEnvironmental enrichment (EE) is a non-pharmacological intervention known to enhance neuroplasticity and resilience. However, studies of EE on brain redox balance have focused predominantly on males and single regions, leaving the developing female brain and region-specific responses largely uncharacterized. This study investigated the effects of a three-week EE protocol on oxidative balance in the hippocampus, hypothalamus, and brainstem of adolescent female C57BL/6 mice.MethodsLipid peroxidation was measured by thiobarbituric acid reactive substances (TBARS), and protein oxidation by carbonyl content. The enzymatic antioxidant system was evaluated through the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione S-transferase (GST). Non-enzymatic antioxidant defenses included quantification of reduced glutathione (GSH), oxidized glutathione (GSSG), the GSH

Astragaloside IV attenuates hypoxia-reoxygenation-induced endothelial senescence and vascular inflammation by modulating the NOTCH1/VCAM-1 axis

ObjectiveAlzheimer's disease (AD) progression involves cerebral microvascular endothelial cell senescence induced by brain hypoperfusion, which contributes to blood-brain barrier (BBB) dysfunction. While Notch1 signaling is known to exacerbate endothelial senescence and neuroinflammation via vascular cell adhesion molecule-1 (VCAM-1), the mechanism by which it mediates hypoxia-induced endothelial aging in AD remains unclear. Furthermore, although Astragaloside IV (AS-IV) has been shown to alleviate cerebral hypoperfusion in AD, whether it acts by directly modulating the Notch1/VCAM-1 axis is unknown. This study aimed to determine whether AS-IV mitigates endothelial senescence and AD pathology by modulating the Notch1/VCAM-1 pathway.MethodsTranscriptomic analysis of AD patient data and network pharmacology identified NOTCH1 as a key target. Molecular docking and 100-ns molecular dynamics

Mitochondrial DNA leakage in oocytes activates cGAS-STING signaling to drive ovarian aging

Why Turning Off Cancer Genes Doesn’t Always Work

A recent study has examined whether senescence might allow cancer cells to survive oncogene withdrawal and become even more dangerous [1]. Some blocking techniques are temporary Many cancers […]

Scientists may have found a shortcut to calorie restriction’s anti-aging benefits

Moderate calorie restriction lowered an immune protein called C3 that appears to help drive chronic inflammation as the body ages. Blocking the same protein reduced age related inflammation in mice, raising the possibility that future treatments could mimic some benefits of calorie restriction without severe dieting.

Anavex outlines progress in Alzheimer’s, rare disease studies with cash runway into 2028

Anavex reported a business update and financial results for the third fiscal quarter ended 30 June. The company has submitted all data from its Alzheimer’s disease clinical trials to a newly opened Alzheimer’s IND and intends to use EMA feedback and prior FDA interactions to inform a planned Phase 3 design. Anavex also reported that […] The post Anavex outlines progress in Alzheimer’s, rare disease studies with cash runway into 2028 appeared first on Longevity.Technology.

Scientists create muscle that exercises itself

Self-contracting myografts improved muscle, bone and metabolic measures in aging mice – without requiring the animals to exercise. Researchers have engineered living muscle grafts that spontaneously contract beneath the skin and appear to reproduce some of exercise’s systemic effects, improving measures of muscle function, bone health and metabolism in aging mice [1]. The work, published […] The post Scientists create muscle that exercises itself appeared first on Longevity.Technology.

NRG Therapeutics shows promising lab results for new ALS drug candidate

NRG Therapeutics presented a poster at the ALS Association’s ALS Nexus conference (23–26 August 2026) detailing preclinical and mechanistic data for NRG5051, its orally bioavailable, CNS-penetrant inhibitor of the mitochondrial permeability transition pore. According to the company, NRG5051 acts through a novel NLRX1-mediated mechanism and showed profound anti-inflammatory and neuroprotective effects in acute NLS-TDP43 ALS […] The post NRG Therapeutics shows promising lab results for new ALS drug candidate appeared first on Longevity.Technology.

cGAS-deficient mice display premature aging associated with derepression of LINE1 elements and inflammation

Elevated contractility drives implantation failure in mouse embryos from aged females

A major Alzheimer’s risk gene may shrink brain cells years before symptoms

Researchers have uncovered a possible reason why the Alzheimer’s risk gene APOE4 can disrupt the brain long before memory problems begin. In mice, APOE4 increased a protein called Nell2, shrinking neurons and making memory circuits unusually active. That early hyperactivity predicted worse memory later in life. Reducing Nell2 in adult mice reversed the abnormal changes, raising hopes for a new way to intervene before Alzheimer’s progresses.

