Patient Impact, Research & Innovation, Vitals Magazine Fall 2026

Genetic ALS May Soon Be
Preventable 

Dartmouth Health researchers are exploring new ways to slow or even prevent genetic amyotrophic lateral sclerosis, which has long been considered a death sentence.

A woman with gray hair and a flowered top sits on a bench looking out a window

Linda Commo watched her father pass away just three years after his diagnosis. Now she, too, has ALS. Credit: Kata Sasvari

When Linda Commo first started noticing the symptoms, she recognized what it was right away. Her issues lifting her right arm and holding objects matched what she had watched her dad experience two decades prior. It would take her nearly two years to get tested, but when the results came in, her self-diagnosis was correct: It was amyotrophic lateral sclerosis, or ALS.

Sometimes known as Lou Gehrig’s, ALS is a merciless neurodegenerative disease that attacks motor neurons in the brain, leading to the loss of muscle control. While the symptoms start small, they quickly advance to loss of mobility, speech, and eventually breathing. For a long time, a diagnosis of ALS has been considered fatal, with most patients only having a few years to live. Commo’s dad passed away just three years after his diagnosis.

But with the help of new research at Dartmouth Health’s Dartmouth Hitchcock Medical Center (DHMC), that prognosis is beginning to change, particularly for familial ALS, a genetic form that affects some 10–15% of ALS patients according to the ALS Association, including Commo and her family. From large-scale research projects that are identifying early diagnostics to clinical trials with promising personalized medicine, DHMC researchers are leading the future of ALS treatment so that a diagnosis of familial ALS no longer means what it used to.

“We are moving ALS from a disease with no hope to a treatable disorder,” says Mark Garret, MD, a neurologist and director of the ALS Center at DHMC and assistant professor of neurology at the Geisel School of Medicine at Dartmouth.

An Ounce of Prevention

Typically, ALS isn’t diagnosed until the disease causes significant, debilitating symptoms. At that point, many nerve cells in the brain and spinal cord have already been irrevocably damaged by the disease, Garret says. If ALS could be identified earlier, it could help halt the disease before too much damage is done.

Early diagnosis is a main focus for Garret, who is one of just a handful of researchers nationwide focusing on preventing ALS. In 2024, Garret helped launch a clinical trial with the Access for ALL in ALS consortium, a National Institutes of Health–funded group of 36 clinics that track enrolled participants who are known carriers of genes that cause ALS. The consortium is creating a biobank filled with participants’ blood samples, strength testing, cognitive exams, and more for researchers to use to identify potential biomarkers that could predict onset of ALS.

“We hope to learn more about the earliest biological changes before someone develops ALS to see if there are signs that we could be paying attention to that predict when someone is about to develop ALS,” Garret says of the study, which is called simply PREVENT. “This may be a critical window to start therapies that could eventually prevent the disease.”

A man with white plastic gloves places a spinal fluid sample into a test tube.
Neurologist Mark Garret, MD, is looking for ways to stop the progression of familial ALS before it starts. Credit: Ben DeFlorio

Study participants have often seen the devastating effects of ALS firsthand. PREVENT participant Chris, who lives in Vermont, has taken part in numerous ALS studies since his brother died from ALS in 1999 at the age of 27. In one of the studies, Chris found he carries the same genetic mutation that caused multiple members of his family to develop ALS, but he has not shown any symptoms. For the past two decades he’s had quarterly doctor’s visits and monthly blood draws.

“It’s not something that I’m doing to help myself,” says Chris, who prefers to be anonymous because of stigma about the disease. “But it’s something to maybe help the next generation, my kids or others, with the disease.”

In the two years since PREVENT launched, the study has enrolled nearly 600 people, including 11 at DHMC. Though the PREVENT study, and others like it, are still in the early stages, results are already pointing towards one key blood marker called neurofilament light chain, which is a protein that marks nerve injury. Elevation in neurofilament light chain can also be seen in patients with Alzheimer’s or Parkinson’s, or who have had a stroke. But, due to ALS’s rapid onset, the neurofilament light-chain levels are particularly high in these patients. Early results from the Dominant Inherited ALS study—a precursor to PREVENT that both Garret and Chris were involved in—showed elevated levels of the neurofilament light chain in some participants’ blood 6 to 12 months before they developed ALS symptoms.

