Masking a Splicing Site Compensates for TDP-43 Dysfunction
Antisense oligonucleotides prevent mis-splicing of stathmin-2 when TDP-43 abandons the nucleus in human induced motor neurons or in the mouse brain.
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Antisense oligonucleotides prevent mis-splicing of stathmin-2 when TDP-43 abandons the nucleus in human induced motor neurons or in the mouse brain.
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?
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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.
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