Summary: Frontotemporal dementia (FTD) is a form of dementia that affects personality, behavior, and language before memory. Unlike Alzheimer’s disease, which typically begins with memory loss, FTD often starts with changes in judgment, social behavior, or speech, and tends to appear at a younger age. Researchers funded by the Brain Research Foundation are studying the biological drivers of FTD to help identify future treatment paths.
In this article:
- What Is Frontotemporal Dementia?
- How Does FTD Differ From Alzheimer’s Disease?
- How Is BRF Advancing FTD Research?
- How Is Dementia Diagnosed and Treated?
- Support Research Into FTD
- Frequently Asked Questions
What Is Frontotemporal Dementia?
Frontotemporal dementia, sometimes called frontotemporal lobar degeneration, is a type of dementia that targets the brain’s frontal and temporal lobes. These regions govern personality, motivation, planning, language, and social behavior, so damage here changes who a person is and how they communicate long before it affects memory in the way most people associate with dementia.
FTD is a broad term that covers several related conditions, including behavioral variant FTD (bvFTD), which primarily affects personality and behavior, and Pick’s disease, an older name still used for one specific form of the disease marked by abnormal protein buildup in brain cells.
While FTD is less common than Alzheimer’s disease overall, it is one of the more frequent causes of dementia diagnosed in people under 60, making it a distinct concern for younger patients and their families.
How Does FTD Differ From Alzheimer’s Disease?
The clearest distinction between FTD and Alzheimer’s lies in where the disease starts and which symptoms appear first.
Frontotemporal dementia typically presents with:
- Personality and behavior changes, such as impulsivity, apathy, or loss of social judgment
- Difficulty with language, including trouble finding words or speaking fluently
- Relatively preserved memory in the early stages
- Onset that often occurs earlier, sometimes in a person’s 50s
Alzheimer’s disease typically presents with:
- Memory loss as the first and most prominent symptom
- Gradual difficulty with recent events and conversations
- Progression that more commonly begins after age 65
- The buildup of amyloid plaques and tangles in the brain, a hallmark not seen in FTD
Because FTD symptoms can resemble a psychiatric condition or simply look like a personality shift, it is frequently misdiagnosed or diagnosed later than Alzheimer’s.
A person experiencing early bvFTD might be mistaken as depressed, going through a difficult life transition, or even developing a mood disorder, when the underlying cause is neurological. Recognizing that behavior and language, not memory loss, are often the first warning signs is one of the most important distinctions for families and physicians to understand, and it is often what prompts a more accurate referral for testing.
How Is BRF Advancing FTD Research?
Understanding FTD at the molecular level is central to finding future treatments, and this is where the Brain Research Foundation’s funding has made a direct impact.
Since 2011, Dr. Aimee W. Kao of the University of California, San Francisco, has studied the causes of frontotemporal lobar degeneration. Her research focuses on a protein called progranulin. When the brain doesn’t produce enough of it, the immune cells that normally protect neurons, called microglia, appear to become overactive and begin attacking healthy brain cells instead.
With support from a BRF Seed Grant, Dr. Kao’s team applied this research to induced pluripotent stem cells (IPSCs): adult human cells reprogrammed to behave like early-stage stem cells. Using advanced microscopy, her lab examined how low progranulin levels affect the interaction between neurons and microglia at a level of detail previously unattainable.
Dr. Kao has described this work in terms of everyday stress on the brain. Over a lifetime, the brain manages routine stressors such as infections or minor head injuries, and their effects can accumulate as cellular changes. Her team’s hypothesis is that people with insufficient progranulin develop a faulty stress response over time, one in which microglia lose the ability to tell friend from foe and begin damaging the very neurons they are supposed to defend.
The implications extend beyond FTD alone. Because the same cellular processes are implicated across several neurodegenerative conditions, findings from this research could eventually inform how scientists approach Alzheimer’s and Parkinson’s disease, and potentially certain forms of cancer as well. This is the kind of early-stage, high-risk research that rarely attracts funding through conventional channels, which is precisely the gap BRF Seed Grants are designed to fill. Seed funding enables a researcher to generate preliminary data, and BRF-funded scientists have gone on to secure significantly more funding from other grant programs to continue that work, extending the reach of every donor dollar well beyond its initial impact.
How Is Dementia Diagnosed and Treated?
Diagnosing any form of dementia, including FTD, generally involves a combination of physical exams, cognitive testing, brain imaging such as MRI or CT scans, and blood tests to rule out other conditions that can mimic dementia symptoms.
There is currently no cure for FTD or most other forms of dementia, but treatment can help manage symptoms and support quality of life. Approaches include:
- Medications that help manage specific symptoms, though options approved specifically for FTD remain limited
- Therapies, including cognitive therapy, occupational therapy, and counseling for both patients and caregivers
- Lifestyle support, such as structured routines and safety planning, which can ease day-to-day challenges for both patients and families
Because treatment options for FTD specifically are still limited compared to Alzheimer’s, ongoing research into its underlying biology, like Dr. Kao’s work on progranulin, is critical to closing that gap.
Support Research Into FTD
Progress against frontotemporal dementia depends on sustained funding for the kind of early-stage research that larger institutions often pass over. Every BRF Seed Grant gives a researcher the initial support needed to test a new idea, generate real data, and become competitive for larger, long-term funding. Your donation helps fund the next stage of discovery, whether that means expanding on Dr. Kao’s progranulin research or launching the next scientist’s first investigation into how FTD begins.
Donate to Brain Research Foundation to help advance research into frontotemporal dementia and other neurodegenerative diseases.
Frequently Asked Questions
What is the difference between FTD and Alzheimer’s disease?
FTD usually begins with changes in personality, behavior, or language, while Alzheimer’s typically begins with memory loss. FTD also tends to appear at a younger age and does not involve the amyloid plaques associated with Alzheimer’s.
What is the difference between FTD and dementia with Lewy bodies?
FTD primarily affects personality, behavior, and language due to damage in the frontal and temporal lobes. Lewy body dementia involves abnormal protein deposits that more commonly cause memory issues alongside visual hallucinations and movement symptoms. Read more in our comparison of Lewy body dementia, Alzheimer’s, and Parkinson’s.
Can early-onset Alzheimer’s be confused with frontotemporal dementia?
Yes. Because both can appear before age 65, and because personality or judgment changes can occur in either condition, FTD is sometimes mistaken for early-onset Alzheimer’s. A full clinical evaluation, including brain imaging, helps distinguish between the two.
What is being done to find better treatments for FTD?
Researchers like Dr. Aimee Kao, supported by BRF Seed Grants, are studying the underlying biology of FTD, including how proteins like progranulin affect brain cell health, to lay the groundwork for future treatments.
