Detecting oligomers in the cerebrospinal fluid is no easy feat. The latest test is among the most sensitive yet, but is it useful?
A new initiative in the U.K. will fund research into potential treatments for dementia and neurodegeneration.
In Fragile X syndrome, mRNA from the mutant FMR1 gene binds to its own DNA to suppress protein expression. Could the same thing happen in other repeat expansion diseases?
AstraZeneca’s BACE inhibitor AZD3293 moves forward to a Phase 2/3 trial, joining Merck’s MK-8931 as the most advanced current compounds in this class.
The first longitudinal data from DIAN conflict with some cross-sectional findings, revealing a small drop in CSF injury markers after the first appearance of symptoms of disease.
The scientific spotlight often shines on excitatory neurons as the brain’s main Aβ factories. What about other cell types?
Scientists may have discovered another explanation for why DNA repeat sequences cause neurodegenerative diseases: A six-nucleotide expansion in the C9ORF72 gene forms stable structures that interfere with its transcription.
Scientists claim to turn differentiated mouse cells into pluripotent ones with a brief dip in an acid bath—no genetic tweaks necessary.
Low levels of 10 phospholipids in blood plasma correlated with future cognitive decline in older adults, hinting at diagnostic potential.
A combination of high clusterin and low Aβ42 in cerebrospinal fluid associates with early Alzheimer’s neurodegeneration, hinting at a mechanistic interaction between the proteins.
Researchers at BACE meeting explore how trafficking and degradation of the protease relate to amyloid pathology in AD.
Scientists are trying to help the brain replace lost dopamine in people with Parkinson's. Will gene therapy or cell replacement work eventually?