Clinical, genetic and pathological heterogeneity of frontotemporal dementia: A review
Open accessAbstract
Frontotemporal dementia (FTD) is the second most common young-onset dementia and is clinically characterised by progressive behavioural change, executive dysfunction and language difficulties. Three clinical syndromes, behavioural variant FTD, semantic dementia and progressive non-fluent aphasia, form part of a clinicopathological spectrum named frontotemporal lobar degeneration (FTLD). The classical neuropsychological phenotype of FTD has been enriched by tests exploring Theory of Mind, social cognition and emotional processing. Imaging studies have detailed the patterns of atrophy associated with different clinical and pathological subtypes. These patterns offer some diagnostic utility, while measures of progression of atrophy may be of use in future trials. 30-50% of FTD is familial, and mutations in two genes, microtubule associated protein tau and Progranulin (GRN), account for about half of these cases. Rare defects in VCP, CHMP2B, TARDP and FUS genes have been found in a small number of families. Linkage to chromosome 9p13.2-21.3 has been established in familial FTD with motor neuron disease, although the causative gene is yet to be identified. Recent developments in the immunohistochemistry of FTLD, and also in amyotrophic lateral sclerosis (ALS), have led to a new pathological nomenclature. The two major groups are those with tau-positive inclusions (FTLD-tau) and those with ubiquitin-positive and TAR DNA-binding protein of 43 kDa (TDP-43) positive inclusions (FTLD-TDP). Recently, a new protein involved in familial ALS, fused in sarcoma (FUS), has been found in FTLD patients with ubiquitin-positive and TDP-43-negative inclusions. In this review, the authors discuss recent clinical, neuropsychological, imaging, genetic and pathological developments that have changed our understanding of FTD, its classification and criteria. The potential to establish an early diagnosis, predict underlying pathology during life and quantify disease progression will all be required for disease-specific therapeutic trials in the future.
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The frontal cortex and striatum have been previously shown to be susceptible to age-related neurodegenerative diseases.
“These brain regions have been previously shown to be susceptible to age-related neurodegenerative diseases.”
From Molecular and spatial signatures of mouse brain aging at single-cell resolution (2023) · cites this paper as [33]
The NEUROIMAGING section reports that mild behavioural-variant frontotemporal dementia involves frontal cortices and the striatum. The EPIDEMIOLOGY section gives ages of onset for FTD, but the paper does not establish that both regions are susceptible to age-related neurodegenerative diseases generally; its anatomical finding is specific to FTD. Page numbers were not available in our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measuredCorrelations between clinical syndrome and the type of pathological protein in frontotemporal dementia are generally weak.
“However, there are several different pathological proteins and aggregation morphologies in FTD, with generally weak correlations between clinical syndrome and the type of pathological protein (Seelaar et al., 2011)”
From Neuroinflammation and protein aggregation co-localize across the frontotemporal dementia spectrum (2020) · cites this paper as Seelaar et al., 2011
The Clinical Presentation section (page unavailable) says that associations between PPA syndromes and underlying pathology are “relatively strong,” though not absolute. The Future Directions section (page unavailable) indicates that distinguishing pathological subtypes of behavioural-variant FTD during life remains difficult. Thus, the review supports limited clinical prediction for some FTD presentations, but not the blanket characterization of correlations as generally weak. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThere are several different pathological proteins and aggregation morphologies in frontotemporal dementia.
