At the age of 22, Andre Yarham was diagnosed with young-onset dementia (YOD) — the youngest person in the UK to receive that diagnosis. He died about a year later, in December 2025, at the age of 24.

Ultimately, his family donated his brain to science to help researchers better understand why neurodegenerative disease can occur decades earlier than expected and how timely diagnosis might alter outcomes.

Among individuals with YOD, early symptoms often involve behavioral or executive changes rather than memory loss. These early changes may be subtle and difficult to recognize, often emerging when individuals are at the height of their careers, raising families, and managing financial responsibilities.

The difficulty lies not in the complexity of the diagnosis but in recognizing it. Maintaining an open mind, listening carefully to the family, and having sufficient knowledge to consider the condition as a possibility are ultimately what help guide a correct diagnosis, followed by confirmatory testing, said James Rowe, PhD, professor of cognitive neurology at the University of Cambridge and lead for the Cambridge Centre for Frontotemporal Dementia in Cambridge, England. Rowe was Yarham’s consultant at Addenbrooke’s Hospital.

“Nine times out of 10 it is not hard — building on a conversation with the affected person and their family, examination in-clinic and, where necessary, a scan. Much of the information is in the timeline of events and symptoms,” Rowe told Medscape Medical News.

Cases like Yarham’s highlight the diagnostic and systemic challenges of detecting dementia in younger adults, a population, Rowe said, is often overlooked. And perhaps that isn’t surprising. After all, how often would a clinician need to consider dementia in the differential diagnosis of a patient in their 20s?

What Is Young-Onset Dementia?

YOD is defined as dementia diagnosed before the age of 65 years and covers a wide range of disorders with various causes and clinical presentations. While Alzheimer’s disease (AD) remains a major contributor, younger adults are proportionally more likely than their older counterparts to present with frontotemporal dementia (FTD) — which was Yarham’s diagnosis. Atypical AD variants, vascular dementia, autoimmune or inflammatory causes, and genetic syndromes are also more common in younger patients.

Epidemiologic data suggest that the burden of YOD may be increasing. A 2025 study published in Translational Psychiatry reported increases in disability-adjusted life years attributable to the disorder across several regions over the past three decades. However, trends also varied across countries and some of this increase may reflect improved detection rather than a true rise in disease burden.

Similarly, a 2020 report by Blue Cross Blue Shield, The Health of America, showed that commercially insured US adults experienced increased rates of YOD diagnoses between 2013 and 2017, with particularly steep relative increases among adults aged 30-44 years. While increased awareness and changes in diagnostic coding might partly account for the rise among younger adults, Vincent Nelson, MD, vice president of medical affairs for Blue Cross Blue Shield Association said in a release , “Further education and research is needed to learn more about early-onset dementia and Alzheimer’s, how to treat these conditions and what can be done better to prevent diagnoses.”

And a 2021 systemic review and meta-analysis published in JAMA Neurology estimated the global age-standardized prevalence of YOD to be approximately 119 per 100,000 people aged 30-34 years or roughly 3.9 million individuals worldwide.

Differentiating Memory From Mood Disorders

The first signs of YOD can be subtle and easily attributed to everyday stress or mood disorders. Patients may struggle to remember recent conversations or appointments, follow complex instructions, make sound decisions, find the right words, or regulate emotions.

Studies also suggest that a high proportion of patients with YOD are initially diagnosed with psychiatric or nondementia neurologic disorders, delaying appropriate evaluation. Such diagnostic misclassification was associated with longer times to an accurate diagnosis, particularly when affective or anxiety disorders were initially documented. 

Rowe emphasized the importance of patterns in symptom timing and behavior when differentiating neurodegeneration from psychiatric illness.

For example, “while some of the features of FTD might superficially remind one of autism, people don’t get autism unexpectedly as adults. If that happens, think FTD,” he said.

“Apathy can be a feature of FTD or depression, but again the clue is in the conversation — people with depression are, well, depressed, and people with FTD generally say they feel OK,” despite all of the problems that are going on in life, Rowe said.

Indeed, any later-onset psychiatric symptoms should prompt careful evaluation, noted Carmela Tartaglia, MD, associate professor of medicine, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.

“It is important to recognize that many psychiatric diseases start earlier in life, so if somebody is middle-aged and develops a psychiatric disease, it would be important to consider that a neurodegenerative disease could be causing the symptoms,” she told Medscape Medical News.

Psychiatric symptoms appearing for the first time in someone with no prior history, or cognitive changes accompanying psychiatric illness, may also serve as warning signs.

“New-onset psychiatric disease is a red flag in someone who has never had any issues. Cognitive impairment with psychiatric disease is also a red flag,” Tartaglia said.

When it comes to evaluation, structural imaging remains critical, she emphasized. “Imaging is important as it can reveal structural changes such as excessive shrinkage of the brain that may indicate a neurodegenerative process.”

Certain biomarkers may also help differentiate neurodegenerative disease from psychiatric conditions.

