Aβ, Tau, and Other AD Markers Altered in COVID
Markers of neuronal injury rose in plasma within a few months of severe COVID-19, then fell back to normal by six months. Some cases with brain symptoms had lower Aβ and higher tau in their blood.
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Markers of neuronal injury rose in plasma within a few months of severe COVID-19, then fell back to normal by six months. Some cases with brain symptoms had lower Aβ and higher tau in their blood.
North Carolina and South Texas centers to focus on risk factors and diversity.
Large study confirms that insufficient sleep correlates with amyloid accumulation in otherwise healthy adults. Too much sleep is also bad, but for different reasons.
Higher Aβ42 in these neurons correlated with greater plaque load and cognitive decline in their 53 donors, suggesting amyloid overproduction in sporadic AD.
Tau oligomers ensnare an RNA-binding protein and its partner, a type of methylated RNA, in the cytosol of neurons. This triad stresses the cells, leading to neurodegeneration in mice. In people, tau draws in more methylated RNA as Alzheimer's pathology worsens.
This latest and largest GWAS identified 38 risk loci. The seven new ones highlight aging microglia, protein catabolism, and the LilR protein family.
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.
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.
In an aging cohort, weak LC signal intensity on MRI correlated with plaques, tangles, and memory problems.
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.
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.
When microglia get overwhelmed by α-synuclein, they pass off aggregates to unburdened neighbors. which pass fresh mitochondria back in exchange.
The sandwich immunoassay recognizes small soluble oligomers in both cerebrospinal fluid and plasma with high sensitivity and specificity.
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.
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.
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