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.
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.
Study reports protein aggregates within cells are cleared out by the endocytosis process. The findings could help with the development of new treatments for ALS.
Researchers have identified a set of drug-like compounds, including a common ingredient in throat lozenges, that can help protect mitochondria from the stresses associated with neurodegenerative diseases.
A new study challenges existing theories about spinal cord neurons. New findings suggest neurological signals originate from a major, scattered network of cells that send signals to only a few other neurons.
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.
When a motor neuron-specific pool of heat shock protein 90 (Hps90) was inhibited, motor neuron apoptosis was triggered.
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.
Retroviruses may be a missing causal link in diseases like ALS, multiple sclerosis and schizophrenia.
Open sharing of scientific data and standard methods will allow researchers to collaborate on projects and accelerate understanding of neurodegenerative diseases.
Treatment with copper-ATSM helped mouse models retain behavioral performance and prevented extensive motor neuron degeneration and microglial activation associated with ALS.
