Not Just Aβ—Glymphatic Flow Clears Tau, Too, Slowing Its Aggregation
Retarding glymphatic clearance in mice caused p-tau to accumulate faster, and hastened neurodegeneration.
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Retarding glymphatic clearance in mice caused p-tau to accumulate faster, and hastened neurodegeneration.
The comment period ends with nearly 10,000 submissions split between pro and con, letter-writing campaigns, and scrutiny from U.S. Congress. Even so, scientists say, not much has changed.
Heterogenous oligomers that include shorter Aβ peptides, such as Aβ37 and Aβ38, along with Aβ42 do not form fibrils, slowing plaque growth.
CSF Aβ and tau are abnormal in older people with psychiatric problems. Are these symptoms an effect of AD pathogenesis, or risk factors for it?
In a career that spanned more than 40 years, Trojanowski broadened and deepened the field's understanding of the molecular pathology of neurodegenerative diseases.
A person's burden and spatial distribution of plaques, as measured by PiB-PET, varied greatly depending on his or her mutation. Their CSF Aβ42 or cognitive decline did not.
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.
Large multinational meta-analysis also found that among people without dementia, CSF Aβ42 edged out PET in detecting amyloid pathology.
Certain MHC class II subtypes reduce a person’s risk of Alzheimer's and Parkinson's. They bind an acetylated snippet of tau.
Protein networks unseen in RNA data correlated closely with plaques, tangles, cognitive decline. Many are in the extracellular matrix.
Dementia risk nearly doubled after each minor stroke and tripled after each major one, regardless of vascular risk factors. Risk climbed almost sevenfold after multiple major strokes.
An unbiased “interactome” generated from human neurons could shed light on what goes wrong in tauopathies, and help identify new therapeutic targets.
When this retromer faltered in mice, Aβ levels rose in the brain and synaptic signaling waned in the transentorhinal cortex. General retromer loss in hippocampal neurons evoked dystrophic microglia similar to those seen in AD.
MK-6884 measures allosteric changes to the M4 subtype of muscarinic receptors. Ligand binding tightened when people took donepezil, an acetylcholinesterase inhibitor.
Among 39 sets of identical twins, tau tangles accumulated in a strikingly similar pattern within each pair. A pair's discordance was due to Aβ and factors such as exercise.
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