TREM2 knockout causes a metabolic meltdown in microglia, but treating mice with cyclocreatine restores ATP levels and rejuvenates the cells to fight amyloid.
Findings from a 25-year longitudinal study in a large, biracial cohort point to preventable mid-life vascular problems as a top dementia risk factor.
FUS proteins tend to link up and form liquid droplets and, from those, aggregates. Phosphorylation of the protein’s low-complexity domain repels these associations.
Researchers will enroll young adults who carry familial AD mutations in the first trial of a mechanism-based, investigational drug to try to prevent amyloid from depositing in the brain.
In London, researchers claimed that a monomer is the minimal structure required for tau strains. On the other hand, the sky seems the limit for the number of Aβ strains that form in an individual brain.
At AAIC 2017, researchers presented new approaches to find genetic variants linked to AD risk and to understand their contributions to disease.
CRISPR-Cas9 gene editing rids embryos of a mutation causing heart disease, evoking a future where autosomal-dominant disease is prevented at the DNA level. What about AD, FTD, and ALS?
The aging brain winds down rapid glucose metabolism in regions that will go on to accumulate amyloid, perhaps raising the risk of neurodegeneration.
Interim data from IDEAS study find that amyloid PET has a greater effect in real-world practice than in research settings. Nearly half of people diagnosed with AD did not have the disease.
Using single-cell mass cytometry, scientists have spotted myriad different immune cells hiding in the mouse brain.
One report implicates APP’s intracellular domain in neuron loss due to LRRK2; another accuses the AICD fragment of regulating mitochondrial dynamics via Pink-1.
Markers of necroptosis peppered postmortem brain tissue from people with AD. Gene expression implicates RIP kinases. Could shuttering this cell death pathway save neurons?
Finally, a Blood Test for Alzheimer’s? In Clinical Use, Amyloid Scans Change Two-Thirds of Treatment Plans Searching for New AD Risk Variants? Move Beyond GWAS Monomeric Seeds and Oligomeric Clouds—Proteopathy News from AAIC Planning the First Primary ...
At AAIC, researchers debuted a method that detects changes in plasma Aβ42 in people with brain amyloid. If confirmed, a widely available screening test for presymptomatic AD could follow.
Gaps surrounding blood vessels in the brain may predict cognitive decline and vascular dementia.
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