Granules in the nucleus and cytoplasm may owe their genesis and shape to liquefied forms of ALS-linked proteins, such as FUS and hnRNPA1.
Researchers report the first known enzyme that combines disaggregase and protease activity.
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.
Avanir Pharmaceuticals’ AVP-923 calmed Alzheimer’s patients in a small 10-week study.
Mutations in CHMP2B gene have been linked to mysterious lysosomal inclusions.
Abnormal protein aggregation is common to neurodegenerative diseases—but what if aggregation were a consequence of normal organelle formation taken to the extreme? Defining a new area of research, scientists are realizing that certain proteins condense into liquid droplets within the cell, lending a modicum of structure to transient, membrane-free organelles such as stress granules. While this newly appreciated feat of cellular biophysics may serve a physiological purpose, it also puts proteins at risk of condensing even further, into the solid fibrils seen in neurodegeneration. This could be important in ALS and beyond. Learn about this emerging disease hypothesis from Simon Alberti, Cliff Brangwynne, Nicolas Fawzi, and Paul Taylor, who will present recent findings in an Alzforum Webinar on October 30.
To get rid of protein aggregates, cells must first break up the clumps, then digest the individual pieces. Now researchers have identified the first known enzyme that can do both. HTRA1 is known to be a serine protease, but it can also weakly tease apart tangled tau strands. With some engineering to optimize this activity, the protein might make a promising candidate to bust up deposits, researchers said.
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.
- Ana Griciuc, Lars Bertram, Raj Hooli and Rudy Tanzi on Alzheimer’s Risk Genes Interact in Immune Cells
- Rita Guerreiro on Alzheimer’s Risk Genes Interact in Immune Cells
- 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.