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.
This alternative approach to Aβ immunotherapy targets unlipidated, plaque-associated ApoE.
Unbiased screen turns up genes expressed in immune cells, both inside and outside the CNS.
Diminishing Alzheimer’s pathology in mice appears to be as easy as shining a light in their eyes. Could it work in people?
Microglia internalize pathogenic forms of tau more robustly when anti-tau antibodies adorn the protein.