Nicotinamide Adenine Dinucleotide Phosphate Oxidases Are Everywhere in Brain Disease, but Not in Huntington’s Disease?

Huntington’s disease (HD) is an inherited neurodegenerative disorder characterized by neuronal loss and tissue atrophy mainly in the striatum and cortex. In the early stages of the disease, impairment of neuronal function, synaptic dysfunction and white matter loss precedes neuronal death itself. Re...

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Autores principales:	Luisana Villegas, Anne Nørremølle, Kristine Freude, Frederik Vilhardt
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	Huntington’s (disease) NADPH (nicotinamide adenine dinucleotide phosphate) oxidase neuron Huntingtin (HTT) NMDAR (NMDA receptor) LTP (long term potentiation) Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571
Acceso en línea:	https://doaj.org/article/a2319712680544fca900d3b65930a9f1
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spelling	oai:doaj.org-article:a2319712680544fca900d3b65930a9f12021-11-05T08:17:12ZNicotinamide Adenine Dinucleotide Phosphate Oxidases Are Everywhere in Brain Disease, but Not in Huntington’s Disease?1663-436510.3389/fnagi.2021.736734https://doaj.org/article/a2319712680544fca900d3b65930a9f12021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fnagi.2021.736734/fullhttps://doaj.org/toc/1663-4365Huntington’s disease (HD) is an inherited neurodegenerative disorder characterized by neuronal loss and tissue atrophy mainly in the striatum and cortex. In the early stages of the disease, impairment of neuronal function, synaptic dysfunction and white matter loss precedes neuronal death itself. Relative to other neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease and Amyotrophic Lateral Sclerosis, where the effects of either microglia or NADPH oxidases (NOXs) are recognized as important contributors to disease pathogenesis and progression, there is a pronounced lack of information in HD. This information void contrasts with evidence from human HD patients where blood monocytes and microglia are activated well before HD clinical symptoms (PET scans), and the clear signs of oxidative stress and inflammation in post mortem HD brain. Habitually, NOX activity and oxidative stress in the central nervous system (CNS) are equated with microglia, but research of the last two decades has carved out important roles for NOX enzyme function in neurons. Here, we will convey recent information about the function of NOX enzymes in neurons, and contemplate on putative roles of neuronal NOX in HD. We will focus on NOX-produced reactive oxygen species (ROS) as redox signaling molecules in/among neurons, and the specific roles of NOXs in important processes such as neurogenesis and lineage specification, neurite outgrowth and growth cone dynamics, and synaptic plasticity where NMDAR-dependent signaling, and long-term depression/potentiation are redox-regulated phenomena. HD animal models and induced pluripotent stem cell (iPSC) studies have made it clear that the very same physiological processes are also affected in HD, and we will speculate on possible roles for NOX in the pathogenesis and development of disease. Finally, we also take into account the limited information on microglia in HD and relate this to any contribution of NOX enzymes.Luisana VillegasAnne NørremølleKristine FreudeFrederik VilhardtFrontiers Media S.A.articleHuntington’s (disease)NADPH (nicotinamide adenine dinucleotide phosphate) oxidaseneuronHuntingtin (HTT)NMDAR (NMDA receptor)LTP (long term potentiation)Neurosciences. Biological psychiatry. NeuropsychiatryRC321-571ENFrontiers in Aging Neuroscience, Vol 13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Huntington’s (disease) NADPH (nicotinamide adenine dinucleotide phosphate) oxidase neuron Huntingtin (HTT) NMDAR (NMDA receptor) LTP (long term potentiation) Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571
spellingShingle	Huntington’s (disease) NADPH (nicotinamide adenine dinucleotide phosphate) oxidase neuron Huntingtin (HTT) NMDAR (NMDA receptor) LTP (long term potentiation) Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Luisana Villegas Anne Nørremølle Kristine Freude Frederik Vilhardt Nicotinamide Adenine Dinucleotide Phosphate Oxidases Are Everywhere in Brain Disease, but Not in Huntington’s Disease?
description	Huntington’s disease (HD) is an inherited neurodegenerative disorder characterized by neuronal loss and tissue atrophy mainly in the striatum and cortex. In the early stages of the disease, impairment of neuronal function, synaptic dysfunction and white matter loss precedes neuronal death itself. Relative to other neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease and Amyotrophic Lateral Sclerosis, where the effects of either microglia or NADPH oxidases (NOXs) are recognized as important contributors to disease pathogenesis and progression, there is a pronounced lack of information in HD. This information void contrasts with evidence from human HD patients where blood monocytes and microglia are activated well before HD clinical symptoms (PET scans), and the clear signs of oxidative stress and inflammation in post mortem HD brain. Habitually, NOX activity and oxidative stress in the central nervous system (CNS) are equated with microglia, but research of the last two decades has carved out important roles for NOX enzyme function in neurons. Here, we will convey recent information about the function of NOX enzymes in neurons, and contemplate on putative roles of neuronal NOX in HD. We will focus on NOX-produced reactive oxygen species (ROS) as redox signaling molecules in/among neurons, and the specific roles of NOXs in important processes such as neurogenesis and lineage specification, neurite outgrowth and growth cone dynamics, and synaptic plasticity where NMDAR-dependent signaling, and long-term depression/potentiation are redox-regulated phenomena. HD animal models and induced pluripotent stem cell (iPSC) studies have made it clear that the very same physiological processes are also affected in HD, and we will speculate on possible roles for NOX in the pathogenesis and development of disease. Finally, we also take into account the limited information on microglia in HD and relate this to any contribution of NOX enzymes.
format	article
author	Luisana Villegas Anne Nørremølle Kristine Freude Frederik Vilhardt
author_facet	Luisana Villegas Anne Nørremølle Kristine Freude Frederik Vilhardt
author_sort	Luisana Villegas
title	Nicotinamide Adenine Dinucleotide Phosphate Oxidases Are Everywhere in Brain Disease, but Not in Huntington’s Disease?
title_short	Nicotinamide Adenine Dinucleotide Phosphate Oxidases Are Everywhere in Brain Disease, but Not in Huntington’s Disease?
title_full	Nicotinamide Adenine Dinucleotide Phosphate Oxidases Are Everywhere in Brain Disease, but Not in Huntington’s Disease?
title_fullStr	Nicotinamide Adenine Dinucleotide Phosphate Oxidases Are Everywhere in Brain Disease, but Not in Huntington’s Disease?
title_full_unstemmed	Nicotinamide Adenine Dinucleotide Phosphate Oxidases Are Everywhere in Brain Disease, but Not in Huntington’s Disease?
title_sort	nicotinamide adenine dinucleotide phosphate oxidases are everywhere in brain disease, but not in huntington’s disease?
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/a2319712680544fca900d3b65930a9f1
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Nicotinamide Adenine Dinucleotide Phosphate Oxidases Are Everywhere in Brain Disease, but Not in Huntington’s Disease?

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