Longevity, genes,
and disease-modifying AI.

Sex-specific biological aging clocks across organs and omics

Resource of 38 sex-specific clocks across 15 organ systems; sex-stratified training shows female/male clocks diverge in genetics, proteomics, and disease/mortality prediction, including sex-dependent links between a brain aging clock and cognitive decline in a preclinical AD trial setting.

Caveat: Observational/modeling resource — not a diagnostic device or approved therapy; sex-pooled clocks remain complementary.

Factor IX Padua AAV gene therapy in adolescents with hemophilia B (BBM-H901)

Multicenter phase 1, n=11 adolescents (12–18) with severe/moderately severe hemophilia B in China (NCT05709288); single dose 5×10¹² vg/kg; no DLT; mean FIX:C at week 52 ≈ 41.8 IU/dL; annualized bleeding rate fell from 13.9 to 0.5.

Caveat: Early phase 1 / single-arm; one SAE and grade-3 AEs reported; liver enzyme elevation in one participant resolved after immunosuppression — not a broad label expansion.

PTCHD4 as a candidate senescence / aging-fibrosis target (AKT axis)

Preclinical work ties PTCHD4 upregulation to faster senescence; knockout MEFs senesce later; PTCHD4-null mice live longer, resist D-galactose aging mimic and bleomycin lung fibrosis — effects attributed to reduced AKT signaling rather than Hedgehog.

Caveat: Preclinical mouse/cell data only; no human therapeutic; initial study needing replication and safety of targeting.

De novo mutations bridge parental reproductive factors and offspring health

WGS of 7,851 parent–offspring families maps parent-of-origin and post-zygotic DNMs linked to ART procedures independent of parental age; increased paternal mutational burden statistically mediates effects of advanced parental age and ART on gestational duration and early outcomes.

Caveat: Association/mediation genomics — not a clinical genetic test change or fertility recommendation by itself.

Clinical-scale WAS CRISPR-Cas9-AAV6 HSPC editing meets GMP/safety benchmarks

Clinical-scale runs (~115M CD34+ cells) reached ~61% targeted integration with preserved viability/stemness; mouse engraftment OK but corrected fraction declined post-transplant (~10% at 14 weeks) — i53 + lower AAV6 improved engrafted corrected cells; limited genotoxicity signals underscore need for long-term monitoring.

Caveat: Preclinical/process paper toward Wiskott-Aldrich gene therapy — not an approved product; engraftment of corrected stem cells remains the hard problem.

Research AI ≠ clinical cure claims

Sex-stratified clocks, early-phase gene therapy, and senescence targets are different evidence classes. This site keeps them labeled so a headline never collapses into “AI cured aging.”