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The orphan nuclear receptor TLX (Nr2e1) is a key regulator of hippocampal neurogenesis. Impaired adult hippocampal neurogenesis has been reported in neurodegenerative and psychiatric conditions including dementia and stress-related depression. Neuroinflammation is also implicated in the neuropathology of these disorders, and has been shown to negatively affect hippocampal neurogenesis. To investigate a role for TLX in hippocampal neuroinflammation, we assessed microglial activation in the hippocampus of mice with a spontaneous deletion of TLX. Results from our study suggest that a lack of TLX is implicated in deregulation of microglial phenotype and that consequently, the survival and function of newborn cells in the hippocampus is impaired. TLX may be an important target in understanding inflammatory-associated impairments in neurogenesis., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Inflammation is involved in the pathology of Parkinson's disease, a disorder characterised by degeneration of dopaminergic neurons. This study demonstrates that conditioned medium (CM) from lipopolysaccharide (LPS)-treated rat glial-enriched cortical cultures induced death of embryonic rat dopaminergic neurons in vitro, an effect which was additive to the toxicity of the neurotoxin 6-hydroxydopamine. Interleukin-1β (IL-1β) in the CM may mediate this neuronal death. IL-1R1 was found to be expressed on dopaminergic neurons. Blockade of IL-1R1 prevented CM-induced dopaminergic neuronal death. This study suggests that IL-1β in CM from LPS-stimulated glia contributes to dopaminergic neuronal death induced by glia-conditioned medium., (Copyright © 2010 Elsevier B.V. All rights reserved.)