NAD<sup>+</sup> Metabolism and Diseases with Motor Dysfunction

Neurodegenerative diseases result in the progressive deterioration of the nervous system, with motor and cognitive impairments being the two most observable problems. Motor dysfunction could be caused by motor neuron diseases (MNDs) characterized by the loss of motor neurons, such as amyotrophic lat...

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Autores principales:	Samuel Lundt, Shinghua Ding
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	NAD<sup>+</sup> Nampt energy metabolism motor neuron diseases motor dysfunction Genetics QH426-470
Acceso en línea:	https://doaj.org/article/a8a630e311744613a9a1167cbd775774
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spelling	oai:doaj.org-article:a8a630e311744613a9a1167cbd7757742021-11-25T17:41:50ZNAD<sup>+</sup> Metabolism and Diseases with Motor Dysfunction10.3390/genes121117762073-4425https://doaj.org/article/a8a630e311744613a9a1167cbd7757742021-11-01T00:00:00Zhttps://www.mdpi.com/2073-4425/12/11/1776https://doaj.org/toc/2073-4425Neurodegenerative diseases result in the progressive deterioration of the nervous system, with motor and cognitive impairments being the two most observable problems. Motor dysfunction could be caused by motor neuron diseases (MNDs) characterized by the loss of motor neurons, such as amyotrophic lateral sclerosis and Charcot–Marie–Tooth disease, or other neurodegenerative diseases with the destruction of brain areas that affect movement, such as Parkinson’s disease and Huntington’s disease. Nicotinamide adenine dinucleotide (NAD<sup>+</sup>) is one of the most abundant metabolites in the human body and is involved with numerous cellular processes, including energy metabolism, circadian clock, and DNA repair. NAD<sup>+</sup> can be reversibly oxidized-reduced or directly consumed by NAD<sup>+</sup>-dependent proteins. NAD<sup>+</sup> is synthesized in cells via three different paths: the de novo, Preiss–Handler, or NAD<sup>+</sup> salvage pathways, with the salvage pathway being the primary producer of NAD<sup>+</sup> in mammalian cells. NAD<sup>+</sup> metabolism is being investigated for a role in the development of neurodegenerative diseases. In this review, we discuss cellular NAD<sup>+</sup> homeostasis, looking at NAD<sup>+</sup> biosynthesis and consumption, with a focus on the NAD<sup>+</sup> salvage pathway. Then, we examine the research, including human clinical trials, focused on the involvement of NAD<sup>+</sup> in MNDs and other neurodegenerative diseases with motor dysfunction.Samuel LundtShinghua DingMDPI AGarticleNAD<sup>+</sup>Namptenergy metabolismmotor neuron diseasesmotor dysfunctionGeneticsQH426-470ENGenes, Vol 12, Iss 1776, p 1776 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	NAD<sup>+</sup> Nampt energy metabolism motor neuron diseases motor dysfunction Genetics QH426-470
spellingShingle	NAD<sup>+</sup> Nampt energy metabolism motor neuron diseases motor dysfunction Genetics QH426-470 Samuel Lundt Shinghua Ding NAD<sup>+</sup> Metabolism and Diseases with Motor Dysfunction
description	Neurodegenerative diseases result in the progressive deterioration of the nervous system, with motor and cognitive impairments being the two most observable problems. Motor dysfunction could be caused by motor neuron diseases (MNDs) characterized by the loss of motor neurons, such as amyotrophic lateral sclerosis and Charcot–Marie–Tooth disease, or other neurodegenerative diseases with the destruction of brain areas that affect movement, such as Parkinson’s disease and Huntington’s disease. Nicotinamide adenine dinucleotide (NAD<sup>+</sup>) is one of the most abundant metabolites in the human body and is involved with numerous cellular processes, including energy metabolism, circadian clock, and DNA repair. NAD<sup>+</sup> can be reversibly oxidized-reduced or directly consumed by NAD<sup>+</sup>-dependent proteins. NAD<sup>+</sup> is synthesized in cells via three different paths: the de novo, Preiss–Handler, or NAD<sup>+</sup> salvage pathways, with the salvage pathway being the primary producer of NAD<sup>+</sup> in mammalian cells. NAD<sup>+</sup> metabolism is being investigated for a role in the development of neurodegenerative diseases. In this review, we discuss cellular NAD<sup>+</sup> homeostasis, looking at NAD<sup>+</sup> biosynthesis and consumption, with a focus on the NAD<sup>+</sup> salvage pathway. Then, we examine the research, including human clinical trials, focused on the involvement of NAD<sup>+</sup> in MNDs and other neurodegenerative diseases with motor dysfunction.
format	article
author	Samuel Lundt Shinghua Ding
author_facet	Samuel Lundt Shinghua Ding
author_sort	Samuel Lundt
title	NAD<sup>+</sup> Metabolism and Diseases with Motor Dysfunction
title_short	NAD<sup>+</sup> Metabolism and Diseases with Motor Dysfunction
title_full	NAD<sup>+</sup> Metabolism and Diseases with Motor Dysfunction
title_fullStr	NAD<sup>+</sup> Metabolism and Diseases with Motor Dysfunction
title_full_unstemmed	NAD<sup>+</sup> Metabolism and Diseases with Motor Dysfunction
title_sort	nad<sup>+</sup> metabolism and diseases with motor dysfunction
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/a8a630e311744613a9a1167cbd775774
work_keys_str_mv	AT samuellundt nadsupsupmetabolismanddiseaseswithmotordysfunction AT shinghuading nadsupsupmetabolismanddiseaseswithmotordysfunction
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NAD<sup>+</sup> Metabolism and Diseases with Motor Dysfunction

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