In an Instagram post, Bruce Willis’ family revealed that the actor has been diagnosed with frontotemporal dementia (FTD). The diagnosis comes nearly a year after his family revealed Willis has aphasia, which is characterized by difficulty speaking.
“Since we announced Bruce’s diagnosis of aphasia in spring 2022, Bruce’s condition has progressed and we now have a more specific diagnosis: frontotemporal dementia (known as FTD),” the family said in its statement, which was also posted on the Association for Frontotemporal Degeneration’s website.
Here’s what to know about the condition.
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What is FTD?
FTD refers to a collection of conditions that involve deterioration of brain nerves in the frontal and temporal parts of the brain, which contribute to behavior, personality, and language. Willis’ earlier diagnosis of aphasia, his family said, may be a symptom of FTD.
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There are several types of FTD. One primarily affects behavior and personality, as nerves cells critical to judgement, conduct, and empathy start degenerating. Another, which affects language, speaking, and writing, most often occurs in midlife. Another type of FTD primarily damages motor nerves; amyotrophic lateral sclerosis, or ALS is a form of this type. Estimates of how many people are affected by FTD aren’t conclusive, but the Alzheimer’s Association speculates that about 50,000 to 60,000 people in the U.S. have the behavior and language versions of the condition.
Is FTD the same as Alzheimer’s disease?
While FTD involves the gradual loss of brain nerves, it differs from Alzheimer’s in important ways. Most people are diagnosed with FTD in their 40s to 60s, while Alzheimer’s patients are typically diagnosed later in life. Memory loss and disorientation are more common in Alzheimer’s than in FTD, while speech problems are more frequent in FTD.
In FTD, patients develop abnormal deposits of one of two proteins—a form of a protein called tau and TDP-43—but not both. Patients with Alzheimer’s also build up tau, but it’s a different form from the one involved in FTD. It’s also typically more difficult to diagnose FTD. “There is an effort to develop blood, spinal fluid, and PET scan markers to diagnose FTD, but those are still in the works, and right now, we don’t have effective ways to test for FTD like we do for Alzheimer’s,” says Dr. Ryan Darby, director of the Frontotemporal Dementia Clinic at Vanderbilt University Medical Center. Doctors diagnose patients based on their suite of symptoms and sometimes with the help of brain scans, which can provide some useful hints but aren’t definitive. In addition, says Dr. Nicole Purcell, a neurologist and senior director of clinical practice at the Alzheimer’s Association, “we often do tests to rule out other types of dementia like Alzheimer’s dementia.”
According to the Alzheimer’s Association, about a third of FTD cases are genetic, and there are no known risk factors for the non genetic cases, so it’s difficult to identify people who might develop the condition.
Understanding which of the two proteins is abnormally building up is critical for developing the right treatments. Darby says that while some forms of language-related FTD involve TDP43, patients with behavioral symptoms can harbor excess forms of either protein, making it difficult to know which protein to target in drug trials.
Are there treatments?
While there is considerable research to better understand FTD and its causes, there are no treatments yet for the neurodegenerative condition. Anti-anxiety medications and antidepressants can ease some of the agitation and stress patients experience, but no therapies are available yet to combat the slow deterioration of neurons in the affected areas of the brain.
Researchers are focusing on the genetic forms of the disease in order to learn more about how it works, and how best to intervene with possible treatments, says Dr. Claire Clelland, assistant professor of neurology at the University of California San Francisco. “We think that is the best and fastest path to clinical trials for new therapies,” she says. “In genetic cases through which we know the underlying cause from the gene mutation, we will learn about the disease more broadly so we can help more patients.”
Research into the condition has picked up in recent years, and doctors who treat FTD patients at academic centers have collaborated to identify and monitor patients to pool information and be prepared to test promising new drug treatments when they are developed. “Our understanding of FTD really accelerated dramatically in the past two decades,” says Darby. “A lot of our understanding has come since the 1990s when we identified the clinical syndrome, and the gene for the most common inherited form wasn’t discovered until 2011. A lot of innovation has happened recently, so a lot of us are optimistic that will translate into therapies.”
Clelland shares that optimism. “These are becoming solvable problems,” she says. “My lab has already essentially cured patient cells in a dish. We just need to figure out how to deliver the therapy to patients.”
She credits Willis and his family for sharing their story to raise awareness about the condition, which will hopefully fuel more research.
“Bruce always believed in using his voice in the world to help others, and to raise awareness about important issues both publicly and privately,” Willis’ family said in their statement. “We know in our hearts that — if he could today — he would want to respond by bringing global attention and connectedness with those who are also dealing with this debilitating disease and how it impacts so many individuals and their families…As Bruce’s condition advances, we hope that any media attention can be focused on shining a light on this disease that needs far more awareness and research.”
