The DOI matches its Crossref record; 225 of the 225 references it cites were found in a registry or an index.
Mitochondrial Dysfunction and Biogenesis in Neurodegenerative diseases: Pathogenesis and Treatment
Open accessAbstract
Summary: Neurodegenerative diseases are a heterogeneous group of disorders that are incurable and characterized by the progressive degeneration of the function and structure of the central nervous system (CNS) for reasons that are not yet understood. Neurodegeneration is the umbrella term for the progressive death of nerve cells and loss of brain tissue. Because of their high energy requirements, neurons are especially vulnerable to injury and death from dysfunctional mitochondria. Widespread damage to mitochondria causes cells to die because they can no longer produce enough energy. Several lines of pathological and physiological evidence reveal that impaired mitochondrial function and dynamics play crucial roles in aging and pathogenesis of neurodegenerative diseases. As mitochondria are the major intracellular organelles that regulate both cell survival and death, they are highly considered as a potential target for pharmacological‐based therapies. The purpose of this review was to present the current status of our knowledge and understanding of the involvement of mitochondrial dysfunction in pathogenesis of neurodegenerative diseases including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS) and the importance of mitochondrial biogenesis as a potential novel therapeutic target for their treatment. Likewise, we highlight a concise overview of the key roles of mitochondrial electron transport chain (ETC.) complexes as well as mitochondrial biogenesis regulators regarding those diseases.
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2 retracted
SIRT1 Protects against α-Synuclein Aggregation by Activating Molecular Chaperones
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RetractedMitochondrial Dysfunction and Oxidative Stress in Neurodegenerative Diseases
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AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activity
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PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin
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NLRP3 is activated in Alzheimer’s disease and contributes to pathology in APP/PS1 mice
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Park, M. W., Cha, H. W., Kim, J., Kim, J. H., Yang, H., Yoon, S., Boonpraman, N., Yi, S. S., Yoo, I. D., & Moon, J.-S. (2021) · Redox Biology · doi:10.1016/j.redox.2021.101947 · Cited by 683
The Peroxisome-Mitochondria Connection: How and Why?
Fransen, M., Lismont, C., & Walton, P. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18061126 · Cited by 351
“Mutations in proteins impairing peroxisome or mitochondrial biogenesis and/or function have been shown to lead to inherited disorders with different, and severe, phenotypic presentations [8,155].”
BackgroundShared molecular and cellular mechanisms of premature ageing and ageing-associated diseases
Kubben, N., & Misteli, T. (2017) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm.2017.68 · Cited by 320
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Metadata
- Authors
- Golpich, M., Amini, E., Mohamed, Z., Azman Ali, R., Mohamed Ibrahim, N., & Ahmadiani, A.
- Venue
- CNS Neuroscience & Therapeutics
- Publisher
- Wiley
- Published
- 2016-11-22
- Volume
- 23
- Issue
- 1
- Pages
- 5-22
- ISSN
- 1755-5930 (ISSN-L)
- 1755-5949
- OpenAlex
- W2555953028
- Cited by
- 532
- References
- 225
- FWCI
- 15.50
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: Mitochondrial Dysfunction and Biogenesis in Neurodegenerative diseases: Pathogenesis and Treatment. https://app.cochat.ai/papers/10.1111/cns.12655
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- Golpich, M., Amini, E., Mohamed, Z., Azman Ali, R., Mohamed Ibrahim, N., & Ahmadiani, A. (2017). Mitochondrial Dysfunction and Biogenesis in Neurodegenerative diseases: Pathogenesis and Treatment. CNS Neuroscience & Therapeutics. https://doi.org/10.1111/cns.12655
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
