Traumatic Tau: Filaments from CTE Share Distinct Structure
Atomic resolution structures of tau filaments from three people with CTE revealed a common strain of tau induced by chronic head injuries.
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Atomic resolution structures of tau filaments from three people with CTE revealed a common strain of tau induced by chronic head injuries.
Using rigorous tissue-processing techniques, researchers find thousands of newborn neurons in older human hippocampi, but a dearth in brains with AD pathology.
Blocking the receptor clears toxic proteins and improves memory in old mice. The work proposes a new role in microglia for a well-known B-cell receptor.
Ever wonder why it’s so easy to nod off in a hammock? Turns out swaying back and forth improves sleep and even enhances memory in people.
Studies in mice and humans show that sleep suppresses extracellular tau and slows its spread.
Neural progenitor cells derived from people with sporadic AD are missing the transcriptional repressor REST in the nucleus. This lets neurogenesis run wild, exhausting a person’s stem cell pool.
In cognitively normal people, a set of blood proteins may predict whether or not amyloid plaques have deposited in a person’s brain.
The approach provides an in vitro system that more closely resembles the brain milieu than do cell cultures, and can be used to model other proteinopathies as well.
Knocking down or blocking the CCR5 receptor with an HIV drug improved motor symptoms and learning and memory in a mouse model of stroke. Recently, researchers in China knocked out this gene in babies using CRISPR.
Only 16 percent of seniors report being assessed for cognition during yearly checkups. Eighty-two percent think it should be routine.
In people at intermediate risk for cardiovascular disease, the meds had no effect on cognitive decline over six years.
Among British civil servants, the quality of their diet did not correlate with their risk of developing dementia cognitive decline over 25 years.
A prospective progeria drug revs up cellular autophagy and clears tau in neurons derived from patients with frontotemporal dementia. In mouse models, the drug rescues abnormal behavior.
Senolytic drugs kill these cells, temper Aβ, and improve cognition in transgenic mice.
Stakeholders have until February 11 to comment on draft FDA guidance for biomarker qualification.