Not All Bad? APOE4 Sharpens Memory in Older People
Cognitively intact 70-year-old people carrying APOE4 recalled objects and their locations slightly better than did noncarriers. The advantage persisted even among people who had amyloid plaques.
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Cognitively intact 70-year-old people carrying APOE4 recalled objects and their locations slightly better than did noncarriers. The advantage persisted even among people who had amyloid plaques.
That long-sought astrocyte toxicity factor? Scientists say it's certain long-chain fatty acids. No, not the ones we get from our diet.
In a collaborative tour de force, scientists for the first time compared eight Aβ assays in the same plasma samples. Mass-spectrometry assays more accurately picked up brain amyloid than did most immunoassays, but one fully automated immunoassay was on par.
High-resolution structures of tau fibrils from a variety of tauopathies reveal distinct folds—and important similarities—among syndromes. The folds facilitate a classification of tauopathies.
Therapies targeting key neurodegenerative disease proteins, or biomarkers, are failing. Can Mendelian randomization test cherished assumptions?
The APOE3-Jacksonville variant generates a protein whose greater lipid-hauling capacity renders it less prone to self-aggregate. This boosted phospholipid trafficking and reduced the number of plaques and downstream damage.
The sandwich immunoassay recognizes small soluble oligomers in both cerebrospinal fluid and plasma with high sensitivity and specificity.
When microglia get overwhelmed by α-synuclein, they pass off aggregates to unburdened neighbors. which pass fresh mitochondria back in exchange.
Amyloid Time: Because amyloid burden grows at a constant rate after having crossed a tipping point, scientists were able to predict when a person’s symptoms will begin, using only his or her age and one PET scan.
With initial funding secured, DAC is attempting to link Alzheimer's research cohorts, support global clinical trials, and prepare health-care systems around the world.
In an aging cohort, weak LC signal intensity on MRI correlated with plaques, tangles, and memory problems.
When provoked by cytokines, astrocytes change their gene expression so as to make their lysosomes overly alkaline, rendering them dysfunctional. Astrocytes then dump lysosomes' contents outside, creating a neurotoxic culture medium.
Centenarians had nearly as many pathogenic variants as controls, but they also sported protective variants in insulin and AMPK signaling genes—longevity pathways known from animal models. Functional variants in the Wnt pathway counteracted damage from ApoE4.
Misfolded tau travels from a subset of neurons in the entorhinal cortex directly into CA1 neurons in the hippocampus, fouling synaptic transmission and memory in mice.
This latest and largest GWAS identified 38 risk loci. The seven new ones highlight aging microglia, protein catabolism, and the LilR protein family.
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