Behold, the Human Brain Like Never Seen Before
Reported in 21 papers, a collaborative effort describes brain-wide gene expression, epigenetics, morphology, and activity at single-cell resolution.
215 RESULTS
Sort By:
Reported in 21 papers, a collaborative effort describes brain-wide gene expression, epigenetics, morphology, and activity at single-cell resolution.
The Alzheimer’s risk allele locks microglia in a state of homeostasis. They ignore amyloid plaques and neurofibrillary tangles.
We all know oligodendrocytes maintain myelin. According to scientists at the 2nd Symposium on Lipids in Diseases, they need microglia to do it.
The largest genome-wide association study for PSP tied six risk loci to the tauopathy, including one new locus near the complement C4A gene.
Smartphone- and web-based cognitive tasks detected amyloid positivity, early Alzheimer’s, better than in-person tests. Some are being used in clinical trials.
A new method tags individual cells in a tissue slice with a DNA barcode. This allows isolated cells to be mapped to their original location.
Axons touch arterioles, releasing glutamate that makes smooth muscle cells relax. This increases cerebral blood flow in mice.
In people on Entresto, Aβ42 and Aβ40 shot up over six months. The Aβ42/40 ratio fell by a third.
The biomarker may signal tau’s early days of entanglement, and serve as a useful disease staging indicator, according to a new immunoassay.
A U.K. Biobank analysis generated 15 risk factors for young-onset dementia. Many factors also correlated with late-onset disease.
In amyloid immunotherapy trials to date, abolishing plaque leads to better outcomes months later. Cognitive benefits lag behind amyloid removal.
Roche’s “brain shuttle” antibody, trontinemab, cleared plaque in Phase 1 with little ARIA, highlighting that bypassing vascular amyloid could be the key.
Risk variant promotes TMEM106b fibrillization; protective variant discourages it.
In early phase trials, therapy lowering tau translation hinted at cognitive benefit, while going after APP lowered its fragments and Aβ peptides.
A new, stem-cell-based method generated neural cultures that live long enough to suffer the consequences of TDP-43 dysregulation.