Hyperactive microglia immune cells may play a significant role in the development of ALS, researchers report.
Researchers found an increased inflammatory signal in patients with the C90rf72 subtype of ALS. The increased inflammatory biomarkers could be found in peripheral serum tests.
Researchers have identified a causal link between strenuous exercise and ALS in people with genetic risk factors for the neurodegenerative disease. The study reports intense physical exercise contributes to motor neuron injury in those susceptible to ALS.
c9ASO, an investigational ASO drug, targets the TDP-43 protein, reducing its buildup and decreasing neurological decline associated with ALS and FTD.
Study reveals why some people with ALS are prone to developing autoimmune diseases. A genetic mutation that decreases the expression of C9orf72 causes the stimulation of interferon genes (STING) protein to become hyperactive. The hyperactivity leads to increased production of interferons. This can lead to systemic inflammation and the development of autoimmune diseases.
Study reveals a new gut-brain connection in amyotrophic lateral sclerosis (ALS). The gut microbiome could influence the severity of the neurodegenerative disease. Altering the bacteria in the gut may prevent or improve symptoms of ALS.
Researchers discovered increased inflammatory activity in a subgroup of patients with frontotemporal dementia. The increased inflammation was indicated by elevated levels of cytokines known to increase inflammatory response and decreased levels of IL-10, which reduces inflammation. The inflammation was associated with Parkinsonism's symptoms and rapid cognitive and functional decline. The study also revealed patients with FTD are less likely to develop cancer.
Researchers have identified the normal function of C9orf72, a gene commonly implicated in ALS and FTD.
Researchers reveal a small region of Ataxin-2, a protein implicated in long term memory, may drive the progression of ALS.
Using CRISPR, researchers have identified a new set of genes that may be implicated in both ALS and frontotemporal dementia.
Researchers report the C9ORF72 genetic mutation can lead to toxicity in neurons, causing 10 percent of all ALS cases and 10 percent of FTD cases.
Researchers reveal a repeat element in the DNA of C9orf72 gene becomes toxic when faced with starvation, toxins and viral infection.
