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Every week in a Finnish operating room, bits of human cortex get lifted from brains and straight into electrophysiology rigs. Other tissues go to diagnostic and research labs, or biobanks, for ADRD research. Read how it happens.
Scientists have established acute slice recordings from cerebral cortex biopsies. They find circuitry and basic function to be preserved. They also find changes in the presence of Alzheimer's pathology.
Functional, genetic, and epidemiological evidence converges on SORL1 as the fourth autosomal-dominant AD gene.
While each disease features distinct proteomes in the brain, cerebrospinal fluid, and blood, some proteins overlap. They are more dysregulated in familial than in sporadic AD.
Synuclein fibrils from Parkinson’s disease, PD dementia, and dementia with Lewy bodies share the same protofilament structure. MSA fibrils are different.
Is transfer of tau from one neuron to the next a normal activity, hijacked by pathogenic protein in the case of tauopathies?
The NIA invites scientists to submit data to create diverse, open datasets and design diagnostic algorithms for more accurate, early prediction of Alzheimer’s.
In dementia with Lewy bodies, basic scans are used in routine diagnosis. Multimodal imaging and new PET tracers for affected neurotransmitters of pathological deposits in the brain and gut are entering research settings.
Provocative new data suggest that glial engulfment of synapses dampens network hyperexcitability early in disease. Key mediators: TREM2 and phosphatidylserine.
A consortium of pharma companies mined data from 50,000 people in the U.K. Biobank to turn up thousands of new gene-protein connections.
Researchers identify where proteases snip the microglial receptor TREM2 to release its extracellular domain: exactly at the site of a rare AD risk variant.
At a conference on lipids in the brain, scientists reported how unsaturated fatty acids might worsen or ameliorate the effects of proteinopathies.
A cholesterol metabolite magnifies pathology in a tauopathy mouse. Microglia need cholesterol to rein in amyloid. ApoE4 jams the fat's export from neuron to glia.
At Leiden conference, scientists discussed how shifting cells toward “specialized pro-resolving mediators” could counter inflammation.
A new study defined the location and expression profile of this astrocyte subtype, pegging the protein myocilin as a marker.
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