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Is there a role for the p75 neurotrophin receptor in mediating degeneration during oxidative stress and after hypoxia?
Author(s) -
Sankorrakul Kornraviya,
Qian Lei,
Thangnipon Wipawan,
Coulson Elizabeth J.
Publication year - 2021
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/jnc.15451
Subject(s) - neurotrophin , low affinity nerve growth factor receptor , neuroscience , oxidative stress , programmed cell death , microbiology and biotechnology , biology , basal forebrain , signalling , cholinergic neuron , signal transduction , receptor , cholinergic , apoptosis , endocrinology , biochemistry
Cholinergic basal forebrain (cBF) neurons are particularly vulnerable to degeneration following trauma and in neurodegenerative conditions. One reason for this is their characteristic expression of the p75 neurotrophin receptor (p75 NTR ), which is up‐regulated and mediates neuronal death in a range of neurological and neurodegenerative conditions, including dementia, stroke and ischaemia. The signalling pathway by which p75 NTR signals cell death is incompletely characterised, but typically involves activation by neurotrophic ligands and signalling through c‐Jun kinase, resulting in caspase activation via mitochondrial apoptotic signalling pathways. Less well appreciated is the link between conditions of oxidative stress and p75 NTR death signalling. Here, we review the literature describing what is currently known regarding p75 NTR death signalling in environments of oxidative stress and hypoxia to highlight the overlap in signalling pathways and the implications for p75 NTR signalling in cBF neurons. We propose that there is a causal relationship and define key questions to test this assertion.