NIH Summit Sets Agenda for AD-Related Dementias Alzheimer's Disease Research Summit 2019 ...
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.
At AAT-AD/PD, scientists showed that correlated amyloid patches are an even earlier marker than brain-wide positivity, while others puzzled over why tau signals are lower in older people.
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 ...
Besides further broadening the Alzheimer’s therapeutic pipeline, researchers urge a return to Phase 2, using artificial intelligence tools to streamline aspects of trials.
An expanded set of CSF biomarkers exposed tight connections between p-tau, synaptic dysfunction, and neuroinflammation in people with brain amyloid.
This past year, therapeutic antibodies massively reduced brain amyloid, blood tests came into their own, and systems-based approaches transformed the study of gene expression, glial cells, and selective vulnerability.
Positive allosteric modulators improve learning and memory in mouse models of AD and epilepsy.
In early Alzheimer’s disease, the pattern of tau deposition also strongly predicts areas destined for subsequent degeneration.
New potential immunotherapies and insight into single-cell responses were highlights of a small meeting in Denmark.
These oily microglia resemble the foamy macrophages seen in atherosclerotic plaques. They correlate with aging, inflammation, and neurodegenerative disease.
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.
Data from different next-generation tracers look similar. It shows spreading plaques kick off tangles by Braak region; memory starts slipping later.