Built to cross the blood-brain barrier, the vehicle delivers therapeutic antibodies, enzymes, and potentially small molecules such as oligonucleotides.
Many Alzheimer’s trials had minimal dosing interruptions, but recruitment stopped for a time. Others trials fared worse, with some scrapped altogether. One administered study drug in an ambulance.
The first ever cryoEM structures of Aβ fibrils extracted from AD tissue look quite different than prior structures of fibrils generated in vitro. For starters, they are right-hand twisted, not left-hand.
Sex-specific polygenic hazard scores predict pathology and cognitive decline.
Tissue from 13-week-old fetuses carrying the huntingtin repeat expansion shows defects in neuronal polarity and proliferation, which lead to fewer neurons populating some brain regions.
In vicinity of plaques, astrocytes and glia change gene expression in concert.
Homozygous carriers of GM17—a common IgG1 variant the HSV-1 virus has evolved to evade—had quadruple the risk of developing AD. In a small Swedish cohort, that is.
Spewed by stressed microglia, fragments of the organelles provoke mitochondrial fission in other cells, causing astrogliosis and neuronal loss.
Resident T cells in the membrane surrounding the healthy mouse brain influence both short-term memory and synaptic plasticity.
The resource boasts 56 stem cell lines derived from tau mutation carriers, patients with sporadic disease, healthy controls, and engineered isogenic lines, including some that have their mutation corrected by CRISPR.
The rare ApoE3 Christchurch variant prevented tau tangles, neurodegeneration, and cognitive decline in a woman’s brain for decades, despite massive amyloid buildup from a familial presenilin AD mutation.
A new study argues that the duration of a person’s amyloid positivity predicts whether they’ll develop tau accumulation and cognitive decline.
No link found with amyloid deposition.
While former professional soccer players have less risk for heart disease and cancer than the general population, they are five times more likely to die with a neurodegenerative disease in old age.
While gene-based therapy for late-onset AD may seem distant, rare neurological disorders could point the way.