Antibodies Boost Microglial Appetite for Tau
Microglia internalize pathogenic forms of tau more robustly when anti-tau antibodies adorn the protein.
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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.
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.
PET scans indicate no more AD pathology in PD-MCI than healthy controls, suggesting their cognitive decline results from other factors.
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