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.
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.
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.
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.
The phenotype of ApoE4 astrocytes and microglia resembles that of these cells in Alzheimer’s brain. Could defects in lipid metabolism and the extracellular matrix bring on the disease?
Using a collection of isogenic iPSC-derived neurons harboring different familial AD mutations, researchers found that, across the board, the mutations meddled with endosomes via elevated β-CTF.
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.