Human-on-a-chip technology could provide a more valuable clinical-based model for ALS.
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.
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.