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Uncovering disease mechanisms in frontotemporal dementia: neuroinflammation under the spotlight
There is increasing clinical, genetic, molecular and cellular evidence that neuroinflammation plays an important role in sporadic and genetic frontotemporal dementia (FTD), with mutations in Progranulin (GRN), microtubule-associated protein tau (MAPT) or repeat expansions in chromosome nine open reading frame 72 (C9orf72).1 GRN and C9orf72 are highly expressed in microglia.2 Genes involved in immune pathways are significantly associated with FTD, and upregulated expression of astrocytic and microglial proteins are found in FTD brains. Furthermore, higher levels of neuroinflammatory biomarkers are found in the cerebrospinal fluid (CSF) of patients with FTD compared with controls or presymptomatic mutation carriers.2
Translocator protein 18 kDa (TSPO) positron emission tomography (PET) ligands are used as …
Contributors Both authors contributed equally to the manuscript.
Funding This study was funded by ZonMw (grant 733050513).
Competing interests None declared.
Patient consent for publication Not required.
Provenance and peer review Commissioned; internally peer reviewed.