As Health Problems Pile Up, Dementia Climbs on Top of the Heap
According to findings from more than 200,000 people 60 and older, having multiple chronic diseases nearly doubles the risk of dementia within the next 12 years.
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According to findings from more than 200,000 people 60 and older, having multiple chronic diseases nearly doubles the risk of dementia within the next 12 years.
Aligning single-cell gene expression in “pseudotime” models longitudinal change. It explores how healthy cells become sick during Alzheimer's.
By pooling single-nucleus RNA-sequencing datasets, scientists found consistent changes across Alzheimer’s cohorts. Examples: hypermetabolic transcription, and a new neuron population that dies early on.
Analysis identified neuronal populations that die early in AD and glial subtypes that expand. Gliosis signaled fast memory decline.
Fewer requirements and simpler agreements should improve accessibility, use.
In this classification scheme, T, i.e. tau, means different things. Phospho-tau predicts tangle buildup, whereas tau-PET signals neurodegeneration and cognitive decline.
Gonadotrophin-releasing hormone improved memory in a mouse model of DS, and it nudged up test scores in a pilot trial. The key? Dosing in pulses.
In human cerebral organoid cultures, mutant tau spurred astrocytes to make excess cholesterol and fatty acids. This happened before overt tau pathology.
Whether TDP-43 behaves itself in the nucleus or gets mixed up with a gelatinous blob in the cytoplasm may come down to HSPB1, which acts as TDP-43’s chief handler in the cytoplasm.
Super-resolution microscopy spots tiny tau clusters in live cell cultures. They come and go. Why do they form? What do they do?
Microglial ApoE4 hobbled these cells' protective responses against Aβ and tau. In the meninges, ApoE4 made by myeloid cells slowed lymphatic drainage; at the blood-brain barrier, ApoE4 steered aging endothelial cells and pericytes toward dysregulation.
A tetravalent IgG1 prompts TREM2 to cluster, boosting the receptor’s activation 100-fold. Treated mice had fewer plaques, better memories.
Soluble p-tau, aggregation epicenters, and gene variants emerged as potential forces that might influence how quickly tangles propagate through the brain.
In a large European study, the scans changed the diagnosis in a third of cases. They boosted the doctor's confidence in making the call, and predicted cognitive decline.
The autopsy of a woman with a the PSEN1 Paisa mutation plus a homozygous ApoE3 variant showed an unusual distribution of tau tangles. Gene-expression studies pinpointed vulnerable neurons that were spared, and riled-up microglia in tangle-ridden zones.
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