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?
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.
An antioxidant thought to boost mitochondrial function came up short in a large multicenter trial for PD treatment.
PINK1 mutations cripple mitochondrial energy production, raising new questions about Parkinson’s disease.
A Keystone symposium underscores the role of lysosomal dysfunction and vesicle trafficking in neurodegenerative disease.
Astrocytes kindle neuronal hyperexcitability in mouse models of Huntington’s.
When a calcium sensor disappears from dendritic spines, synapse loss soon follows in Alzheimer’s models, aging mice, and diseased human brains.
Older adults with amyloid in their brains develop abnormal activity in the entorhinal cortex even while memory and hippocampal function remain unaffected.
If new results hold up, enhanced phosphorylation of a ribosomal protein may explain the toxicity of mutations that cause Parkinson's.
Scientists claim that AV-133, an imaging agent that visualizes dopaminergic neurons, can gauge progression of Parkinson’s disease.
Scientists generate human embryonic stem cell lines from adult donor cells, building on earlier studies that showed this was possible with fetal cells.
A small longitudinal study suggests that atrophy begins in the frontoparietal cortex, not the hippocampus, in early Alzheimer's.
European and U.S. agencies approve a third amyloid PET tracer, florbetaben.
The overused adage of the fountain of youth rears its head again, as four new studies show how young blood rejuvenates old brain and muscle, pumping up the vasculature, stem cells, and restoring microglia’s appetite for waste products. Researcher are isolating the responsible factors, for example GDF11.