“There are some biomarkers that are being considered as possibly useful for differentiating psychiatric disease from neurodegenerative disease. Neurofilament light chain is the one with the most evidence,” Tartaglia noted.

What Drives YOD?

Beyond recognizing early warning signs, researchers are also working to better understand what drives YOD. Scientists suspect it may stem from a combination of genetic and environmental factors. While many cases are sporadic, some are hereditary.

Mutations in the amyloid protein precursor (APP), presenilin-1(PSEN1), and presenilin-2 (PSEN2) genes cause autosomal dominant early-onset AD, particularly in families with multiple affected members. In these high-risk populations, genetic testing can guide monitoring, counseling, and early intervention, although routine testing is not recommended for all patients.

Metabolic health is increasingly recognized as a contributor to the risk for YOD. A 2023 observational cohort study published in JAMA Neurology showed that type 2 diabetes, insulin resistance, and midlife obesity were associated with increased risk in adults younger than 50 years. These findings suggest that modifiable midlife factors may influence the trajectory of neurodegeneration, suggesting potential opportunities for prevention.

Although the study did not directly evaluate interventions, broader evidence suggests that lifestyle measures, such as physical activity, a balanced diet, and cognitive engagement, may help maintain brain health over time.

Toward Earlier Detection

Research is increasingly focused on blood testing for earlier detection, said Courtney Kloske, PhD, director, Scientific Engagement, Alzheimer’s Association, Chicago. She noted that two blood tests were cleared by the FDA in 2025 for use in primary and specialty care settings to help determine whether AD pathology is present.

In May 2025, the FDA cleared the Lumipulse G pTau217/beta-amyloid-1-42 plasma ratio test, which measures the ratio of pTau217 and beta-amyloid-1-42 in plasma to help detect amyloid plaques in adults aged 55 years or older with cognitive impairment. It is intended to help clinicians to evaluate likelihood of AD in conjunction with other clinical data.

In October 2025, the Elecsys pTau181 plasma test was cleared for use in primary care to help rule out AD-related amyloid pathology in patients aged 55 years or older who present with cognitive symptoms. This test helps identify individuals who may not require further invasive testing, such as PET imaging or cerebrospinal fluid analysis.

Kloske said the test may help clinicians in primary care settings distinguish whether cognitive symptoms in patients younger than 65 years are driven by AD pathology or another cause.

Meanwhile, Kloske noted that antiamyloid therapies are indicated for early symptomatic AD and may include some younger patients depending on age criteria and biomarker confirmation.

Current FDA-approved therapies that slow disease progression in AD are indicated for patients aged 55 years or older, meaning some individuals with young-onset disease may be eligible for treatment, Kloske said.

These drugs include lecanemab and donanemab for patients with early symptomatic AD and confirmed biomarker evidence. Although these FDA approvals were based on trials in older adults, the Alzheimer’s Association’ ALZ-NET program has found that some patients younger than age 55 years and some older than those in the trials are receiving these medications. Treatment decisions should be made in consultation with physicians and consider factors such as age, disease stage, biomarker status, and insurance or cost considerations, she cautioned.

In addition, the LEADS may be an option for patients and clinicians interested in contributing to YOD research.

“LEADS is an observational study that we’re able to see how individuals with younger onset progress in the disease and now we have a subset of those people that are also on therapy,” Kloske said.

The Real-World Cost of Delayed Diagnosis

Beyond research advances and emerging therapies, delayed diagnosis can carry significant real-world consequences for patients and families for employment, relationships, financial stability, and overall quality of life. Early recognition can make a significant difference, said Rowe.

“A diagnosis can save marriages, save the home, save them from severe poverty, save the positive memory, and legacy of relationships for years to come,” he said. “Delays can mean people get sacked, get sent to prison, become homeless, or develop severe malnutrition.”

Tartaglia has observed similar patterns in her own practice. When changes in personality or cognition are not recognized as symptoms of disease, she said, the consequences can be far-reaching, including job loss, family strain, and worsening health. Workplace and marital fallout are common. Tartaglia noted that many of her younger patients lose their jobs before anyone realizes that changes in behavior or performance stem from a neurologic condition rather than carelessness or lack of effort.

Financial vulnerability can also become an early issue. Impaired judgment may lead patients to fall victim to scams or make risky financial decisions before the underlying brain disease is recognized, she said.

Early detection is critical not only for treatment eligibility but also for planning and support as well. Persistent cognitive or behavioral changes in younger adults should prompt thorough evaluation. Increased awareness of YOD may help expand dementia services beyond those designed primarily for adults aged 65 years or older.

“A day center aiming to help 80-year-olds with memory loss from AD is unlikely to be well set up and trained to help a big strong 22-year-old with challenging behaviors from FTD,” Rowe noted.

“Fortunately, others have special teams, providing brilliant help, focused on the needs and challenges of young adults.”

Rowe, Tartaglia, and Kloske reported no relevant financial disclosures.