Ask Onix
Updated 20 February 2026 - Recent developments in ALS research offer new insights into the disease's causes, while the deaths of prominent figures underscore its devastating impact.
ALS claims lives of well-known figures
Actor Kenneth Mitchell, known for his roles in Star Trek: Discovery and Captain Marvel, died on 24 February 2024 after a five-and-a-half-year battle with amyotrophic lateral sclerosis (ALS). Mitchell, who documented his struggle on social media, described the disease as "absolutely horrific" in an August 2023 Instagram post. He acknowledged the support of family, friends, and caregivers but lamented the losses he endured.
Mitchell's death followed that of photographer Bryan Randall, partner of actress Sandra Bullock, who died in August 2023 at age 57 after a three-year fight with ALS. In April 2025, actor Eric Dane, famous for Grey's Anatomy and Euphoria, revealed his ALS diagnosis at 52. He passed away less than a year later, in February 2026.
The mysteries of ALS
ALS, also known as Lou Gehrig's disease, is a progressive motor neuron disease (MND) that destroys nerve cells controlling voluntary muscle movement. It leads to gradual loss of bodily function, often resulting in paralysis. In the U.S., approximately five in every 100,000 people are affected, with men at higher risk than women. While most patients survive only a few years post-diagnosis, exceptions like physicist Stephen Hawking-who lived for over five decades after his diagnosis at 21-highlight the disease's unpredictable nature.
Genetic and environmental factors
For 10-15% of ALS cases, the disease is hereditary, linked to mutations in specific genes passed through families. However, the affected gene varies even among familial cases. The remaining 85% of cases are classified as sporadic, with no clear family history. Recent research suggests these cases may involve subtle genetic mutations across multiple genes, rather than a single defect.
Scientists have identified up to 40 genes that may increase sporadic ALS risk, though the condition remains rare. Four genes-C9orf72, SOD1, TARDBP, and FUS-are most commonly implicated. C9orf72, involved in nerve and muscle regulation, accounts for 30% of cases, while SOD1, which codes for an antioxidant enzyme, is faulty in 20%.
"The extent that disease can be explained by genetic factors is only about 8% to 60%, depending on the type of ALS."
Eva Feldman, Professor of Neurology, University of Michigan
Environmental triggers under scrutiny
Emerging evidence points to environmental factors as potential contributors to ALS, particularly in sporadic cases. Eva Feldman and her team at the University of Michigan propose the concept of an "ALS exposome"-a cumulative effect of toxic exposures that may elevate risk. Prolonged contact with organic pollutants, metals, pesticides, construction dust, and poor air quality has been linked to higher ALS incidence.
Neil Thakur, chief mission officer of the ALS Association, emphasizes that no single factor guarantees ALS development. "It is always a combination of factors," he says. "Even with a genetic predisposition, ALS is not inevitable." Studies suggest that exposure to diesel fuel, aviation fuel, burn pits, pesticides, and lead in drinking water may increase risk. Military personnel, for instance, face heightened exposure to such hazards and appear more susceptible to ALS.
Other potential triggers include smoking and contact sports, though research remains inconclusive. Surprisingly, studies indicate that abstaining from alcohol and cigarettes does not necessarily reduce ALS risk, despite their benefits for other health conditions.
Challenges in research and treatment
ALS's rarity complicates research efforts. Limited patient participation and genetic diversity hinder studies, making it difficult to isolate causes or test treatments. "It takes a long time to recruit enough people for clinical trials," Thakur notes, as patients are often only eligible early in the disease's progression.
While ALS remains incurable, the U.S. Food and Drug Administration has approved treatments to slow its progression. These drugs work through various mechanisms, such as reducing harmful chemicals around the brain and spinal cord or preventing nerve cell death. Early trials targeting specific genetic mutations, like SOD1, have shown promise.
Living with ALS and future hopes
The ALS Association focuses on improving quality of life for patients and their families. "Our strategy is to make ALS liveable until we have a cure," Thakur says. The organization advocates for multidisciplinary care to extend active living and plans to release guidelines on reducing ALS risk factors.
Feldman's team is investigating how polygenic risk profiles-combinations of multiple genes-interact with environmental factors to trigger ALS. "The real question is not why people get ALS, but what we can do to prevent or treat it," Thakur asserts. Despite funding challenges, advances in understanding the disease's mechanisms offer hope for more effective therapies and, ultimately, prevention.
For now, ALS continues its relentless progression, leaving families and caregivers to adapt with compassion. Yet, growing scientific insight may one day turn the tide against this devastating condition.
