(NewsNation) — Researchers have identified a set of genes that may cause neuron death in amyotrophic lateral sclerosis commonly known as ALS, offering new insights into the disease’s root causes and potential therapeutic targets.
The small study, funded by the National Institutes of Health and published in Nature Aging, analyzed genetic profiles of thousands of neurons from postmortem brain tissue of ALS patients and healthy donors.
Scientists found higher levels of ALS and frontotemporal dementia (FTD) risk genes, particularly in Betz cells, a type of motor neuron. These genes are among the most commonly associated with ALS/FTD.
In ALS patients, the presence of these genes was linked to disruptions in other neurons, affecting their ability to build, transport, and break down proteins. This may be connected to the toxic accumulation of the protein TDP-43, a hallmark of ALS and some FTD cases.
The study also examined glial cells, which normally support neurons but can become dysfunctional in ALS. Genetic analysis revealed genes related to cellular stress and inflammation in these cells, though further research is needed to determine if glial dysfunction is a cause or consequence of neuron degeneration.
ALS is a progressive neurological disorder that attacks motor neurons in the brain and spinal cord, leading to muscle weakness, paralysis, and eventually death. Most cases are sporadic, occurring in people without a family history or clear risk factors.
