Amyloid Clearance: Check. Cognitive Benefit: Um … Maybe.
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.
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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?
Frequent heading weakened verbal memory in amateur soccer players, and more so in ApoE4 carriers.
Poor lysosomal function in dopaminergic neurons derived from people with YOPD points to disease origin and potential therapies.
New research presented at the HAI conference also finds links between UCB-J uptake and plaques, tangles, and cognitive decline.
PET Tracer Detects Synapse Loss Across Alzheimer’s Brain Multimodal Imaging of Neurodegenerative Diseases Links Pathology and Cellular Dysfunction Tau PET: The Field Expands Rapidly Can PET Match Up Areas of Protein Deposit With Alzheimer’s Symptoms? How