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.
The updated, expanded manual helps doctors diagnose this rare tauopathy and its variants earlier, in hopes that more patients can take advantage of clinical trials.
The prevalence of chronic traumatic encephalopathy supports a link between multiple concussions and this degenerative tauopathy, though the sample is self-selected.
An astrocytic Aβ protease, destabilization of γ-secretase by FAD mutations, and an sAPP receptor all made their debuts at Heidelberg conference.
Run-on repeats not only break DNA, they thwart the crucial repair pathways needed to sew the strands back together.
Knockout mice suggest opposing effects on lysosomal enzymes and neurodegeneration in frontotemporal dementia, implicating an ATPase.
Analysis of brain tissue from Alzheimer’s patients offers a glimpse of proteomic changes in the disease.
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