Hyperactive microglia immune cells may play a significant role in the development of ALS, researchers report.
NU-9, a novel, non-toxic compound, targets upper motor neurons and reverses damage associated with ALS within 60 days of treatment.
A novel method detected conformational changes to the TDP-43 protein in cerebral spinal fluid associated with ALS.
c9ASO, an investigational ASO drug, targets the TDP-43 protein, reducing its buildup and decreasing neurological decline associated with ALS and FTD.
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.