As the Alzheimer’s field suffers smackdowns in trials of small molecules and antibodies, antisense oligonucleotides are quietly coming along—and looking safe so far.
A brother’s survival guilt, a journalist tracing her mutation to Lebanon, a student freezing her eggs ahead of a primary prevention trial—DIAN family members are stirring their growing community to act against Alzheimer’s disease.
Nearly 30 years after the first Alzheimer’s gene discoveries, genetics once again drives recruitment, scientific progress, and therapy development in the Dominantly Inherited Alzheimer’s Network.
At AAIC, researchers presented baseline data from an ongoing, five-year study asking whether the anti-Aβ antibody crenezumab can forestall cognitive decline in autosomal-dominant Alzheimer’s disease.
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?
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 ...
In 2,144 Colombian ADAD family members, plasma NfL in gene carriers rises as early as two decades before their symptoms start.
A plasma assay for Alzheimer’s could radically speed up screening for clinical trials; alas, competing assays don’t measure the same thing.
At AAIC, researchers touted phospho-tau species, especially p217 and p181. They tick up in CSF as an early response to amyloid accumulation.
At this year’s AAIC, no sooner had scientists reported that phospho-tau in the CSF might reflect early responses to amyloid, than they reported parallel data for phospho-tau in blood.
Protein levels track with cognitive function and can distinguish Alzheimer’s patients from controls.
New genes linked to early and late-onset AD offer up mechanistic insight, potential targets for treatment.