Mitochon receives $1m award for ALS phase 2 study

Mitochon Pharmaceuticals has been awarded a $1 million Hoffman ALS Clinical Trial Award from the ALS Association to support a 24-week sporadic amyotrophic lateral sclerosis study. The funding is intended to expand on recent clinical work in Europe that the company claims showed a rapid reduction in neurofilament light levels among sporadic ALS participants taking […] The post Mitochon receives $1m award for ALS phase 2 study appeared first on Longevity.Technology.

How Old Fat Cells Trigger Inflammation and Raise Risks

Using cohort studies and a mouse model, researchers have found that the circulating factor ANGPTL8, which is produced by senescent fat cells, is related to age-related diseases and mortality in mice and people. Too much of a regulator […]

Citrus compound reverses some signs of liver aging in older mice

The liver is a jack-of-all-trades and a master of all. From removing harmful substances and secreting bile to metabolizing proteins, carbohydrates and fats and managing the immune system, the liver does it all. As we age, liver cells undergo major structural changes, making the body prone to metabolic liver diseases such as fatty liver and inflammation, which, over time, can increase the risk of liver cancer.

Inhibiting cyclin D1–CDK6 suppresses senescence-associated inflammatory gene expression and age-related functional decline

OncoC4 begins testing experimental T-cell therapy in advanced solid tumor patients

OncoC4 announced that it has dosed the first patient in a Phase 1 clinical trial of ONC-783 following U.S. IND clearance. ONC-783 is an investigational T-cell engager developed from the neoCD24 platform, which the company claims is the first clinical-stage T-cell engager targeting the cancer-specific glycoform of CD24. The ONC-783-001 study (NCT07408258) is an open-label, […] The post OncoC4 begins testing experimental T-cell therapy in advanced solid tumor patients appeared first on Longevity.Technology.

Amylyx to share Phase 3 results for low blood sugar treatment after weight loss surgery

Amylyx Pharmaceuticals will announce topline results from its Phase 3 Lucidity clinical trial of Avexitide in post-bariatric hypoglycemia on 18 August 2026, and will host a conference call and audio webcast at 8:00 a.m. ET. The live webcast will be available through the company’s investor events and will be archived for 90 days. Amylyx is […] The post Amylyx to share Phase 3 results for low blood sugar treatment after weight loss surgery appeared first on Longevity.Technology.

Biological age clocks face a regulatory reckoning

Designerly’s Cooper Adwin explains why the ‘Biological Age’ metric Is threatening to derail longevity venture capital. Longevity venture capital is experiencing a breakout moment, with billions flowing into companies developing proprietary biological age clocks. Companies position epigenetic, proteomic and transcriptomic dashboards as the gold standard for measuring intervention efficacy. Yet beneath the hype lies a […] The post Biological age clocks face a regulatory reckoning appeared first on Longevity.Technology.

A little-known protein may be fueling Alzheimer’s — and scientists found a way to block it

An experimental Alzheimer’s compound prevented damaging protein clumps from forming in the brains of mice, helping nerve cells survive longer and reducing amyloid buildup. The treatment also appeared to improve heart health and slow some signs of aging, raising hopes for an entirely new way to combat dementia.

ZEUS does not end inflammation drug discovery – it raises the bar

Novo’s ziltivekimab failure challenges the “lower hsCRP, improve outcomes” thesis – DLT data point to NLRP3 and senescent-cell biology next. Novo Nordisk’s phase 3 ZEUS failure has shaken the cardiovascular inflammation field. Ziltivekimab was designed to block interleukin-6, a cytokine associated with residual inflammatory risk in patients with cardiovascular disease. In ZEUS, the drug produced […] The post ZEUS does not end inflammation drug discovery – it raises the bar appeared first on Longevity.Technology.