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.
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.
In response to the peptide, these little cells squeeze capillaries, constricting them. This may contribute to neuronal dysfunction.
Co-sponsors Banner, Novartis, and Amgen announced that they will stop testing CNP520 in two Phase 2/3 studies in people at risk of AD. The drug worsened cognition.
A leaky blood-brain barrier in the hippocampus correlated with cognitive impairment, independently of other vascular risk factors or Alzheimer’s pathology.
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.
The hippocampus trickles out new neurons throughout life, a process that falters without BACE1 or in the presence of ApoE4.
Vascular microchannels linking the skull bone marrow to the dura mater supply the brain with neutrophils in response to stroke and inflammation.
Computational models predict that ALS mutations tax the flexibility of profilin-1, weaken binding with key partners including actin, and boost the protein’s propensity to aggregate.
By promoting the exocytosis of cellular debris, the kinase may facilitate spread of α-synuclein aggregates.