Brain Drain—“Glymphatic” Pathway Clears Aβ, Requires Water Channel
Researchers have shown that the CSF goes into the brain along very specific anatomical structures...
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Researchers have shown that the CSF goes into the brain along very specific anatomical structures...
Topline data yesterday showed that intravenous immunoglobulin (IVIG) therapy, known as Gammagard™, failed to meet primary endpoints of slowing cognitive and functional decline...
In mouse models, the Alzheimer’s risk gene TREM2 affects microglial behavior but does not lead to more amyloid deposition.
Microglia internalize pathogenic forms of tau more robustly when anti-tau antibodies adorn the protein.
A C-terminal fragment of APP recruits the protein APPL1 to endosomes, causing the enlarged, overactive vesicles seen early in Alzheimer’s disease.
In two trials, moderate exercise or supplements of omega-3 fatty acids and antioxidants failed to alter the course of cognitive decline in older adults.
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.
Diminishing Alzheimer’s pathology in mice appears to be as easy as shining a light in their eyes. Could it work in people?
Imatinib, previously reported to inhibit γ-secretase, now appears to isolate APP from BACE as well.
If it works in neurons, this disposal pathway could have implications for neurodegenerative disease.
Unbiased screen turns up genes expressed in immune cells, both inside and outside the CNS.
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.
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