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Donanemab Data Anchors Upbeat AAIC Give BACE Inhibitors a Second Chance? CSF MTBR-tau-243 Tracks Tangles, Plummets in Response to Antibody Cohort LEADS Toward Better Understanding of Sporadic Early Onset AD Spying on α-Synuclein Inclusions: PET Tracers In
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.
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.
Two interference screens netted a thousand proteins that affect tau oligomerization. The affected pathways? Mitochondrial malfunction, and UFMylation.
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.
The endocytic receptor SORL1 has come to fruition both literally and figuratively. An interactive diagram of the 2,214 amino acid behemoth—filled with findings about hundreds of rare variants—is live for viewing on the Alzforum Mutations database. A handf
Functional, genetic, and epidemiological evidence converges on SORL1 as the fourth autosomal-dominant AD gene.
The comprehensive survey of brain-wide gene expression over the lifespan flagged glial cells in white matter as potential drivers of aging.
When human neurons and brain organoids lack G3BP2, they contain more tau oligomers. The protein binds to tau’s microtubule-binding domain.
As massive, complex datasets burst onto the scene, scientists are using machine learning to analyze the data and uncover hidden patterns. AI may also come in handy in detecting dementia before humans do.
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.
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.
Layer 1 interneurons vanish. Layer 2/3 excitatory neurons become hyperactive, then fade. Microglia change state. Astrocytes react. No symptoms yet. Is this preclinical Alzheimer's?
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.
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