“However, there are several different pathological proteins and aggregation morphologies in FTD, with generally weak correlations between clinical syndrome and the type of pathological protein (Seelaar et al., 2011)”
From Neuroinflammation and protein aggregation co-localize across the frontotemporal dementia spectrum (2020) · cites this paper as Seelaar et al., 2011
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Epidemiology of Frontotemporal Lobar Degeneration
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Atrophy patterns in histologic vs clinical groupings of frontotemporal lobar degeneration
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Self-citationMutations in progranulin explain atypical phenotypes with variants in MAPT
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Chromosome 9p-linked families with frontotemporal dementia associated with motor neuron disease
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Variations in regional SPECT hypoperfusion and clinical features in frontotemporal dementia
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Gene expression study on peripheral blood identifies progranulin mutations
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Confabulation, but not executive dysfunction discriminate AD from frontotemporal dementia
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FUS Mutations in Familial Amyotrophic Lateral Sclerosis in the Netherlands
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Qualitative Assessment of Verbal Fluency Performance in Frontotemporal Dementia
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Considering sex and gender in Alzheimer disease and other dementias
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Enhanced Protein Degradation by Branched Ubiquitin Chains
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Self-citationSerum neurofilament light chain protein is a measure of disease intensity in frontotemporal dementia
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Self-citationMolecular and spatial signatures of mouse brain aging at single-cell resolution
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“These brain regions have been previously shown to be susceptible to age-related neurodegenerative diseases.(33,34) We sequenced 50,000 nuclei from two female animals at each age and performed unsupervised clustering analysis of the 80,000 cells that passed quality control (Figures S1A–S1F).”
BackgroundClinical and neuroanatomical signatures of tissue pathology in frontotemporal lobar degeneration
Rohrer, J. D., Lashley, T., Schott, J. M., Warren, J. D., Mead, S., Isaacs, A. M., Beck, J. A., Hardy, J., de Silva, R., Warrington, E. K., et al. (2011) · Brain · doi:10.1093/brain/awr198 · Cited by 359 · see citing works
Self-citationMotor Neuron dysfunction in frontotemporal dementia
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Self-citationNeurofilament light chain: a biomarker for genetic frontotemporal dementia
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Imaging and fluid biomarkers in frontotemporal dementia
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Trajectories of cognitive decline in different types of dementia
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- Authors
- Seelaar, H., Rohrer, J. D., Pijnenburg, Y. A. L., Fox, N. C., & van Swieten, J. C.
- Affiliations
- Erasmus MC (NL)
- National Hospital for Neurology and Neurosurgery (GB)
- Amsterdam UMC Location Vrije Universiteit Amsterdam (NL)
- Venue
- Journal of Neurology, Neurosurgery & Psychiatry
- Publisher
- BMJ
- Published
- 2010-10-22
- Volume
- 82
- Issue
- 5
- Pages
- 476-486
- ISSN
- 0022-3050 (ISSN-L)
- OpenAlex
- W2102932082
- Cited by
- 609
- References
- 222
- Citations by year
- 2026: 16 · 2025: 22 · 2024: 39 · 2023: 23 · 2022: 35 · 2021: 33 · 2020: 44 · 2019: 42 · 2018: 34 · 2017: 31 · 2016: 49 · 2015: 41 · 2014: 45 · 2013: 65 · 2012: 54
- FWCI
- 6.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neurology Neurosurgery & Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- HAL (submittedVersion, other-oa)
- Digital Academic REpository of VU University Amsterdam (Vrije Universiteit Amsterdam) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- HighWire Press Open Archive (submittedVersion)
- Pure Amsterdam UMC (submittedVersion)
- Trinity's Access to Research Output (TARA) (Trinity College Dublin) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- Alzheimer's Research Trust
- National Institute for Health and Care Research (NF-SI-0508-10123)
- Hersenstichting
- Stichting Dioraphte
- Medical Research Council
- Topics
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- frontotemporal dementia, frontotemporal lobar degeneration, semantic dementia, progressive nonfluent aphasia, tauopathy, TDP-43, FUS, progranulin, tau protein, VCP, CHMP2B, amyotrophic lateral sclerosis, neuroimaging, brain atrophy, neuropsychological assessment, disease progression, early diagnosis, genetic heterogeneity
- MeSH terms
- Progranulins, Brain, Cognition, Humans, Magnetic Resonance Imaging, Risk Factors, Social Perception, Biomarkers, tau Proteins, Intercellular Signaling Peptides and Proteins, Executive Function, Frontotemporal Dementia
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