“This research is promising, and we’re looking for additional tools,” Garret says. “Neurofilament might elevate 6 to 12 months before, but there may be other proteins that elevate a little earlier.”

For now, these studies are being conducted on a small percentage of people who have familial ALS or its carrier gene. Non-inherited, or sporadic, ALS is much more difficult to diagnose early given its rarity in the general population. But the hope is that one day advancements in familial ALS can be extended to sporadic ALS, Garret says.

A Miracle Drug

Finding early-onset familial ALS symptoms is, of course, only half the battle. Ultimately that knowledge needs to be met with treatments that can halt the progression of ALS. However, until recently, the drug options for ALS remain limited.

Garret was first introduced to one potential ALS drug in 2020, during his medical training in neurology at Washington University in St. Louis, when he helped administer a clinical trial for a promising new drug called tofersen. Tofersen, now the first of three FDA-approved treatments for ALS, targets the second most common type of familial ALS, caused by a mutation that leads to a buildup of SOD1, a toxic protein in motor neurons of the brain and spinal cord. By blocking the production of SOD1, tofersen can halt the development of ALS symptoms in some patients.

“ALS is this universally fatal, incurable, rapidly progressive disease, but we saw people who were doing really well and seemed to have significant slowing of progression and stabilization of their disease with tofersen,” Garret says. “In the last couple of years, we’ve seen patients who are actually stable or even improving in terms of their muscle strength, which was really previously thought to be impossible in ALS.”

One of those success stories is Dale Kandoll, who started receiving tofersen soon after his ALS diagnosis in 2024. The strength in Kandoll’s legs had been decreasing, but the drug stabilized his condition, and he’s still able to walk short distances and drive.

“There are people like me who are improving,” says Kandoll, who’s also involved in one of the ALS consortium studies. “I hope what can be learned from me and others with ALS can make it easier for the next generation of people with ALS.”

A woman's right hand grips a tool that looks like a pencil, using it to carefully pick up small plastic gems and place them onto a canvas
Linda Commo diamond painting, in which crafters adhere plastic gems to a canvas with a preset design. Credit: Kata Sasvari

Commo also found relief with tofersen. She began taking the drug when it was approved in 2023 and is also now taking riluzole, another ALS drug. In the past three years she’s seen her symptoms stabilize and has had improvements in her speech and balance. Though she can no longer knit, Commo is still able to enjoy doing jigsaw puzzles on her phone and diamond painting, in which crafters adhere plastic gems to a canvas with a preset design. Now six years out from her diagnosis, Commo has lived longer than she ever dreamed.

“My doctor says that I’m still right about where I was when I went into the program,” Commo says. “So that makes me feel good. I didn’t think I’d live as long as my dad did after his diagnosis.”

The Future of ALS Treatment

Garret is also working with clinical trials of other ALS drugs like NUZ-001, which, like tofersen, works to reduce levels of toxic proteins that damage nerve cells. Currently, three patients at DHMC’s nationally recognized ALS Center are enrolled. The Center uses a multidisciplinary approach, with in-house neurologists, speech therapists, dietitians, physical therapists, and more to deliver the best possible care.

Several of Garret’s patients at DHMC are also in line for a tailored genetic therapy to treat a type of familial ALS that affects the TARDBP gene. Genetic therapies work by modulating the gene or its end product associated with the disease. For ALS, one genetic therapy aims to switch off the TARDBP gene so it cannot produce its problematic protein. Personalized treatments like these are becoming increasingly common, not just for ALS but for many neurological diseases, and have demonstrated success with diseases like spinal muscular atrophy and genetic epilepsy.

Patients interested in DHMC’s ALS Center can go to dartmouth-hitchcock.org/als to learn more.

“The future of neurology in general is shifting to genetic therapies,” says Barbara Jobst, MD, chair of neurology at DHMC. “There are a lot of studies tailored to a particular gene in a particular person.”

With advances in predicting onset and new genetic therapies, the future of ALS is brighter than it’s ever been. “Unlike when I first got involved in ALS studies, there is now hope and there are now treatments—at least for SOD1—that are game changing,” Chris says.

“I believe that every day that we move forward, there’s more and more hope. And I hope that someday nobody gets this terrible disease.”

To support ALS research at Dartmouth Health, contact Matthew Hall at 603-667-6309 or Matthew.R.Hall@hitchcock.org.