X-ray crystallography yields high-resolution structure.
In AD brain, scientists see a genome-wide histone acetylation pattern replete with peaks near familiar AD genes such as APP, presenilin, tau, complement receptor, and more.
Much like tau, Aβ, and α-synuclein, pathological TDP-43 spreads through the mouse brain, following the trail of neuronal connections and corrupting healthy protein along the way.
Case study in early onset AD finds PET ligand tracks regional tau burden.
A new finding questions the usefulness of some mouse models.
A new technique helps researchers single out and characterize toxic aggregates of TDP-43 from human brain.
Multiplexed marker analysis in single cells from human brain corroborates expression data, identifies microglia subsets in human brain.
With buckets of new data at AAIC, blood NfL grabbed attention as a telltale of neurodegeneration. The protein predicts progression, and might one day track treatment effects.
Studies in mice and humans show that sleep suppresses extracellular tau and slows its spread.
Neural progenitor cells derived from people with sporadic AD are missing the transcriptional repressor REST in the nucleus. This lets neurogenesis run wild, exhausting a person’s stem cell pool.
A large multicenter study confirms the tau PET ligand identifies AD at the dementia stage, but not so well at prodromal stages.
In cognitively normal people, a set of blood proteins may predict whether or not amyloid plaques have deposited in a person’s brain.
The approach provides an in vitro system that more closely resembles the brain milieu than do cell cultures, and can be used to model other proteinopathies as well.
Knocking down or blocking the CCR5 receptor with an HIV drug improved motor symptoms and learning and memory in a mouse model of stroke. Recently, researchers in China knocked out this gene in babies using CRISPR.
Only 16 percent of seniors report being assessed for cognition during yearly checkups. Eighty-two percent think it should be routine.