Last year, four independent research groups reported a linkage between polymorphisms in the complement factor H (CFH) gene to age-related macular degeneration...
Robert Katzman was a pioneer in bringing Alzheimer disease out of obscurity and into the forefront of medical, scientific, and social agenda of this country...
Topline data yesterday showed that intravenous immunoglobulin (IVIG) therapy, known as Gammagard™, failed to meet primary endpoints of slowing cognitive and functional decline...
A C-terminal fragment of APP recruits the protein APPL1 to endosomes, causing the enlarged, overactive vesicles seen early in Alzheimer’s disease.
Excess Aβ42 trips up calcium homeostasis and precipitates the loss of spines thought to be important for memory.
The FTC imposed a $2 million fine on Lumos Labs for overstating the benefits of the company’s Lumosity brain-training software.
Researchers may soon add another imaging agent to their tool kit—one that tracks synapse loss.
At least one phosphate tag may quell Aβ excitotoxicity.
If it works in neurons, this disposal pathway could have implications for neurodegenerative disease.
Electrodes entering the brain through a hole above the jaw detected epileptic spikes in the hippocampi of Alzheimer’s patients. Scalp recordings missed the action.
An antibody that activates Notch 3 signaling helps keep retinal blood vessels intact in a mouse model of the small vessel disease CADASIL.
A longitudinal study identified regions in the default mode network as among the first to accumulate Aβ.
The trial’s sponsor announced an early end to the large Alzheimer’s prevention study based on an interim futility analysis.
In people with an autosomal-dominant AD mutation, Aβ and tau start accumulating long before the estimated onset of symptoms.
A CRISPR knockout screen in human cells and mouse neurons found genes that tweak C9ORF72 toxicity, zeroing in on ER stress as a potential therapeutic target.