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The monoclonal antibody activated TREM2 signaling on mouse microglia. It supported their survival and stimulated their clearance of amyloid plaques.
In the human brain, alpha waves fell out of sync, while delta-theta waves swelled in concert with amyloid plaques, neurofibrillary tangles. Alpha modulation correlated with cognitive decline.
Under diabetic conditions, SERP1 binds secretase subunit, cranking up cleavage of APP but not Notch. The finding offers a mechanistic link between diabetes and Alzheimer’s.
In motor neurons of TMEM106b knockout mice, swollen vacuoles piled up in axons near the soma, rendering the mice wobbly and slow to react. The finding contradicts prior reports.
Different forms of p-tau in cerebrospinal fluid reflect worsening plaque load, metabolism, and atrophy in the brain. They could help stage Alzheimer’s disease.
United Kingdom’s DRI pivots to fight COVID-19. The facility could test 10,000 samples per day.
A survey conducted by the Alzheimer’s Association finds that three-quarters of these physicians had little to no residency training in dementia care.
From caregivers going it alone to understaffed nursing homes on lockdown, people with neurodegenerative disease and their caregivers are feeling enormous strain from the novel coronavirus. They are adapting to the new normal with technology.
Two papers report that phosphorylated tau in the blood distinguishes people with AD from healthy controls and from people with frontotemporal and vascular dementias.
A trial of nearly 20,000 participants found no benefit over five years.
Most observational cohorts are on pause, and many clinical trials have stopped dosing. The long-term effects on the integrity of AD studies are unclear.
The slowdown of proteasomes stymied TDP-43’s entry into the nucleus and promoted its aggregation in the cytoplasm.