Davos Alzheimer’s Consortium to Link Global Cohorts
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.
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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.
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.
Data shown at CTAD suggests the Aβ42/40 ratio falls in the blood before it does in the CSF, offering perhaps the earliest glimpse at the pathophysiology of Alzheimer's. Measuring that change prospectively might be a tall order.
AAV-based CRISPR snipped a piece of mutant APP and limited plaques in mice. Viruses that infiltrate only the CNS—and only neurons there—may facilitate localized gene editing in the brain.
APP or presenilin mutation carriers who also carried the Met66 allele had more p-tau217 at presymptomatic stages, and more p-tau205 at symptomatic stages, than did Val carriers.
Longitudinal ADNI data tie higher sTREM2 in CSF to slower cognitive decline, reinforcing the idea that TREM2 activity protects the brain from AD pathology.
Heterogenous oligomers that include shorter Aβ peptides, such as Aβ37 and Aβ38, along with Aβ42 do not form fibrils, slowing plaque growth.
A population of AGTR1-expressing dopaminergic neurons in the ventral slice of the human substantia nigra were selectively vulnerable in Parkinson's disease. These cells also expressed the most PD risk genes.
Depleted of cholesterol, neurons laid out the welcome mat for tau aggregates, which readily crossed into the cytosol and seeded aggregation there. Adding cholesterol blocked entry and seeding.
Proteins stuck around longer in the oldest mice. Those involved in neurodegeneration had the most extended lifespans.
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.
While TMEM175 ushers potassium ions out of neutral lysosomes, it shuttles protons out of acidic ones. Sans TMEM175, lysosomes become too “tart,” and stop working. Two papers say so.
Mutations spur fibrillization, while methylation and autophagy keep droplets nice and fluid.
Certain mutations in TDP-43, tau, and NfL add one hydrogen bond to their low-complexity domains. This warps phase transition and strengthens self-aggregation.
In young adults with Down’s, plasma phospho-tau217 correlated with amyloid and tau PET positivity. With great accuracy.