Analysis of MRI brain volume data identifies multiple AD and FTD/ALS disease subtypes with distinct patterns of degeneration over time.
A small molecule that protects neurons fends off a short region of Aβ from a specific pocket on the LilrB2 receptor.
In DIAN, participants who are more physically active may also have slower disease progression.
In several model systems, α-synuclein boosts oleic acid production and the fatty acid worsens α-synuclein pathology.
In presynapses, binding sequesters synaptic vesicles.
Microfluidic tri-culture of neurons, astrocytes, and microglia models how glia impose deadly neuroinflammation on top of amyloid and tau pathology.
Two independent studies find that loss of nuclear TDP-43 leads to mis-splicing of stathmin 2, an essential protein for axon growth and repair.
Aberrant gene-expression patterns found to be common to human neurodegenerative disease and animal models. MicroRNA and epigenetic modification may be to blame.
Boosting sTREM2 in the brain rallied microglia to clear Aβ plaques, restored synaptic plasticity, and even rescued memory deficits in mice.
A leaky blood-brain barrier in the hippocampus correlated with cognitive impairment, independently of other vascular risk factors or Alzheimer’s pathology.
Clusters of neurons harboring somatic mutations in 56 genes linked to neurodegenerative diseases may be commonplace in the human brain.
A molecular-level view of tau filaments from a person with Pick’s disease reveals that the protein folds up differently than it does in Alzheimer’s disease.
Better tissue extraction and Aβ assays could help identify the most toxic Aβ species and most promising immunotherapies.
The findings offer one way this RNA-binding protein gets into cytoplasm, where it sets the stage for pathological aggregation.
UCB-J hints at early synaptic loss in the hippocampus, but not the cortex. Researchers puzzle over the pattern.