Study reveals an association between intestinal inflammation and the gut microbiome in the development and progression of ALS.
Ebselen, a Selenium-based drug molecule, and several other novel compounds can change the characteristics of SOD1. The findings could help with the development of new therapeutics for ALS.
Human-on-a-chip technology could provide a more valuable clinical-based model for ALS.
Increasing the activity of interneurons in later 5 of the primary motor cortex in mouse models of ALS effectively slowed the onset of the disease.
The TBK1 gene regulates the disease progression of ALS in mouse models of the neurodegenerative disease. Loss of the TBK1 gene in motor neurons increases SOD1 aggregation and accelerates the onset of the disease.
Exposure to the environmental toxin BMAA may elevate the risk of ALS. BMAA is produced by cyanobacteria, a blue-green alga that commonly occurs in marine ecosystems and accumulates in shellfish, sharks, and other sea-life. Those most reliant on sea-foods for their food source may be most at risk.
Researchers have isolated a molecule that may be under-produced in the gut of those with ALS. Using mouse models of the disease, researchers identified 11 microbial strains that became altered as the disease progressed, or before the development of symptoms.
During early Alzheimer's disease, SOD1 initially weakens levels of Tau protein. However, as the disease progresses, the antioxidant becomes less effective at protecting the brain against neurodegeneration.
A new study reveals peripheral nerve damage may trigger the onset and spread of ALS in mouse models of the neurodegenerative disease.
Researchers report activating microglia may help reduce the imbalance between neuroprotection and neurotoxicity for neurodegenerative diseases.
A new method reveals some ALS affected neurons display hypo-excitability. Researchers say these changes most likely represent early steps in the disease progression.
Researchers report transplanting altered neural stem cells into the brains of mice genetically engineered to exhibit symptoms of ALS, delayed the progression of the disease and extended lifespan.
