The NAD+-mitophagy axis in healthy longevity and in artificial intelligence-based clinical applications

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

The NAD+-mitophagy axis in healthy longevity and in artificial intelligence-based clinical applications. / Aman, Yahyah; Frank, Johannes; Lautrup, Sofie Hindkjær; Matysek, Adrian; Niu, Zhangming; Yang, Guang; Shi, Liu; Bergersen, Linda H.; Storm-Mathisen, Jon; Rasmussen, Lene J.; Bohr, Vilhelm A.; Nilsen, Hilde; Fang, Evandro F.

In: Mechanisms of Ageing and Development, Vol. 185, 111194, 2020.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Aman, Y, Frank, J, Lautrup, SH, Matysek, A, Niu, Z, Yang, G, Shi, L, Bergersen, LH, Storm-Mathisen, J, Rasmussen, LJ, Bohr, VA, Nilsen, H & Fang, EF 2020, 'The NAD+-mitophagy axis in healthy longevity and in artificial intelligence-based clinical applications', Mechanisms of Ageing and Development, vol. 185, 111194. https://doi.org/10.1016/j.mad.2019.111194

APA

Aman, Y., Frank, J., Lautrup, S. H., Matysek, A., Niu, Z., Yang, G., Shi, L., Bergersen, L. H., Storm-Mathisen, J., Rasmussen, L. J., Bohr, V. A., Nilsen, H., & Fang, E. F. (2020). The NAD+-mitophagy axis in healthy longevity and in artificial intelligence-based clinical applications. Mechanisms of Ageing and Development, 185, [111194]. https://doi.org/10.1016/j.mad.2019.111194

Vancouver

Aman Y, Frank J, Lautrup SH, Matysek A, Niu Z, Yang G et al. The NAD+-mitophagy axis in healthy longevity and in artificial intelligence-based clinical applications. Mechanisms of Ageing and Development. 2020;185. 111194. https://doi.org/10.1016/j.mad.2019.111194

Author

Aman, Yahyah ; Frank, Johannes ; Lautrup, Sofie Hindkjær ; Matysek, Adrian ; Niu, Zhangming ; Yang, Guang ; Shi, Liu ; Bergersen, Linda H. ; Storm-Mathisen, Jon ; Rasmussen, Lene J. ; Bohr, Vilhelm A. ; Nilsen, Hilde ; Fang, Evandro F. / The NAD+-mitophagy axis in healthy longevity and in artificial intelligence-based clinical applications. In: Mechanisms of Ageing and Development. 2020 ; Vol. 185.

Bibtex

@article{8874389896e04613bc5f3fca60ac436e,
title = "The NAD+-mitophagy axis in healthy longevity and in artificial intelligence-based clinical applications",
abstract = "Nicotinamide adenine dinucleotide (NAD+) is an important natural molecule involved in fundamental biological processes, including the TCA cycle, OXPHOS, β-oxidation, and is a co-factor for proteins promoting healthy longevity. NAD+ depletion is associated with the hallmarks of ageing and may contribute to a wide range of age-related diseases including metabolic disorders, cancer, and neurodegenerative diseases. One of the central pathways by which NAD+ promotes healthy ageing is through regulation of mitochondrial homeostasis via mitochondrial biogenesis and the clearance of damaged mitochondria via mitophagy. Here, we highlight the contribution of the NAD+-mitophagy axis to ageing and age-related diseases, and evaluate how boosting NAD+ levels may emerge as a promising therapeutic strategy to counter ageing as well as neurodegenerative diseases including Alzheimer's disease. The potential use of artificial intelligence to understand the roles and molecular mechanisms of the NAD+-mitophagy axis in ageing is discussed, including possible applications in drug target identification and validation, compound screening and lead compound discovery, biomarker development, as well as efficacy and safety assessment. Advances in our understanding of the molecular and cellular roles of NAD+ in mitophagy will lead to novel approaches for facilitating healthy mitochondrial homoeostasis that may serve as a promising therapeutic strategy to counter ageing-associated pathologies and/or accelerated ageing.",
keywords = "Age-related diseases, Ageing, Alzheimer's disease, Artificial intelligence, Mitophagy, NAD",
author = "Yahyah Aman and Johannes Frank and Lautrup, {Sofie Hindkj{\ae}r} and Adrian Matysek and Zhangming Niu and Guang Yang and Liu Shi and Bergersen, {Linda H.} and Jon Storm-Mathisen and Rasmussen, {Lene J.} and Bohr, {Vilhelm A.} and Hilde Nilsen and Fang, {Evandro F.}",
year = "2020",
doi = "10.1016/j.mad.2019.111194",
language = "English",
volume = "185",
journal = "Mechanisms of Ageing and Development",
issn = "0047-6374",
publisher = "Elsevier Ireland Ltd",

