Researchers discovered both immune system and central nervous system dysfunction in animal models and people with ALS4, a genetic, juvenile, and slow-progressing form of ALS.
Study reveals an association between intestinal inflammation and the gut microbiome in the development and progression of ALS.
PolyP, an inorganic polyphosphate released by astrocytes in people with ALS and frontotemporal dementia contributes to the signature motor neuron death associated with the disease pathologies.
Mislocalization of the TDP-43 protein alters the genetic instructions for UNC13A. The findings provide a potential new therapeutic target for the treatment of ALS and frontotemporal dementia.
Measuring the level of neurofilaments in the blood may be a reliable biomarker for the early diagnosis of ALS.
In patients with ALS, astrocytes within the brain become pro-inflammatory and tend to lose their protective function, resulting in changes in the ability to uptake glutamate.
Post-mortem studies of brain tissue from ALS patients reveal an abnormal form of tau is present in novel brain areas, and the tau interacts with DRP1. The tau appears to cause the brain cell's mitochondria to fragment and increase oxidative stress. Reducing tau reversed the effect, decreasing oxidative stress and mitochondrial fragmentation.
Researchers reveal how proteins accumulate in the incorrect parts of brain cells in ALS, and demonstrate how it may be possible to reverse the accumulation.
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.
