The plasma biomarker neurofilament light was able to distinguish individual mutation carriers from noncarriers three years prior to onset.
The modeling approach reinforces the idea that tau pathology propagates through the brain’s physical architecture, including neuronal networks.
Researchers identify a way to isolate human astrocytes generated from induced pluripotent stem cells. And astrocytes stand out in FTD-prone brain areas.
As the SARS-Cov-2 infection peak passes in some areas, scientists are resuming lab work and clinical studies, albeit with new safety protocols in place. Regions differ greatly in how fast they can reopen.
A GWAS of co-expression modules identifies a haplotype that disrupts lysosomes and myelination. ApoE4 and Aβ regulate the same module.
This neuronal protein regulates the complement cascade in the developing brain. Could it do the same in aging or neurodegenerative disease?
Carriers accumulate fewer tangles than noncarriers for a given amount of amyloid, explaining how the gene variant may lower a person’s Alzheimer’s risk.
Without the WD domain of Atg16L1, required for a newly discovered type of endocytosis, old mice develop hallmark pathologies of AD.
In the Alzheimer’s brain, too, plaques trigger a coordinated inflammatory response from microglia and astrocytes. A preprint paper had shown the same for mice.
A 2018 report that had spotted extra copies of APP lurking in neuronal genomes has come under scrutiny, with claims that the result is due to contamination. Does a response from the original authors bolster their claim?
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.
Induced neurons lacking the Alzheimer’s risk gene can’t properly recycle APP.
In stark contrast to Aβ and tau fibrils, α-synuclein fibrils are asymmetric, comprising two different protofibrils.
In cell culture, slashing Aβ production by more than half harmed neuronal signaling, but a smaller cut maintained it.
New research suggests the R47H variant protects neurons from neurodegeneration, raising questions about staging and direction of future TREM2-based therapy.