}

RIS

TY - JOUR

T1 - The NAD+-mitophagy axis in healthy longevity and in artificial intelligence-based clinical applications

AU - Aman, Yahyah

AU - Frank, Johannes

AU - Lautrup, Sofie Hindkjær

AU - Matysek, Adrian

AU - Niu, Zhangming

AU - Yang, Guang

AU - Shi, Liu

AU - Bergersen, Linda H.

AU - Storm-Mathisen, Jon

AU - Rasmussen, Lene J.

AU - Bohr, Vilhelm A.

AU - Nilsen, Hilde

AU - Fang, Evandro F.

PY - 2020

Y1 - 2020

N2 - Nicotinamide adenine dinucleotide (NAD+) is an important natural molecule involved in fundamental biological processes, including the TCA cycle, OXPHOS, β-oxidation, and is a co-factor for proteins promoting healthy longevity. NAD+ depletion is associated with the hallmarks of ageing and may contribute to a wide range of age-related diseases including metabolic disorders, cancer, and neurodegenerative diseases. One of the central pathways by which NAD+ promotes healthy ageing is through regulation of mitochondrial homeostasis via mitochondrial biogenesis and the clearance of damaged mitochondria via mitophagy. Here, we highlight the contribution of the NAD+-mitophagy axis to ageing and age-related diseases, and evaluate how boosting NAD+ levels may emerge as a promising therapeutic strategy to counter ageing as well as neurodegenerative diseases including Alzheimer's disease. The potential use of artificial intelligence to understand the roles and molecular mechanisms of the NAD+-mitophagy axis in ageing is discussed, including possible applications in drug target identification and validation, compound screening and lead compound discovery, biomarker development, as well as efficacy and safety assessment. Advances in our understanding of the molecular and cellular roles of NAD+ in mitophagy will lead to novel approaches for facilitating healthy mitochondrial homoeostasis that may serve as a promising therapeutic strategy to counter ageing-associated pathologies and/or accelerated ageing.

AB - Nicotinamide adenine dinucleotide (NAD+) is an important natural molecule involved in fundamental biological processes, including the TCA cycle, OXPHOS, β-oxidation, and is a co-factor for proteins promoting healthy longevity. NAD+ depletion is associated with the hallmarks of ageing and may contribute to a wide range of age-related diseases including metabolic disorders, cancer, and neurodegenerative diseases. One of the central pathways by which NAD+ promotes healthy ageing is through regulation of mitochondrial homeostasis via mitochondrial biogenesis and the clearance of damaged mitochondria via mitophagy. Here, we highlight the contribution of the NAD+-mitophagy axis to ageing and age-related diseases, and evaluate how boosting NAD+ levels may emerge as a promising therapeutic strategy to counter ageing as well as neurodegenerative diseases including Alzheimer's disease. The potential use of artificial intelligence to understand the roles and molecular mechanisms of the NAD+-mitophagy axis in ageing is discussed, including possible applications in drug target identification and validation, compound screening and lead compound discovery, biomarker development, as well as efficacy and safety assessment. Advances in our understanding of the molecular and cellular roles of NAD+ in mitophagy will lead to novel approaches for facilitating healthy mitochondrial homoeostasis that may serve as a promising therapeutic strategy to counter ageing-associated pathologies and/or accelerated ageing.

KW - Age-related diseases

KW - Ageing

KW - Alzheimer's disease

KW - Artificial intelligence

KW - Mitophagy

KW - NAD

U2 - 10.1016/j.mad.2019.111194

DO - 10.1016/j.mad.2019.111194

M3 - Journal article

C2 - 31812486

AN - SCOPUS:85076247604

VL - 185

JO - Mechanisms of Ageing and Development

JF - Mechanisms of Ageing and Development

SN - 0047-6374

M1 - 111194

ER -

ID: 234637988