Lifestyle Coaching Slows Cognitive Decline in African-Americans with MCI
A behavioral intervention slowed memory slippage and functional decline over two years.
281 RESULTS
Sort By:
A behavioral intervention slowed memory slippage and functional decline over two years.
In DIAN, participants who are more physically active may also have slower disease progression.
A small molecule that protects neurons fends off a short region of Aβ from a specific pocket on the LilrB2 receptor.
Analysis of MRI brain volume data identifies multiple AD and FTD/ALS disease subtypes with distinct patterns of degeneration over time.
Clusters of neurons harboring somatic mutations in 56 genes linked to neurodegenerative diseases may be commonplace in the human brain.
In several model systems, α-synuclein boosts oleic acid production and the fatty acid worsens α-synuclein pathology.
In presynapses, binding sequesters synaptic vesicles.
A leaky blood-brain barrier in the hippocampus correlated with cognitive impairment, independently of other vascular risk factors or Alzheimer’s 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.
Scientists know that the retina changes in people with preclinical AD; alas, there is neither consensus nor convergence in the field of retinal imaging. An upcoming initiative aims to determine which measures are most robust.
Males are inflammatory, females are neuroprotective: Profiling of microglia from adult mice suggests sex-specific phenotypes, likely set at birth.
An 856-patient, proof-of-concept trial of the anti-protofibril Aβ antibody suggests the highest dose slowed cognitive decline and cleared plaques.
Better tissue extraction and Aβ assays could help identify the most toxic Aβ species and most promising immunotherapies.