When Faced with Amyloidosis, Human Transplants Die by Necroptosis
In mice, the long noncoding RNA MEG3 mediated the death of human neurons, which accumulated tau tangles.
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In mice, the long noncoding RNA MEG3 mediated the death of human neurons, which accumulated tau tangles.
In people over 60, sitting for 12 hours per day increased dementia risk. An exercise-induced hormone, irisin, protects via astrocytes, at least in vitro.
A curated panel of 48 proteins foretold cognitive decline. It also illuminated biological pathways involved in Alzheimer's disease.
A retrospective study found an increased risk of brain bleeds in people who received blood from someone else with such bleeds, hinting at a soluble agent. Aβ?
The NIA invites scientists to submit data to create diverse, open datasets and design diagnostic algorithms for more accurate, early prediction of Alzheimer’s.
In a mouse amyloidosis model, a protective variant tightened the reins on plaques and spared synapses; a risk variant did the opposite.
Provocative new data suggest that glial engulfment of synapses dampens network hyperexcitability early in disease. Key mediators: TREM2 and phosphatidylserine.
These greasy particles carry more than 300 different proteins. Some oil the immune response, inflammation, and wound healing.
Droplets of triglycerides accumulate in microglia exposed to Aβ fibrils. These cells barely ate Aβ, and released molecules that damage neurons.
Together, the two immune-cell types deal a neurodegenerative blow more powerful than either can inflict alone.
Compared to AD, tau tangles in PART accumulated slowly, and only in the medial temporal lobe. Cognition slipped subtly, and no amyloid amassed over three years.
Experts say the low specificity of Quest Diagnostics’ plasma Aβ test could lead to more false than true positives, causing distress and confusion.
Proteins involved in the extracellular matrix, metabolism, immunity, proteostasis, and synaptic function change in the CSF and plasma up to 30 years before dementia sets in.
Few people with Down's syndrome have cardiovascular risk factors, yet most develop cerebrovascular disease. Will this complicate anti-amyloid immunotherapy?
Two men with loss-of-function variants in their APOE4 alleles escaped amyloid pathology. One was in his 90s.