Plasma p-Tau217 Set to Transform Alzheimer’s Diagnostics Could Common Vaccines Protect Against Alzheimer’s Disease? Doubling Down on Sequencing Serves up More Alzheimer’s Genes IDEAS Finds Small Drop in Hospitalizations, Missing Goal Lancet Commission’s ...
This early marker distinguishes Alzheimer’s from controls and other neurodegenerative diseases more accurately than other biomarkers.
Poor coordination among grid cells in the entorhinal cortex and place cells in the hippocampus compromises navigation. Grid cells fail first.
This neuronal protein regulates the complement cascade in the developing brain. Could it do the same in aging or neurodegenerative disease?
In striatal spiny projection neurons with mutant huntingtin, mitochondria spill immunogenic RNAs into the cytosol. These touch off innate antiviral signaling inside the neurons, which may spell their demise.
A 2018 report that had spotted extra copies of APP lurking in neuronal genomes has come under scrutiny, with claims that the result is due to contamination. Does a response from the original authors bolster their claim?
Tissue from 13-week-old fetuses carrying the huntingtin repeat expansion shows defects in neuronal polarity and proliferation, which lead to fewer neurons populating some brain regions.
Behold single proteins on the move: Super-resolution microscopy of living cells suggests the infamous protease does not form complexes with other secretases in the plasma membrane—in mouse fibroblasts, that is.
The tracer distinguished people with progressive supranuclear palsy from controls with a sensitivity of 85 percent, suggesting potential as a diagnostic for 4R tauopathies.
The findings hint at a liver-brain axis that transmits inflammation from periphery to brain, and could suggest therapeutic targets for preserving brain function.
New drug application is first for Alzheimer’s disease in the U.S. since 2003, and first based on amyloid hypothesis.
Released from hippocampal neurons in response to experience, the cytokine prompted microglia to eat extracellular matrix around synapses. This facilitated growth of new spines, and sharpened memory.
As mice age, a busy receptor-mediated protein transport across the barrier wanes; inhibiting an alkaline phosphatase restores it. Meanwhile, the aging barrier becomes generally leaky to large molecules.
Sex-specific polygenic hazard scores predict pathology and cognitive decline.
Cognitive enrichment in early life correlated with less Alzheimer’s pathology, and slower cognitive decline, in late life.