How Is Frontotemporal Dementia Different From Alzheimer's?
At a Glance
Frontotemporal dementia usually begins before age 65 with changes in behavior, personality, or language, while Alzheimer's more often begins after 65 with recent-memory loss. Symptoms overlap, so diagnosis relies on history, cognitive testing, and supportive scans.
In this answer
5 sections
Alzheimer’s disease and frontotemporal dementia (FTD) are both progressive brain disorders, but they differ significantly in who they affect, how they typically begin, and what causes the damage in the brain. The most noticeable difference is their initial presentation: Alzheimer’s typically begins with memory loss in older adults, while FTD often begins with gradual changes in behavior, personality, or language in middle-aged adults. However, these are general patterns, not absolute rules, and it is important to remember that the behavioral changes in FTD are symptoms of a physical brain disease, not intentional choices or flaws in character.
Age of Onset
While dementia is often associated with the elderly, FTD follows a different timeline. FTD most often strikes people in their 50s or 60s, typically before the age of 65 [1][2]. Though it can occasionally happen earlier or later in life, FTD is one of the most common causes of dementia in people under 65. When FTD symptoms do appear after age 65, it is more commonly misdiagnosed as Alzheimer’s disease because of the patient’s older age [1][3]. In contrast, the vast majority of Alzheimer’s cases occur in people over age 65, and the risk increases significantly with advancing age.
Initial Symptoms (Patterns, Not Rules)
The earliest signs of these two diseases are generally distinct, reflecting the different areas of the brain they target first.
- Alzheimer’s Disease: The hallmark early symptom is progressive loss of episodic memory (the ability to remember recent events and personal experiences) [4]. People with typical Alzheimer’s often struggle to recall recent conversations or frequently misplace items.
- Frontotemporal Dementia: Memory is generally preserved in the early stages of typical FTD, though memory issues can occasionally occur. Instead, families first notice profound shifts in the person’s behavior or communication skills. In the behavioral variant of FTD (bvFTD), early symptoms include apathy (loss of motivation), a loss of empathy, inappropriate social behavior, compulsive actions, and dietary changes, such as intensely craving sweets [2][5][6].
- Language Symptoms (PPA): Primary Progressive Aphasia (PPA) is a clinical syndrome where language declines first. The “semantic” and “nonfluent” variants of PPA involve struggling to understand words or speak fluidly and are usually caused by FTD pathology [7][8]. However, a third variant called “logopenic” PPA, where people struggle to find the right words in conversation, is actually most often associated with Alzheimer’s disease pathology [9].
Changes in the Brain (Proteins and Pathology)
Both diseases involve the abnormal buildup of proteins in the brain, but the specific culprit proteins are different.
- Alzheimer’s Proteins: Alzheimer’s disease is defined by two specific protein abnormalities: amyloid plaques (clumps of beta-amyloid protein outside the cells) and neurofibrillary tangles (twisted strands of tau protein inside the cells) [10][11].
- FTD Proteins: The clinical syndrome of FTD is caused by underlying brain changes known as frontotemporal lobar degeneration (FTLD). FTLD typically does not involve amyloid plaques. Instead, it is most commonly driven by abnormal accumulations of either Tau protein or TDP-43 protein, and rarely a protein called FUS [12][13][14].
It is currently very difficult for clinicians to determine the exact protein subtype (Tau vs. TDP-43) during life using standard clinical tests; definitive classification often requires examination of brain tissue after passing, though genetic testing or research scans can sometimes provide clues [12]. Furthermore, overlaps are common. Older individuals may have multiple types of protein buildup happening simultaneously [15].
How Clinicians Use Brain Scans
Because FTD and Alzheimer’s affect different parts of the brain, doctors use neuroimaging as supportive tools. Scans are not definitive standalone answers and must be interpreted alongside a patient’s medical history and cognitive testing [16].
- MRI Scans: An MRI looks at the physical structure of the brain. In FTD, the shrinkage (atrophy) is typically early and most prominent in the frontal lobes (behind the forehead) and anterior temporal lobes (behind the ears) [17][18]. In Alzheimer’s, the shrinkage usually starts in the medial temporal regions, including the hippocampus (a deep brain structure vital for memory), and the temporoparietal areas towards the back of the brain [17].
- FDG-PET Scans: A functional scan called an FDG-PET measures how the brain uses sugar for energy. FTD usually shows decreased energy use (hypometabolism) in the frontal and anterior temporal regions, whereas Alzheimer’s shows reduced energy use in the parietotemporal and posterior areas [19][20].
