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Neuroinflammation contributes to ALS and FTD pathophysiology
The pathophysiological mechanisms underlying the development of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) remain to be fully elucidated, although overlapping biological processes expressed in different proportions in neuronal and non-neuronal cells seem to predispose to regional neuronal vulnerability and ultimately disease symptomology in seemingly disparate neurodegenerative diseases.1–5 There is now emerging evidence for the importance of neuroinflammation ALS and FTD pathogenesis.6 7 In patients with ALS, the neuroinflammatory response is characterised by microglial activation and T cell infiltration, the profile of which changes with disease stage.8 Specifically, in early stages of ALS, the immune profile is characterised by increased regulatory T cells, upregulation of anti-inflammatory cytokines and activation of …
Contributors SV was commissioned to write the manuscript.
Funding Funding support from the National Health and Medical Research Council of Australia (Project grant numbers 510233, 1024915, 1055778, Program Grant #1037746).
Competing interests None declared.
Patient consent Not required.
Provenance and peer review Commissioned; internally peer reviewed.