A SARS-CoV-2 protease cleaves the transcription factor NEMO, which protects the brain's endothelial cells. In people who had COVID, and mice lacking NEMO, blood vessels shriveled. Could long COVID increase risk for dementia?
Microglia regurgitate tau seeds. Then they retreat into a senescent torpor. In this state, they nonetheless pump out potentially hazardous metalloproteases.
A combination of retinoic acid and the cholesterol drug gemfibrozil prompted astrocytes to ingest and degrade Aβ. Mice treated this way had fewer amyloid plaques and performed better on cognitive tests.
A paper marrying math modeling with biological data proposes that, past Braak Stage III, tau aggregates double every five years in the neocortex. By this stage, they were already distributed throughout, de-emphasizing spread.
Having a serious flu upped a person's odds of getting PD a decade later; a sedentary life dimmed prospects of living with PD; and cerebrovascular pathology implied more severe parkinsonism. Deaths due to PD have risen in the United States.
At a recent conference, researchers presented more evidence tying the APOE4 allele to disrupted lipid metabolism. They linked this problem to Aβ production.
In Alzheimer's mice without the AD risk gene Abi3, fewer microglia crowd around amyloid plaques. Cultured microglia without Abi3 appear stuck in a torpor, even though their phagocytosis mostly works.
The new gene JADE1 encodes an adaptor protein that sits in tangles and nonetheless appears neuroprotective. The study also turned up three AD and two PSP genes, suggesting PART overlaps with these conditions.
Data shown at CTAD suggests the Aβ42/40 ratio falls in the blood before it does in the CSF, offering perhaps the earliest glimpse at the pathophysiology of Alzheimer's. Measuring that change prospectively might be a tall order.
In a mouse model of amyloidosis, microglia carried Aβ aggregates into grafted wild-type tissue. The immune cells played a key part in the subsequent growth of plaques in the graft.
While Phase 3 trials of subcutaneous gantenerumab continue, scientists say delivering the antibody to the brain via the transferrin receptor might be twice as efficient.
The same 24 proteins that are downregulated in an Alzheimer’s proteomic study are turned up in young APOE4 carriers. Two proteins, the kinases Yes1 and Fyn1, are targets of the drug dasatinib, which is being tested as an anti-aging senolytic in AD.
Transcriptomics pinpoints an expansion of pro-inflammatory microglia in people who carried the R47H-TREM2 variant. A similar cadre of microglia arose in female tauopathy mice carrying a single copy of the AD risk variant.
By integrating plasma proteomics data from 35,000 Icelanders with data on disease-associated variations in their genomes, scientists cinched connections between gene variants that change protein levels in plasma, causing disease.