A new study reports an antidepressant temporarily inhibits the blood-brain barrier, allowing drugs to enter the brain. The findings could have implications for treating neurological diseases from ALS to epilepsy.
Study implicates abnormalities in SOD1 with Parkinson's disease and ALS.
By increasing the signaling activity of a protein called muscle skeletal receptor tyrosine-protein kinase (MuSK), researchers were able to keep nerve cells attached to muscle longer into the progression of the disease in a mouse model 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.
According to researchers, a drug that has been used for decades to help treat malaria can lower levels of a biomarker associated with ALS.
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.
Human-on-a-chip technology could provide a more valuable clinical-based model for ALS.
Researchers report the formation of larger, more visible SOD1 aggregates may help to protect brain cells.
Researchers report a collapse of the mitochondria-associated membrane is a common halmark in two genetic forms of 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.
Researchers report activating microglia may help reduce the imbalance between neuroprotection and neurotoxicity for neurodegenerative diseases.
Researchers have identified a modifier gene that affects the risk of developing degenerative myelopathy, a canine disease similar to ALS in Welsh corgis.
