The role of mitochondrial dysfunction in the progression of Alzheimer’s disease

Research output: Contribution to journal › Review › Research › peer-review

Standard

The role of mitochondrial dysfunction in the progression of Alzheimer’s disease. / Desler, Claus; Lillenes, Meryl S.; Tønjum, Tone; Rasmussen, Lene Juel.

In: Current Medicinal Chemistry, Vol. 25, No. 40, 2018, p. 5578 - 5587.

Research output: Contribution to journal › Review › Research › peer-review

Harvard

Desler, C, Lillenes, MS, Tønjum, T & Rasmussen, LJ 2018, 'The role of mitochondrial dysfunction in the progression of Alzheimer’s disease', Current Medicinal Chemistry, vol. 25, no. 40, pp. 5578 - 5587. https://doi.org/10.2174/0929867324666170616110111

APA

Desler, C., Lillenes, M. S., Tønjum, T., & Rasmussen, L. J. (2018). The role of mitochondrial dysfunction in the progression of Alzheimer’s disease. Current Medicinal Chemistry, 25(40), 5578 - 5587. https://doi.org/10.2174/0929867324666170616110111

Vancouver

Desler C, Lillenes MS, Tønjum T, Rasmussen LJ. The role of mitochondrial dysfunction in the progression of Alzheimer’s disease. Current Medicinal Chemistry. 2018;25(40):5578 - 5587. https://doi.org/10.2174/0929867324666170616110111

Author

Desler, Claus ; Lillenes, Meryl S. ; Tønjum, Tone ; Rasmussen, Lene Juel. / The role of mitochondrial dysfunction in the progression of Alzheimer’s disease. In: Current Medicinal Chemistry. 2018 ; Vol. 25, No. 40. pp. 5578 - 5587.

Bibtex

@article{07e8d69603fb4f99a93fd5899b188a02,
title = "The role of mitochondrial dysfunction in the progression of Alzheimer{\textquoteright}s disease",
abstract = "The current molecular understanding of Alzheimer{\textquoteright}s disease (AD) has still not resulted in successful interventions. Mitochondrial dysfunction of the AD brain is currently emerging as a hallmark of this disease. One mitochondrial function often affected in AD is oxidative phosphorylation responsible for ATP production, but also for production of reactive oxygen species (ROS) and for the de novo synthesis of pyrimidines. This paper reviews the role of mitochondrial produced ROS and pyrimidines in the aetiology of AD and their proposed role in oxidative degeneration of macromolecules, synthesis of essential phospholipids and maintenance of mitochondrial viability in the AD brain.",
author = "Claus Desler and Lillenes, {Meryl S.} and Tone T{\o}njum and Rasmussen, {Lene Juel}",
year = "2018",
doi = "10.2174/0929867324666170616110111",
language = "English",
volume = "25",
pages = "5578 -- 5587",
journal = "Current Medicinal Chemistry",
issn = "0929-8673",
publisher = "Bentham Science Publishers",
number = "40",

}

RIS

TY - JOUR

T1 - The role of mitochondrial dysfunction in the progression of Alzheimer’s disease

AU - Desler, Claus

AU - Lillenes, Meryl S.

AU - Tønjum, Tone

AU - Rasmussen, Lene Juel

PY - 2018

Y1 - 2018

N2 - The current molecular understanding of Alzheimer’s disease (AD) has still not resulted in successful interventions. Mitochondrial dysfunction of the AD brain is currently emerging as a hallmark of this disease. One mitochondrial function often affected in AD is oxidative phosphorylation responsible for ATP production, but also for production of reactive oxygen species (ROS) and for the de novo synthesis of pyrimidines. This paper reviews the role of mitochondrial produced ROS and pyrimidines in the aetiology of AD and their proposed role in oxidative degeneration of macromolecules, synthesis of essential phospholipids and maintenance of mitochondrial viability in the AD brain.

AB - The current molecular understanding of Alzheimer’s disease (AD) has still not resulted in successful interventions. Mitochondrial dysfunction of the AD brain is currently emerging as a hallmark of this disease. One mitochondrial function often affected in AD is oxidative phosphorylation responsible for ATP production, but also for production of reactive oxygen species (ROS) and for the de novo synthesis of pyrimidines. This paper reviews the role of mitochondrial produced ROS and pyrimidines in the aetiology of AD and their proposed role in oxidative degeneration of macromolecules, synthesis of essential phospholipids and maintenance of mitochondrial viability in the AD brain.

U2 - 10.2174/0929867324666170616110111

DO - 10.2174/0929867324666170616110111

M3 - Review

C2 - 28618998

VL - 25

SP - 5578

EP - 5587

JO - Current Medicinal Chemistry

JF - Current Medicinal Chemistry

SN - 0929-8673

IS - 40

ER -

ID: 189863451