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Exposure, Exposure, Exposure? At CTAD, Aducanumab Scientists Make a Case Fluid AD Biomarkers Link P-Tau to Synapses, Inflammation Blood Tests of Phospho-Tau, Aβ42, Track With Brain Amyloid Amyloid Clearance: Check. Cognitive Benefit: Um … Maybe. Picking T
In PASSPORT study, the antibody failed to slow progressive supranuclear palsy. Alzheimer’s trial to continue.
An expanded set of CSF biomarkers exposed tight connections between p-tau, synaptic dysfunction, and neuroinflammation in people with brain amyloid.
Using mass spectrometry to detect teensy amounts of phospho-tau species in plasma, researchers reported that p-tau-217 and p-tau-181 picked out people with Aβ pathology. Differences between groups appear to be huge. An MS-based test for plasma Aβ42 corresponded to brain amyloid, and is going in for regulatory approval.
Plaque-busting antibodies reset the time course of amyloid accumulation, but so far provide only hints of a clinical benefit in mild AD. Good news: once gone, plaque stays gone for a while.
Apabetalone, an epigenetic drug that tamps down vascular inflammation, slowed cognitive decline in people with MCI. A new statistical analysis of results from AMBAR claimed the plasma-exchange therapy might boost cognition by removing pathogenic proteins from blood.
Bringing the total NIH funding for Alzheimer’s research up to $2.8 billion, the Senate continued its steady upward climb in spending for the disease.
NIH Summit Sets Agenda for AD-Related Dementias Alzheimer's Disease Research Summit 2019
Data from different next-generation tracers look similar. It shows spreading plaques kick off tangles by Braak region; memory starts slipping later.
Besides further broadening the Alzheimer’s therapeutic pipeline, researchers urge a return to Phase 2, using artificial intelligence tools to streamline aspects of trials.
In early Alzheimer’s disease, the pattern of tau deposition also strongly predicts areas destined for subsequent degeneration.
Positive allosteric modulators improve learning and memory in mouse models of AD and epilepsy.
These oily microglia resemble the foamy macrophages seen in atherosclerotic plaques. They correlate with aging, inflammation, and neurodegenerative disease.
When observed over an eight-year period, people with the highest plasma concentrations were more likely to die than people with lower levels.
Aberrant protein-protein interactions centered on HSP90 may contribute to Alzheimer’s disease. Can an inhibitor set things right?
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