American Aging Association

The next generation of geroscience should look like the communities it serves.

Applications are open for the AGE Early Career Scholars Program, an award from the American Aging Association to support diversity in AGE and in the broader geroscience research community.

What 25 selected scholars receive:

• A 2-year AGE membership
• A $1,300 travel award for the 2027 AGE annual meeting
• The opportunity to present your research at AGE 2027
• Ongoing mentorship from a senior AGE trainee chapter member
• Additional 1-year memberships and virtual 2027 meeting registrations will also be awarded

Who should apply:

• Undergraduates, postbaccs, graduate students and postdocs
• Trainees who identify as under-represented minorities in biomedical sciences, or who have faced significant barriers to scientific development or networking
• Anyone studying aging or age-related diseases. If you work on metabolic, neurodegenerative, cardiovascular or infectious disease, or cancer, that counts.

How to apply: submit one PDF with (1) a CV or biosketch, (2) a research abstract of up to 300 words that explains how your work relates to aging or geroscience (no results needed), and (3) a paragraph of up to 500 words on why you want to join AGE and how this award would benefit your career.

Deadline: December 1, 2026 at 11:59pm ET. Early career investigators outside these stages are not eligible, but are encouraged to apply for a travel award.

Know a trainee who should apply? Tag them or share this post, and apply here: clicks.memberclicks-mail.net

AGE 2027 annual meeting: americanagingassociation.org/annual-meeting

#AGE2027 #Geroscience #AgingResearch #EarlyCareer #DiversityInSTEM

Rapamycin is the most talked-about drug in aging biology. What does a first look in healthy middle-aged people actually show?

A pilot trial from the @Mizzou (University of Missouri), published in the Journal of Cerebral Blood Flow & Metabolism (online Sept 10, 2026, and widely covered this week), gave low-dose rapamycin to cognitively normal adults aged 45 to 65, stratified by APOE genotype.

Key findings:

• Design: single-arm, 1 mg/day for 4 weeks, 23 completers (9 APOE4 carriers, 14 non-carriers).
• Cerebral blood flow, the primary outcome, rose by more than 15% across multiple brain regions in APOE4 carriers.
• Non-carriers showed no significant change, pointing to genotype-dependent effects.
• Metabolic and inflammatory profiles improved, with minimal adverse effects reported.

What this does and does not tell us: this is a very small pilot with no placebo group. Blood flow is a biomarker, not evidence of better memory or prevention of Alzheimer's disease, and the effects of longer or repeated dosing are unknown. It is not a reason to take rapamycin, which is a prescription immunosuppressant.

Why it matters for geroscience: APOE4 carriers show vascular dysfunction decades before symptoms. A genotype-specific response is exactly the kind of signal that supports precision trials, with placebo control, larger samples and cognitive endpoints.

Should geroscience trials stratify by genotype from the start? Share your view below.

Paper: Aware et al., J Cereb Blood Flow Metab 2026. doi.org/10.1177/027167… (ClinicalTrials.gov NCT05386914)

#AGE2026 #Geroscience #AgingResearch #Healthspan #TranslationalMedicine

Two people score the same on a memory test today. Could their brain wiring already predict who declines faster?

A new Stanford-led study in Science Advances (published Nov 4, 2026) says it might. Researchers built the Alzheimer's Resilience-Vulnerability Connectome (ARC) by contrasting SuperAgers, people with unusually preserved late-life memory, against people with Alzheimer's disease, using resting-state fMRI.

Key findings:

• ARC separated SuperAgers from Alzheimer's patients with an AUC of 0.85 in a discovery cohort (n=290) and replicated in an independent cohort (n=143).
• Applied to cognitively unimpaired adults (n=818, replicated in n=497), it revealed SuperAger-like and Alzheimer-like subgroups with comparable baseline cognition.
• The Alzheimer-like subgroup showed faster cognitive decline, greater amyloid-β accumulation and higher risk of converting to Alzheimer's.
• The signal involved prefrontal, temporal and insular networks and tracked with brain age.

What this does and does not tell us: ARC is a research signature, not a clinical test. The subgroups are statistical, group-level labels, and the candidate genetic loci from the exploratory GWAS need independent confirmation. It should not be used to label an individual.

Why it matters for geroscience: trials that wait for symptoms start late. Early risk stratification by functional brain organization could help enrich prevention trials for the people most likely to progress, and test whether interventions shift people toward the resilient end of the spectrum.

Which biomarker do you think prevention trials should use first: imaging, blood, or a combination? Tell us below.

Paper: Zhao et al., Sci Adv 2026;12(45):eaed9351. doi.org/10.1126/sciadv…

#AGE2026 #Geroscience #AgingResearch #Healthspan #TranslationalMedicine

@StanfordMed

Why do women carry more of the dementia burden, and could lifetime estrogen exposure be part of the story?

A new peer-reviewed study in Neurology (published Nov 4, 2026) followed 352 cognitively healthy women from the Gothenburg H70 cohort, with brain MRI at age 70 and again five years later. Researchers from Karolinska Institutet and the University of Gothenburg asked how reproductive years and hormone use relate to brain vascular health.

Key findings:

• A longer reproductive span (age at menopause minus age at menarche) was linked to lower cerebral small vessel disease burden, about 8% lower odds per extra year (OR 0.92, 95% CI 0.86-0.99).
• Menopausal hormone therapy use was associated with fewer microbleeds and fewer enlarged perivascular spaces.
• Oral contraceptive and hormone therapy use were each linked to better white matter integrity, highest in women who used both.
• Among APOE-ε4 carriers only, hormone therapy use was associated with greater cortical thickness in Alzheimer's-vulnerable regions.

What this does and does not tell us: this is observational, hormone use was self-reported as yes or no (no dose, timing or formulation), and the outcomes were MRI markers, not cognition. It cannot show that hormones protect the brain, and it is not a reason to start hormone therapy. Whether to use it remains an individualized decision with a clinician.

What the field can act on now: cerebral small vessel disease is tied to vascular risk, so established levers like blood pressure control, physical activity and not smoking remain the evidence-based priorities for brain aging in both sexes. Sex-specific prevention research like this helps define who to study next, ideally in randomized trials with timing and dose built in.

How should geroscience trials account for lifetime hormone exposure and APOE genotype? Share your view below.

Paper: Lorenzon et al., Neurology 2026;107(11):e218706. doi.org/10.1212/WNL.00…

#AGE2026 #Geroscience #AgingResearch #Healthspan #TranslationalMedicine

Could restoring the liver's filtration system help the aging body clear Alzheimer's-linked protein? A new study points in that direction, in rats.

With age, the liver's sinusoidal endothelial cells (LSECs) lose structure and function, and clearance of circulating cargo declines. In a @KeckMedicineUSC study published in the Journal of Biological Chemistry, aged rats received the sGC activator cinaciguat for two weeks. Treatment restored LSEC structure and function, including their microscopic pores, and engaged HB-EGF signaling to hepatocytes. Blood amyloid beta fell by about 50%, to levels similar to young rats, and LDL cholesterol fell to young-animal levels. Untreated aged rats showed no comparable improvement.

Caveats: this is a rat study with no human data. Lower blood amyloid beta does not by itself show fewer brain plaques or protection from Alzheimer's, and the drug's safety profile was not reported. The authors say further translational work is needed.

For geroscience, it adds to the case that peripheral organs, not only the brain, shape age-related proteostasis and lipid handling. Follow AGE for more research linking aging biology to healthspan.

Paper: doi.org/10.1016/j.jbc.…

#AgingResearch #Geroscience #Healthspan #Alzheimers