In Tauopathy, ApoE Destroys Neurons Via Microglia
Ablating the immune cells protected mouse models of frontotemporal dementia from the neurodegeneration caused by human ApoE4.
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Ablating the immune cells protected mouse models of frontotemporal dementia from the neurodegeneration caused by human ApoE4.
Using chemical cross-linkers to map contacts among amino acids, structural biologists predict that soluble tau is, in fact, a compact globule containing β-sheets poised to snap into a pathological formation.
The transcriptional repressor quiets neural activity and lengthens lifespan in worms. It is abundant in the brains of cognitively healthy centenarians.
By analyzing a single MRI scan, researchers pinpointed the origin of frontotemporal dementia pathology and predicted its future progression.
The resource boasts 56 stem cell lines derived from tau mutation carriers, patients with sporadic disease, healthy controls, and engineered isogenic lines, including some that have their mutation corrected by CRISPR.
Based on high school personality tests taken nearly 60 years ago, researchers associated certain traits with future risk of dementia.
After shutting down a Phase 3 program last March, Biogen now says the futility analysis it did was incorrect, and that a new analysis of a larger dataset in fact supports filing for FDA marketing approval next year.
A $400,000 prize is to be awarded as part of the new Rainwater program, and $63 million of NIH money will support a research consortium on frontotemporal dementias.
Cognitive deficits in mice on a high-salt diet are due to tau phosphorylation, not reduced blood flow, according to a new study.
Two papers used different approaches to energize laggard lysosomal function in neurons derived from people with Parkinson’s. Both restored lysosomal trafficking and reduced α-synuclein accumulation.
Evidence from postmortem human brains and cultured human microglia suggests the immune cells make a meal out of synapses, especially near plaques.
The first ever cryoEM structures of Aβ fibrils extracted from AD tissue look quite different than prior structures of fibrils generated in vitro. For starters, they are right-hand twisted, not left-hand.
Imaging studies suggest that ApoE4 carriers may be more susceptible to the effects of tangles, particularly if they are women.
Slow-wave sleep brings on coordinated oscillations in blood flow, which in turn are coupled to waves of cerebrospinal fluid. The data point to a mechanism linking deep sleep to the flow of CSF.
The rare ApoE3 Christchurch variant prevented tau tangles, neurodegeneration, and cognitive decline in a woman’s brain for decades, despite massive amyloid buildup from a familial presenilin AD mutation.
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