- Amyloid PET and Lumbar Punctures: Doctors may use an amyloid PET scan or a lumbar puncture (spinal tap) to help assess whether Alzheimer’s-type amyloid pathology is present. A negative result makes Alzheimer’s much less likely. However, a positive amyloid scan only establishes that amyloid is present—it does not by itself prove that Alzheimer’s is the sole cause of the person’s symptoms, as older individuals can have age-related amyloid buildup alongside FTD [21][22].
What This Distinction Means for Care
Knowing the difference between FTD and Alzheimer’s is critical for planning care. Standard Alzheimer’s medications (like donepezil) do not improve FTD symptoms and can sometimes worsen behavioral issues, so they should not be started or stopped without consulting the treating clinician. Instead, FTD care focuses on targeted symptom management, behavioral adaptations, speech-language therapy for communication difficulties, and robust support systems to help caregivers navigate the unique emotional and practical challenges of the disease.
(Note: Sudden or rapidly evolving changes in behavior, memory, or language are not typical of slowly progressive dementias like FTD or Alzheimer’s, and warrant prompt emergency medical evaluation for other causes.)
Common questions in this guide
How do the first symptoms of FTD and Alzheimer's usually differ?
Does FTD usually happen at a younger age than Alzheimer's?
Can doctors tell FTD from Alzheimer's with a brain scan?
What proteins are involved in FTD and Alzheimer's disease?
Do Alzheimer's medications help people with FTD?
What should I do if behavior or memory changes appear suddenly?
Questions to Ask Your Doctor
Curated prompts to bring to your next appointment.
- 1.Based on the medical history and cognitive exams, which diagnosis is most likely, and what specific uncertainty remains?
- 2.How would additional testing, such as an MRI, FDG-PET, or amyloid test, change our daily management or treatment plan?
- 3.Should we be referred to a specialized behavioral neurologist or a dedicated dementia clinic for further evaluation?
- 4.Since Alzheimer's medications are usually not effective for FTD, what symptom-focused treatments or therapies (like speech therapy) should we consider?
Questions For You
Tap a prompt to share your answer — we'll use it plus this page's context to start a tailored conversation.
Related questions
References
References (22)
- 1
Frontotemporal dementia: Clinical aspects, genetics, and neuropathology of a family with a C9ORF72 expansion in Argentina.
Román KD, Ardohain CA, Surace EI, et al.
Brain pathology (Zurich, Switzerland) 2026; (36(3)):e70057 doi:10.1111/bpa.70057.
PMID: 41500252 - 2
The clinical spectrum of sporadic and familial forms of frontotemporal dementia.
Woollacott IO, Rohrer JD
Journal of neurochemistry 2016; (138 Suppl 1()):6-31 doi:10.1111/jnc.13654.
PMID: 27144467 - 3
Early vs late age at onset frontotemporal dementia and frontotemporal lobar degeneration.
Seo SW, Thibodeau MP, Perry DC, et al.
Neurology 2018; (90(12)):e1047-e1056 doi:10.1212/WNL.0000000000005163.
PMID: 29453245 - 4
The behavioural/dysexecutive variant of Alzheimer's disease: clinical, neuroimaging and pathological features.
Ossenkoppele R, Pijnenburg YA, Perry DC, et al.
Brain : a journal of neurology 2015; (138(Pt 9)):2732-49 doi:10.1093/brain/awv191.
PMID: 26141491 - 5
Frontotemporal Dementia.
Clark DG
Continuum (Minneapolis, Minn.) 2024; (30(6)):1642-1672 doi:10.1212/CON.0000000000001506.
PMID: 39620838 - 6
Distinct early symptoms in neuropathologically proven frontotemporal lobar degeneration.
Kawakami I, Arai T, Shinagawa S, et al.
International journal of geriatric psychiatry 2021; (36(1)):38-45 doi:10.1002/gps.5387.
PMID: 32748432 - 7
Primary Progressive Aphasia Treatment: Current Treatment Options in Neurology Article Topic: Management of Primary Progressive Aphasia.
Cahan JG, Bonakdarpour B
Current treatment options in neurology 2025; (27(1)):39 doi:10.1007/s11940-025-00848-4.
PMID: 40985039 - 8
Verbal Semantics and the Left Dorsolateral Anterior Temporal Lobe: A Longitudinal Case of Bilateral Temporal Degeneration.
Vonk JMJ, Borghesani V, Battistella G, et al.
Aphasiology 2020; (34(7)):865-885 doi:10.1080/02687038.2019.1659935.
