Alzforum spoke with UCSD’s incoming leader for Alzheimer’s research. Where does he want to take the Alzheimer’s Disease Cooperative Study and neurodegeneration research in La Jolla and beyond?
An immunotherapy drug recruits immune cells to the brain, where they help clean up amyloid plaques.
With the most widespread chronic traumatic encephalopathy yet seen in a player that young, the 25-year-old represents the first published case with neuropsychological data.
Gene expression analysis highlights differences from mouse astrocytes as well as from immature and cultured human astrocytes.
The prion concept continues to infiltrate the neurodegeneration field, with models of SOD1 propagation and a bevy of tau strains.
The modified stem cells might slow disease, too, though the trial was too small to say for sure.
Atomic-level analysis of the protein’s C-terminal end suggests a floppy region key for the delicate process of forming functional oligomers. Mutate it slightly, and it becomes an aggregating machine.
The FTC imposed a $2 million fine on Lumos Labs for overstating the benefits of the company’s Lumosity brain-training software.
The drug benefits some patients with mild amyotrophic lateral sclerosis, and is approved in Japan.
Scientists propose and test criteria to detect this treatable disorder without a brain biopsy.
Do α- and γ-secretase band together to cleave substrates such as the amyloid precursor protein?
Alzforum looks back on a year of developments.
When clinicians and pathologists argue, sometimes genetics can settle the dispute. How about DLB?
How α-synuclein aggregates spread, quite possibly starting in the nose in some people, sets DLB apart from its better-known cousins, Alzheimer’s and Parkinson’s.
In transgenic mice, revving up proteasome function lowered tau deposits and improved memory.
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