Exosomes From Living Mice Hint That Sexes Respond Differently to Amyloid
The protein content of extracellular vesicles sampled from hippocampal interstitial fluid depended on age, sex, and amyloid load.
6397 RESULTS
Sort By:
The protein content of extracellular vesicles sampled from hippocampal interstitial fluid depended on age, sex, and amyloid load.
The p-tau217/tau217 ratio in the cerebrospinal fluid tightly correlated with amyloid, while p-tau205/tau205 best detected neurofibrillary tangles and neurodegeneration.
Summoned by microglia, T cells trigger neurodegeneration in a mouse model of tauopathy. Does this happen in Alzheimer’s disease?
The decade-long trial found no benefit for solanezumab in delaying progression, but laid the groundwork for subsequent prevention studies.
These endoplasmic reticulum channels can flood the cytosol with calcium, disrupting lysosomal acidification and stalling autophagy.
Joining the circulatory systems of young mice with old evokes gene-expression changes in the brain that reflect in proteostasis, metabolism, and inflammation.
A new mouse study finds no consistent gamma entrainment, amyloid lowering, or microglial activation in response to 40 hertz light, raising questions about previous findings.
The U.S. Food and Drug Administration will convene an advisory committee to guide its decision, which will affect how widely available the treatment will be.
Carriers of R145C were more likely to get AD, but only if they co-inherited a copy of ApoE4.
When growing among healthy human neurons, astrocytes that lack progranulin cause TDP-43 to aggregate and muck up neuronal gene splicing.
Shrinkage of distinct brain regions in the frontal and temporal lobes may unsuppress neural activity in the dorsal stream, a region involved in visual perception.
A protective variant promotes anti-inflammatory microglia, while a risk variant depletes them.
Across a three-decade span, there was no difference in amyloid pathology, but younger cohorts had healthier cerebrovasculature.
In mice, nixing ApoE4 from neurons squelched tau pathology, myelin loss, and neuronal death.
In mice, the neuronal transcription factor NPAS4 recruits DNA repair machinery to active promoters; without it, double-strand DNA breaks accumulate.