PMID: 33012947 - 9
The ScreeLing: Detecting Semantic, Phonological, and Syntactic Deficits in the Clinical Subtypes of Frontotemporal and Alzheimer's Dementia.
Jiskoot LC, Poos JM, van Boven K, et al.
Assessment 2023; (30(8)):2545-2559 doi:10.1177/10731911231154512.
PMID: 36799220 - 10
Interactions of pathological proteins in neurodegenerative diseases.
Spires-Jones TL, Attems J, Thal DR
Acta neuropathologica 2017; (134(2)):187-205 doi:10.1007/s00401-017-1709-7.
PMID: 28401333 - 11
Detection of Alzheimer Disease (AD)-Specific Tau Pathology in AD and NonAD Tauopathies by Immunohistochemistry With Novel Conformation-Selective Tau Antibodies.
Gibbons GS, Banks RA, Kim B, et al.
Journal of neuropathology and experimental neurology 2018; (77(3)):216-228 doi:10.1093/jnen/nly010.
PMID: 29415231 - 12
The basis of clinicopathological heterogeneity in TDP-43 proteinopathy.
Kawakami I, Arai T, Hasegawa M
Acta neuropathologica 2019; (138(5)):751-770 doi:10.1007/s00401-019-02077-x.
PMID: 31555895 - 13
Transcriptomic and pathological analysis of the hnRNP network reveals glial involvement in frontotemporal lobar degeneration pathological subtypes.
Gatt A, Buhidma Y, Fodder K, et al.
Brain communications 2026; (8(3)):fcag197 doi:10.1093/braincomms/fcag197.
PMID: 42327368 - 14
Frontotemporal Dementia: Correlations Between Psychiatric Symptoms and Pathology.
Scarioni M, Gami-Patel P, Timar Y, et al.
Annals of neurology 2020; (87(6)):950-961 doi:10.1002/ana.25739.
PMID: 32281118 - 15
Neurodegenerative disease concomitant proteinopathies are prevalent, age-related and APOE4-associated.
Robinson JL, Lee EB, Xie SX, et al.
Brain : a journal of neurology 2018; (141(7)):2181-2193 doi:10.1093/brain/awy146.
PMID: 29878075 - 16
The use of neuroimaging techniques in the early and differential diagnosis of dementia.
Chouliaras L, O'Brien JT
Molecular psychiatry 2023; (28(10)):4084-4097 doi:10.1038/s41380-023-02215-8.
PMID: 37608222 - 17
Structural MRI in frontotemporal dementia and Alzheimer's disease: stage-dependent atrophy patterns.
Khalili E, Sodaei F, Noroozian M, et al.
Journal of neural transmission (Vienna, Austria : 1996) 2026; (133(8)):1817-1832 doi:10.1007/s00702-026-03158-4.
PMID: 42082780 - 18
The Use of Biomarkers and Genetic Screening to Diagnose Frontotemporal Dementia: Evidence and Clinical Implications.
Gossye H, Van Broeckhoven C, Engelborghs S
Frontiers in neuroscience 2019; (13()):757 doi:10.3389/fnins.2019.00757.
PMID: 31447625 - 19
Brain fluorodeoxyglucose (FDG) PET in dementia.
Kato T, Inui Y, Nakamura A, Ito K
Ageing research reviews 2016; (30()):73-84.
PMID: 26876244 - 20
Analysis of positron emission tomography hypometabolic patterns and neuropsychiatric symptoms in patients with dementia syndromes.
Gan J, Shi Z, Zuo C, et al.
CNS neuroscience & therapeutics 2023; (29(8)):2193-2205 doi:10.1111/cns.14169.
PMID: 36924296 - 21
Amyloid PET in Dementia Syndromes: A Chinese Multicenter Study.
Shi Z, Fu LP, Zhang N, et al.
Journal of nuclear medicine : official publication, Society of Nuclear Medicine 2020; (61(12)):1814-1819 doi:10.2967/jnumed.119.240325.
PMID: 32385166 - 22
Prevalence of amyloid PET positivity in dementia syndromes: a meta-analysis.
Ossenkoppele R, Jansen WJ, Rabinovici GD, et al.
JAMA 2015; (313(19)):1939-49 doi:10.1001/jama.2015.4669.
PMID: 25988463
This comparison is for informational purposes only and does not constitute medical advice or diagnose FTD or Alzheimer's disease. A neurologist or dementia specialist should interpret testing and guide treatment for your specific situation.
Get notified when new evidence is published on Frontotemporal dementia.
We monitor PubMed for new peer-reviewed studies on this topic and email a short summary when something meaningful changes.