Alzheimer's Disease Research Summit 2019
NIH Summit Sets Agenda for AD-Related Dementias Alzheimer's Disease Research Summit 2019
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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
Synapse loss and mitochondrial stress, as seen by separate PET tracers, go hand-in-hand in Alzheimer’s, Parkinson’s, and frontotemporal dementia.
FDA approves adding safety and efficacy data from an Alzheimer’s trial to the drug’s label.
The creation of long-term memories requires a continual supply of myelin provided by newly formed oligodendrocytes. Alas, the generation of fresh oligodendrocytes diminishes with age, along with memory.
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