When these tiny mural cells carried APOE4, they secreted more ApoE, causing Aβ to deposit in capillary walls. Blocking ApoE production prevented angiopathy.
Acting downstream of TREM2, PLCγ2 facilitates phagocytic microglial behavior such as lipid processing. PLCγ2 also acts downstream of toll-like receptors, where it can throw a switch to inflammation.
A GWAS of co-expression modules identifies a haplotype that disrupts lysosomes and myelination. ApoE4 and Aβ regulate the same module.
People who lived in impoverished neighborhoods in their last year of life had greater odds of having died with AD neuropathology.
In seven papers, researchers presented a dazzling set of findings gleaned from 125,748 exomes and 15,708 genomes housed in a new database. Tidbits emerge on tau, LRRK2, and other proteins implicated in neurodegeneration.
In cell culture, slashing Aβ production by more than half harmed neuronal signaling, but a smaller cut maintained it.
Researchers identify a way to isolate human astrocytes generated from induced pluripotent stem cells. And astrocytes stand out in FTD-prone brain areas.
Induced neurons lacking the Alzheimer’s risk gene can’t properly recycle APP.
Using a form of confocal microscopy and automated software, the method allows researchers to rapidly identify functional synapses within brain structures.
The modeling approach reinforces the idea that tau pathology propagates through the brain’s physical architecture, including neuronal networks.
Built to cross the blood-brain barrier, the vehicle delivers therapeutic antibodies, enzymes, and potentially small molecules such as oligonucleotides.
Umbilical cord stem cells from presenilin 1 E280A carriers, once differentiated into cholinergic-like neurons, pumped out Aβ42 and accumulated phosphorylated tau and apoptotic markers.
In stark contrast to Aβ and tau fibrils, α-synuclein fibrils are asymmetric, comprising two different protofibrils.
The plasma biomarker neurofilament light was able to distinguish individual mutation carriers from noncarriers three years prior to onset.
Separately, cerebrovascular disease drove an uptick in neurofilament light in the brain, indicating neurodegeneration.