Osmotic Stress Ushers FUS Out of Nucleus and Into Stress Granules
The findings offer one way this RNA-binding protein gets into cytoplasm, where it sets the stage for pathological aggregation.
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The findings offer one way this RNA-binding protein gets into cytoplasm, where it sets the stage for pathological aggregation.
UCB-J hints at early synaptic loss in the hippocampus, but not the cortex. Researchers puzzle over the pattern.
The hippocampus trickles out new neurons throughout life, a process that falters without BACE1 or in the presence of ApoE4.
Vascular microchannels linking the skull bone marrow to the dura mater supply the brain with neutrophils in response to stroke and inflammation.
Study links changes in the retina’s microvasculature to brain amyloid in cognitively normal adults.
Computational models predict that ALS mutations tax the flexibility of profilin-1, weaken binding with key partners including actin, and boost the protein’s propensity to aggregate.
Treatments that promote neurogenesis and elevate BDNF act as exercise does to improve memory in mouse models of Alzheimer’s disease.
By promoting the exocytosis of cellular debris, the kinase may facilitate spread of α-synuclein aggregates.
Ablating BACE1 in adult mice spares them from most problems found in germline knockouts. However, axons extending from newborn hippocampal neurons still lose their way.
The largest study so far to compare brain scans and CSF among African-Americans and Caucasians finds differences, but participant numbers remain small.
Amyloid plaques in postmortem human cortex correlated with the proportion of microglia that were activated, not with microglial numbers. Tau pathology and cognitive decline come later.
Reducing these esters with statins and cholesterol-hydroxylase-activating drugs lowers phospho-tau and Aβ in neurons. One such drug is approved to treat HIV AIDS.
Among cognitively normal people with amyloid plaques, women have more tau tangles in the entorhinal cortex than do men. Does this indicate susceptibility, or resilience?
In mouse models of Alzheimer’s, neutrophils stick to capillaries in the cerebral cortex, reducing blood flow. Keeping those cells moving or depleting them altogether improved memory.
A score based on the combined burden of a person’s Alzheimer’s risk variants correlated with plaques, tangles, cognitive decline, and even non-AD pathology. Are polygenic hazard scores ready for direct-to-consumer marketing?