The burgeoning proliferation in glia during neuroinflammation could indicate disease course and the efficacy of potential medicines...
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In neurons derived from FTD patients, microtubules distort the nucleus, warping its normally rounded membrane and disrupting communication with the cytoplasm.
In familial Alzheimer’s disease, rise in NfL in the blood precedes disease onset by 16 years.
Frail people may be more likely to have Aβ plaques and neurofibrillary tangles; when they do, they are more likely to have dementia. Physical activity correlated with better global cognition, regardless of brain pathology.
Reducing systolic blood pressure staves off cognitive decline, but what about dementia?
At AAIC, scientists said that alterations in how the aging female brain uses energy and metabolizes fat may leave APOE4 carriers particularly susceptible to tau pathology.
New work implicates changes in chromatin structure and failed DNA repair in neurodegeneration.
Compared with previously published model lines, these animals develop more features of amyotrophic lateral sclerosis and frontotemporal dementia.
Mouse lines made by two different labs replicate the molecular pathology, but not the neurodegeneration, of ALS and FTD based on C9ORF72 expansions.
In a process known as repeat-associated non-ATG translation, neurons and glia make alanine, serine, cysteine, and leucine chains from the huntingtin gene.
Scientists say treatments to muzzle faulty genes are making some headway.
The RNA-binding protein hnRNP A3 can help rid a cell of the repeat RNAs, but the RNAs interfere with its nuclear localization.
The latest news on C9ORF72 includes a genetic modifier, various animal models, and a potential treatment to untangle stable, guanine-based structures formed by expanded repeats.
A repeat expansion that causes neurodegenerative disease is transcribed both forward and backward, producing sense and antisense RNAs and multiple polypeptides.