FDA Clears Roche’s CSF Aβ42/tTau Assay
The Elecsys-based assay could run on 100,000 fully automated diagnostic machines worldwide.
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The Elecsys-based assay could run on 100,000 fully automated diagnostic machines worldwide.
Known for his work on animal models, APP processing, and the cholinergic system, Price founded one of the first Alzheimer’s Disease Research Centers.
A giant of basic science, Ihara biochemically characterized Aβ and tau deposits in AD brain, laying the groundwork for subsequent discoveries.
The anti-amyloid antibody becomes the first Alzheimer’s treatment in 20 years to receive traditional approval from the FDA. Broader Medicare coverage starts now.
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.
In Kuopio, a collaborative tissue resource supplies the broadest swath of materials found anywhere for functional studies on ADRD genes. Think ABI3, APP, C9ORF72, GRN, PLCG2, TMEM106B—and more.
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.
When human neurons and brain organoids lack G3BP2, they contain more tau oligomers. The protein binds to tau’s microtubule-binding domain.
Functional, genetic, and epidemiological evidence converges on SORL1 as the fourth autosomal-dominant AD gene.
The panel of six marker candidates includes proteins involved in lipid processing and metabolism in microglia.
A trio of studies report that missense variants in SORL1 that disrupt its trafficking or dimerization are highly likely to cause Alzheimer's disease in carriers, strengthening the case for SORL1 being a familial AD gene.
Two interference screens netted a thousand proteins that affect tau oligomerization. The affected pathways? Mitochondrial malfunction, and UFMylation.
A new method for precisely localizing pathological tau in whole mouse brain finds that its spread follows network connections—but it seems to move up axons, not down.
The comprehensive survey of brain-wide gene expression over the lifespan flagged glial cells in white matter as potential drivers of aging.
In cells from people with Down’s syndrome, and in mouse models of DS and Alzheimer’s, excess β-CTF binds vacuolar ATPase, hobbling lysosomal acidification.