Impact of NQO1 dysregulation in CNS disorders

NAD(P)H Quinone Dehydrogenase 1 (NQO1) plays a pivotal role in the regulation of neuronal function and synaptic plasticity, cellular adaptation to oxidative stress, neuroinflammatory and degenerative processes, and tumorigenesis in the central nervous system (CNS). Impairment of the NQO1 activity in...

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Published inJournal of translational medicine Vol. 22; no. 1; pp. 4 - 28
Main Authors Yuhan, Li, Khaleghi Ghadiri, Maryam, Gorji, Ali
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 02.01.2024
BioMed Central
BMC
Subjects
Alzheimer Disease
Alzheimer's disease
Analysis
Antioxidants
Apoptosis
Biological markers
Brain
Brain cancer
Brain Neoplasms
Brain tumors
Carcinogenesis
Care and treatment
Cell cycle
Cell death
Cell growth
Central nervous system
Central nervous system diseases
Cerebrovascular diseases
CNS disorders
Colon
Cyclin-dependent kinases
Demographic aspects
Diagnosis
Drug development
Enzymatic activity
Enzymes
Epilepsy
Gene expression
Health aspects
Humans
Inflammation
Kinases
Lipid peroxidation
Lipids
Measurement techniques
Metabolism
Molecular weight
Movement disorders
Multiple sclerosis
NAD(P)H Dehydrogenase (Quinone)
NADPH dehydrogenase
Neurodegeneration
Neurodegenerative diseases
Neurological diseases
Neurological disorders
Neuronal excitability
Neurons - pathology
Neurophysiology
Neurotransmission
Neurotransmitter release
NQO1
Oxidative Stress
Parkinson's disease
Physiology
Proteins
Review
Ribonucleic acid
RNA
Synaptic plasticity
Transcription factors
Traumatic brain injury
Tumorigenesis
Vitamin E
Iran
Brain
NQO1
Biomarker
Neurodegeneration
CNS disorders
Inflammation
Neuronal excitability
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Abstract NAD(P)H Quinone Dehydrogenase 1 (NQO1) plays a pivotal role in the regulation of neuronal function and synaptic plasticity, cellular adaptation to oxidative stress, neuroinflammatory and degenerative processes, and tumorigenesis in the central nervous system (CNS). Impairment of the NQO1 activity in the CNS can result in abnormal neurotransmitter release and clearance, increased oxidative stress, and aggravated cellular injury/death. Furthermore, it can cause disturbances in neural circuit function and synaptic neurotransmission. The abnormalities of NQO1 enzyme activity have been linked to the pathophysiological mechanisms of multiple neurological disorders, including Parkinson's disease, Alzheimer's disease, epilepsy, multiple sclerosis, cerebrovascular disease, traumatic brain injury, and brain malignancy. NQO1 contributes to various dimensions of tumorigenesis and treatment response in various brain tumors. The precise mechanisms through which abnormalities in NQO1 function contribute to these neurological disorders continue to be a subject of ongoing research. Building upon the existing knowledge, the present study reviews current investigations describing the role of NQO1 dysregulations in various neurological disorders. This study emphasizes the potential of NQO1 as a biomarker in diagnostic and prognostic approaches, as well as its suitability as a target for drug development strategies in neurological disorders.
AbstractList NAD(P)H Quinone Dehydrogenase 1 (NQO1) plays a pivotal role in the regulation of neuronal function and synaptic plasticity, cellular adaptation to oxidative stress, neuroinflammatory and degenerative processes, and tumorigenesis in the central nervous system (CNS). Impairment of the NQO1 activity in the CNS can result in abnormal neurotransmitter release and clearance, increased oxidative stress, and aggravated cellular injury/death. Furthermore, it can cause disturbances in neural circuit function and synaptic neurotransmission. The abnormalities of NQO1 enzyme activity have been linked to the pathophysiological mechanisms of multiple neurological disorders, including Parkinson's disease, Alzheimer's disease, epilepsy, multiple sclerosis, cerebrovascular disease, traumatic brain injury, and brain malignancy. NQO1 contributes to various dimensions of tumorigenesis and treatment response in various brain tumors. The precise mechanisms through which abnormalities in NQO1 function contribute to these neurological disorders continue to be a subject of ongoing research. Building upon the existing knowledge, the present study reviews current investigations describing the role of NQO1 dysregulations in various neurological disorders. This study emphasizes the potential of NQO1 as a biomarker in diagnostic and prognostic approaches, as well as its suitability as a target for drug development strategies in neurological disorders.
