Researchers discover how a genetic code variation in the C9orf72 gene alters the shape of DNA, making cells more vulnerable to stress and apoptosis.
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.
Using neurons created from iPS cells derived from people with ALS, researchers develop a new drug which appears to halt the impact of the genetic mutations in some forms of ALS and dementia.
Researchers believe a newly discovered mechanism may contribute to cell death in people suffering from ALS and dementia.
c9ASO, an investigational ASO drug, targets the TDP-43 protein, reducing its buildup and decreasing neurological decline associated with ALS and FTD.
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.
Hyperactive microglia immune cells may play a significant role in the development of ALS, researchers report.
Researchers report the most common genetic mutation associated with ALS plays an important role in not only the nervous system, but also the blood and immune systems.
Immune cells appear to play a direct role in the development of ALS, a new study reports.
Researchers reveal a repeat element in the DNA of C9orf72 gene becomes toxic when faced with starvation, toxins and viral infection.
Researchers have identified the normal function of C9orf72, a gene commonly implicated in ALS and FTD.
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.
