Researchers discovered mutations of the OPTN gene resulted in increased herpesvirus 1 growth in the brains of mice, leading to the death of local neurons. This resulted in accelerated neurodegeneration. OPTN deficiency was also associated with impairments in immune response. While these findings are specific to the HSV-1 virus, researchers believe the findings may apply to up to eight herpesvirus infections.
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 have identified a key instigator of neural damage in people with ALS.