NAD(P)H Quinone Dehydrogenase 1 (NQO1) plays a pivotal role in the regulation of neuronal function and synaptic plasticity, cellular adaptation to oxidative stress, neuroinflammatory and degenerative processes, and tumorigenesis in the central nervous system (CNS). Impairment of the NQO1 activity in the CNS can result in abnormal neurotransmitter release and clearance, increased oxidative stress, and aggravated cellular injury/death. Furthermore, it can cause disturbances in neural circuit function and synaptic neurotransmission. The abnormalities of NQO1 enzyme activity have been linked to the pathophysiological mechanisms of multiple neurological disorders, including Parkinson's disease, Alzheimer's disease, epilepsy, multiple sclerosis, cerebrovascular disease, traumatic brain injury, and brain malignancy. NQO1 contributes to various dimensions of tumorigenesis and treatment response in various brain tumors. The precise mechanisms through which abnormalities in NQO1 function contribute to these neurological disorders continue to be a subject of ongoing research. Building upon the existing knowledge, the present study reviews current investigations describing the role of NQO1 dysregulations in various neurological disorders. This study emphasizes the potential of NQO1 as a biomarker in diagnostic and prognostic approaches, as well as its suitability as a target for drug development strategies in neurological disorders. Keywords: Brain, CNS disorders, Inflammation, Neurodegeneration, Neuronal excitability, NQO1, Biomarker
NAD(P)H Quinone Dehydrogenase 1 (NQO1) plays a pivotal role in the regulation of neuronal function and synaptic plasticity, cellular adaptation to oxidative stress, neuroinflammatory and degenerative processes, and tumorigenesis in the central nervous system (CNS). Impairment of the NQO1 activity in the CNS can result in abnormal neurotransmitter release and clearance, increased oxidative stress, and aggravated cellular injury/death. Furthermore, it can cause disturbances in neural circuit function and synaptic neurotransmission. The abnormalities of NQO1 enzyme activity have been linked to the pathophysiological mechanisms of multiple neurological disorders, including Parkinson's disease, Alzheimer's disease, epilepsy, multiple sclerosis, cerebrovascular disease, traumatic brain injury, and brain malignancy. NQO1 contributes to various dimensions of tumorigenesis and treatment response in various brain tumors. The precise mechanisms through which abnormalities in NQO1 function contribute to these neurological disorders continue to be a subject of ongoing research. Building upon the existing knowledge, the present study reviews current investigations describing the role of NQO1 dysregulations in various neurological disorders. This study emphasizes the potential of NQO1 as a biomarker in diagnostic and prognostic approaches, as well as its suitability as a target for drug development strategies in neurological disorders.NAD(P)H Quinone Dehydrogenase 1 (NQO1) plays a pivotal role in the regulation of neuronal function and synaptic plasticity, cellular adaptation to oxidative stress, neuroinflammatory and degenerative processes, and tumorigenesis in the central nervous system (CNS). Impairment of the NQO1 activity in the CNS can result in abnormal neurotransmitter release and clearance, increased oxidative stress, and aggravated cellular injury/death. Furthermore, it can cause disturbances in neural circuit function and synaptic neurotransmission. The abnormalities of NQO1 enzyme activity have been linked to the pathophysiological mechanisms of multiple neurological disorders, including Parkinson's disease, Alzheimer's disease, epilepsy, multiple sclerosis, cerebrovascular disease, traumatic brain injury, and brain malignancy. NQO1 contributes to various dimensions of tumorigenesis and treatment response in various brain tumors. The precise mechanisms through which abnormalities in NQO1 function contribute to these neurological disorders continue to be a subject of ongoing research. Building upon the existing knowledge, the present study reviews current investigations describing the role of NQO1 dysregulations in various neurological disorders. This study emphasizes the potential of NQO1 as a biomarker in diagnostic and prognostic approaches, as well as its suitability as a target for drug development strategies in neurological disorders.
