A CD33 variant associated with Alzheimer’s boosts levels of wild-type TREM2, hinting that these risk factors could share a common mechanism.
The genetic relics of ancient, dormant retroviruses pepper the human genome. One such virus reanimates in about one-third of ALS cases.
Analysis of the avagacestat trial of 2012 details the side effects that sank the drug, and the outcomes that support CSF biomarkers for prodromal Alzheimer’s disease.
The 1000 Genomes consortium released its final report and sequence data set. It will help scientists studying neurodegenerative diseases better interpret GWAS findings.
Acetylated tau accumulates in Alzheimer’s disease, and associates with pathology and behavioral measures in mouse models.
Drosophila were just fine, thank you very much, despite carrying the ALS- and FTD-linked repeats in the same intronic context as they occur in people.
In a large population study, middle-aged people who developed atrial fibrillation were about twice as likely as their peers to succumb to dementia over the next 20 years.
GATA4 transcription factor connects selective autophagy to pro-inflammatory state of cells harboring DNA damage. Researchers propose the pathway may play a role in age-related disease.
Some Alzheimer’s risk genes may be partners in crime, influencing each other’s expression or behavior. In this week’s Nature Neuroscience, researchers report immune-related AD risk genes interact in human monocytes. Of particular note, increased expression of the CD33 receptor boosted the amount of wild-type TREM2 on the cell surface, suggesting a functional connection between these proteins.
Scientists looking for amyotrophic lateral sclerosis risk factors may have found a new culprit lurking in the DNA of every person on the planet. Endogenous retroviruses, the relics of ancient infections, dot the human genome. One of these, HERV-K, reawakens and produces RNA and proteins in a subset of people with sporadic ALS, according to a paper in Science Translational Medicine.
Do nuclear aggregates of hexanucleotide repeat RNAs, copied from an intron in the C9ORF72 gene, kill neurons? A study in Drosophila says no. Only when the RNAs escape into the cytoplasm do they cause trouble, probably because they are translated into repeat dipeptides there.
Evidence keeps growing that a person’s cardiovascular health in midlife affects the health of their brain in the future. A large population study in the Netherlands suggests that people who developed atrial fibrillation, a common arrhythmia, in middle age had up to triple the risk of sliding into dementia in old age.
- Jeremy Garson on Do Sleeper Viruses Awaken in ALS?
- Kaycee Sink on Neither Exercise Nor Supplements Boost Cognition in Two Large Studies
- Fred Van Leuven on New Type of Toxic Tau? Acetylated Form Correlates With Memory Defects
- Takaomi Saido on New Type of Toxic Tau? Acetylated Form Correlates With Memory Defects
- Marcia Ratner on Chronic toxic encephalopathy in a painter exposed to mixed solvents.
- Diane Stephenson and Stephen Arneric on Cerebrospinal Fluid Neurogranin Correlates with Markers of Neurodegeneration
- Aaron Gitler on C9ORF72 RNA Foci Acquitted of Toxic Charge—in Fruit Flies