Viral surfaces attract proteins from the extracellular environment of the person they infect. This corona of host proteins makes the virus more or less infective—and promotes amyloid fibrils.
New potential immunotherapies and insight into single-cell responses were highlights of a small meeting in Denmark.
Research on postmortem human brain strengthens the idea that an ebbing of neurogenesis may underlie cognitive decline.
Thousands of stretches of the genome go undetected by standard short-read sequencing techniques. Unmasking these “dark regions” revealed a potential AD risk variant in the CR1 gene.
Using single-nuclei or cell sorting, three separate research groups sequenced RNA from human postmortem brains. They unveiled AD-associated gene-expression signatures, but disease-related transcriptomes from human microglia were quite different from those in mice.
Antisense Oligonucleotides: Can They Take on ALS, SMA, Prions? American Academy of Neurology 2019 Annual Meeting ...
Data on ASOs, presented recently at the annual meeting of the American Academy of Neurology, depict RNA-based therapies as broadly on the rise in neurodegenerative diseases.
In a new, inducible mouse model, poly(GR) damages mitochondria, but its effect is reversible. In flies, turning off transcription of hexanucleotide expansion protects cells.
Expression of VCAM1 on the endothelial cells that line the blood-brain barrier allowed aging factors in the plasma to exact their toll on the brain.
Lanabecestat, elenbecestat, and umibecestat all showed data at the AD/PD conference in Lisbon. Learn what definitely doesn’t work and what might yet.
Long recognized in dendrites, scientists now report that substantial synaptic proteome remodeling happens on the axonal side, too.
More mouse data add to the argument that a flashing light sequence could potentially fight cognitive decline.
The global agency’s report recommends physical activity, a healthy diet, stopping alcohol abuse and smoking, and managing one’s weight, blood pressure, and diabetes.
“We are learning” was the tenor of debate about the latest round of setbacks for anti-amyloid trials in symptomatic Alzheimer’s disease at a recent conference in Lisbon.
An electron microscopy study reveals a jumbled mess of membrane chunks and malfunctioning organelles, bound together by phosphorylated or truncated α-synuclein.