Abstract NAD(P)H Quinone Dehydrogenase 1 (NQO1) plays a pivotal role in the regulation of neuronal function and synaptic plasticity, cellular adaptation to oxidative stress, neuroinflammatory and degenerative processes, and tumorigenesis in the central nervous system (CNS). Impairment of the NQO1 activity in the CNS can result in abnormal neurotransmitter release and clearance, increased oxidative stress, and aggravated cellular injury/death. Furthermore, it can cause disturbances in neural circuit function and synaptic neurotransmission. The abnormalities of NQO1 enzyme activity have been linked to the pathophysiological mechanisms of multiple neurological disorders, including Parkinson's disease, Alzheimer's disease, epilepsy, multiple sclerosis, cerebrovascular disease, traumatic brain injury, and brain malignancy. NQO1 contributes to various dimensions of tumorigenesis and treatment response in various brain tumors. The precise mechanisms through which abnormalities in NQO1 function contribute to these neurological disorders continue to be a subject of ongoing research. Building upon the existing knowledge, the present study reviews current investigations describing the role of NQO1 dysregulations in various neurological disorders. This study emphasizes the potential of NQO1 as a biomarker in diagnostic and prognostic approaches, as well as its suitability as a target for drug development strategies in neurological disorders.
ArticleNumber 4
Audience Academic
Author Gorji, Ali
Khaleghi Ghadiri, Maryam
Yuhan, Li
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Issue 1
Keywords Brain
NQO1
Biomarker
Neurodegeneration
CNS disorders
Inflammation
Neuronal excitability
Language English
License 2023. The Author(s).
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Snippet NAD(P)H Quinone Dehydrogenase 1 (NQO1) plays a pivotal role in the regulation of neuronal function and synaptic plasticity, cellular adaptation to oxidative...
Abstract NAD(P)H Quinone Dehydrogenase 1 (NQO1) plays a pivotal role in the regulation of neuronal function and synaptic plasticity, cellular adaptation to...
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SubjectTerms Alzheimer Disease
Alzheimer's disease
Analysis
Antioxidants
Apoptosis
Biological markers
Brain
Brain cancer
Brain Neoplasms
Brain tumors
Carcinogenesis
Care and treatment
Cell cycle
Cell death
Cell growth
Central nervous system
Central nervous system diseases
Cerebrovascular diseases
CNS disorders
Colon
Cyclin-dependent kinases
Demographic aspects
Diagnosis
Drug development
Enzymatic activity
Enzymes
Epilepsy
Gene expression
Health aspects
Humans
Inflammation
Kinases
Lipid peroxidation
Lipids
Measurement techniques
Metabolism
Molecular weight
Movement disorders
Multiple sclerosis
NAD(P)H Dehydrogenase (Quinone)
NADPH dehydrogenase
Neurodegeneration
Neurodegenerative diseases
Neurological diseases
Neurological disorders
Neuronal excitability
Neurons - pathology
Neurophysiology
Neurotransmission
Neurotransmitter release
NQO1
Oxidative Stress
Parkinson's disease
Physiology
Proteins
Review
Ribonucleic acid
RNA
Synaptic plasticity
Transcription factors
Traumatic brain injury
Tumorigenesis
Vitamin E
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Title Impact of NQO1 dysregulation in CNS disorders
URI https://www.ncbi.nlm.nih.gov/pubmed/38167027
https://www.proquest.com/docview/2914306528
https://www.proquest.com/docview/2910191332
https://pubmed.ncbi.nlm.nih.gov/PMC10762857
https://doaj.org/article/44915be6ad9d472d9d5dd85aed6e1445
Volume 22
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