DIAD: Families from Argentina, Canada, Minnesota Rally a Global Community Genetics Propels DIAN Toward Therapies ASOs: Wave of the Future in Alzheimer’s Therapeutics? As DIAN Wraps Up Anti-Aβ Drug Arms, it Sprouts Tau, Primary Prevention Arms On July 13, ...
Different polymorphisms in MS4A genes up- or downregulate levels of TREM2, modulating levels of the shed ectodomain in the cerebrospinal fluid and AD risk.
Among former National Football League players who died with CTE, tau tangles, crumbling white matter, and arteriolosclerosis independently contributed to dementia.
What’s with all those head-to-head comparison studies of academic and commercial biomarker tests? Could we not just pick one that works, and be done?
In a tauopathy model, knocking out C3 spared synapses and neurons. In an amyloidosis model, deleting C3 preserved dendritic spines, but exacerbated plaque growth.
Older people who lived healthy lifestyles had a third lower risk of dementia than their unhealthy peers, but only if their genetic risk for the disease was low.
Clinical trial design could benefit from new estimates of how slowly amyloid accumulates and how best to detect it at various disease stages.
Loss of ataxin-1 intensifies BACE1 expression, Alzheimer’s pathogenesis. Is that how ataxin GWAS variants increase AD risk?
Smartphones and gamified apps move cognitive testing from the lab into the real world. But keeping people engaged remains a problem. Is passive monitoring the answer?
Passive monitoring of old people in their everyday lives is starting to generate new indicators for cognitive impairment.
New PET Staging Scheme for Amyloid? Physical Activity May Shield the Brain from the Onslaught of Aβ Crenezumab Update: Baseline Data from Colombian Prevention Trial Colombian Cohort Delivers Data on Blood NfL Rare Luck: Two Copies of ApoE2 Shield Against ...
No benefit detected in double-blind trial with sham surgical controls.
The Phase 2 study missed its primary endpoint. While fewer developed dementia in the treatment group, the effect was not statistically significant. People on drug had less brain atrophy than those on placebo.
The study halted early when the primary endpoint was met, but an unusual trial design and lack of detailed data leave questions unanswered.
In neurons derived from FTD patients, morphological changes at the base of the axon render them hyperexcitable.