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Whether neuroinflammation also plays an important role in the pathophysiology of frontotemporal dementia is less well known. Frontotemporal dementia is a heterogeneous classification that covers many subtypes, with the main pathology known as frontotemporal lobar degeneration. The disease can be categorized with respect to the identity of the protein that causes the frontotemporal lobar degeneration in the brain. The most common subgroup describes diseases caused by frontotemporal lobar degeneration associated with tau aggregation, also known as primary tauopathies. Evidence suggests that neuroinflammation may play a role in primary tauopathies with genome-wide association studies finding enrichment of genetic variants associated with specific inflammation-related gene loci. These loci are related to both the innate immune system, including brain resident microglia, and the adaptive immune system through possible peripheral T-cell involvement. This review discusses the genetic evidence and relates it to findings in animal models expressing pathogenic tau as well as to post-mortem and PET studies in human disease. Across experimental paradigms, there seems to be a consensus regarding the involvement of innate immunity in primary tauopathies, with increased microglia and astrocyte density and\/or activation, as well as increases in pro-inflammatory markers. Whilst it is less clear as to whether inflammation precedes tau aggregation or vice versa; there is strong evidence to support a microglial contribution to the propagation of hyperphosphorylated in tau frontotemporal lobar degeneration associated with tau aggregation. Experimental evidence\u2014albeit limited\u2014also corroborates genetic data pointing to the involvement of cellular adaptive immunity in primary tauopathies. However, it is still unclear whether brain recruitment of peripheral immune cells is an aberrant result of pathological changes or a physiological aspect of the neuroinflammatory response to the tau pathology.<\/jats:p>","DOI":"10.1093\/brain\/awaa457","type":"journal-article","created":{"date-parts":[[2020,12,21]],"date-time":"2020-12-21T21:14:26Z","timestamp":1608585266000},"page":"724-745","source":"Crossref","is-referenced-by-count":41,"title":["Glial cells and adaptive immunity in frontotemporal dementia with tau pathology"],"prefix":"10.1093","volume":"144","author":[{"given":"Iain J","family":"Hartnell","sequence":"first","affiliation":[{"name":"Clinical Neurosciences, Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Blum","sequence":"additional","affiliation":[{"name":"University of Lille, Inserm, CHU-Lille, UMR-S 1172\u2014Lille Neuroscience and Cognition, Lille, France"},{"name":"Alzheimer & Tauopathies, LabEx DISTALZ, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James A R","family":"Nicoll","sequence":"additional","affiliation":[{"name":"Clinical Neurosciences, Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, UK"},{"name":"Department of Cellular Pathology, University Hospital Southampton NHS Foundation Trust, Southampton, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5763-3632","authenticated-orcid":false,"given":"Guillaume","family":"Dorothee","sequence":"additional","affiliation":[{"name":"Inserm, Sorbonne University, UMRS 938 Saint-Antoine Research Center, Immune System and Neuroinflammation Laboratory, H\u00f4pital Saint-Antoine, Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5884-130X","authenticated-orcid":false,"given":"Delphine","family":"Boche","sequence":"additional","affiliation":[{"name":"Clinical Neurosciences, Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2021,1,26]]},"reference":[{"key":"2021041219330311900_awaa457-B1","doi-asserted-by":"crossref","first-page":"2","DOI":"10.1186\/s13195-019-0562-4","article-title":"CSF biomarkers of neuroinflammation in distinct forms and subtypes of neurodegenerative dementia","volume":"12","author":"Abu-Rumeileh","year":"2019","journal-title":"Alzheimers Res Ther"},{"key":"2021041219330311900_awaa457-B2","doi-asserted-by":"crossref","first-page":"2018","DOI":"10.1073\/pnas.0812697106","article-title":"Apolipoprotein E epsilon4 is associated with 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