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Originally construed as a disorder of behaviour and executive impairment, FTD is now known also to be associated with alterations in language, conceptual knowledge and praxis. An absence of neurological signs is the hallmark of many FTD patients, but there is also an established association with motor neurone disease (MND), progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD). FTD is commonly defined as an early onset dementia, yet about a quarter of patients present after the age of 65. The underlying pathological protein is tau, TDP\u201043 or more rarely fused\u2010in\u2010sarcoma (FUS). Distinct genetic mutations have been identified in familial FTD. There are predictable relationships between clinical phenotype, pathological substrate and genetic mutation. For example, a circumscribed semantic disorder predicts TDP\u201043 pathology, and speech or limb apraxia tau pathology. The co\u2010occurrence of MND predicts TDP\u201043 pathology, and PSP and CBD tau pathology. FUS pathology is associated with very youthful onset, stereotyped behaviours and caudate atrophy. Non\u2010fluent aphasia is linked to progranulin (\n                    <jats:italic>GRN<\/jats:italic>\n                    ) mutations and MND and psychosis to repeat expansions in the\n                    <jats:italic>C9orf72<\/jats:italic>\n                    gene. Despite striking worldwide consensus in findings there remain some issues of contention, largely related to the classification of FTD and its sub\u2010variants. Understanding the diverse nature of FTD is crucial for effective diagnosis, management and the development of targeted therapies.\n                  <\/jats:p>","DOI":"10.1111\/jnp.12297","type":"journal-article","created":{"date-parts":[[2022,10,31]],"date-time":"2022-10-31T10:46:26Z","timestamp":1667213186000},"page":"211-234","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["Changing perspectives on frontotemporal dementia: A review"],"prefix":"10.1111","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3976-4310","authenticated-orcid":false,"given":"Julie S.","family":"Snowden","sequence":"first","affiliation":[{"name":"Cerebral Function Unit, Manchester Centre for Neurosciences Salford Royal NHS Foundation Trust Salford UK"},{"name":"Division of Neuroscience &amp; Experimental Psychology School of Biological Sciences, University of Manchester Manchester 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