Genetics Propels DIAN Toward Therapies
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.
289 RESULTS
Sort By:
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.
RPS25 helps translate repetitive snippets of RNA that are associated with neurodegenerative diseases. Knocking it down reduces protein aggregates and cell death.
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.
Too much or too little serum hemoglobin increases risk for Alzheimer’s and other dementias by 20 percent or more.
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.
In 2,144 Colombian ADAD family members, plasma NfL in gene carriers rises as early as two decades before their symptoms start.
ApoE2 homozygotes have a dramatically lower risk of AD than even the previously known low-risk E2/3 heterozygotes. More study of this protective allele could reveal roots of resilience.
Among former National Football League players who died with CTE, tau tangles, crumbling white matter, and arteriolosclerosis independently contributed to dementia.
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.
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?
A plasma assay for Alzheimer’s could radically speed up screening for clinical trials; alas, competing assays don’t measure the same thing.
Protein levels track with cognitive function and can distinguish Alzheimer’s patients from controls.
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.