The DOI matches its Crossref record; 103 of the 103 references it cites were found in a registry or an index.
Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases
Abstract
Many lines of evidence suggest that mitochondria have a central role in ageing-related neurodegenerative diseases. Mitochondria are critical regulators of cell death, a key feature of neurodegeneration. Mutations in mitochondrial DNA and oxidative stress both contribute to ageing, which is the greatest risk factor for neurodegenerative diseases. In all major examples of these diseases there is strong evidence that mitochondrial dysfunction occurs early and acts causally in disease pathogenesis. Moreover, an impressive number of disease-specific proteins interact with mitochondria. Thus, therapies targeting basic mitochondrial processes, such as energy metabolism or free-radical generation, or specific interactions of disease-related proteins with mitochondria, hold great promise.
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In the citing paper
“Evidence also suggests that not only does Aβ increase cellular RS but that these RS may in turn increase production of Aβ in a destructive autocatalytic cycle (Misonou et al., 2000; Tamagno et al., 2002, 2005; Lin and Beal, 2006; Quiroz-Baez et al., 2009).”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Lin and Beal, 2006
In the citing paper
“Aβ appears to enhance production of cellular RS, and these RS in turn may to contribute to Aβ toxicity.”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Lin and Beal, 2006
In the citing paper
“On the basis of evidence from post-mortem brain tissues from AD patients as well as different AD mouse models, damaged mitochondria and increased oxidative stress are common features of AD (Lin and Beal, 2006; Mattson et al., 2008).”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Lin and Beal, 2006
In the citing paper
“Due to the content of multiple electron carriers and an extensive antioxidant defence, they represent a key centre for ROS/antioxidant balance regulation [56].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [56]
In the citing paper
“and the AD brain displays insulin resistance and impaired mitochondrial function (45,46)”
From Altered mitochondrial function in insulin-deficient and insulin-resistant states (2018) · cites this paper as [46]
In the citing paper
“a range of distinct aetologies, which manifest as a variety of different syndromes or diseases, converge at some point on an autocatalytic series of reactions, involving imperfectly liganded iron, in the production of the very damaging hydroxyl radical, that by causing the destruction of appropriate cellular structures and proteins liberates further ‘free’ iron and other reactive oxygen species,”
In the citing paper
“Aging-associated expression changes in genes associated with mitochondrial function, protein metabolism, and immune response have been identified in several tissues (173) and are consistent with some proposed mechanisms for late-onset neurodegenerative diseases (98, 113, 124, 166).”
From Unraveling a Multifactorial Late-Onset Disease: From Genetic Susceptibility to Disease Mechanisms for Age-Related Macular Degeneration (2009) · cites this paper as [98]
In the citing paper
“Mitochondrial dysfunction and oxidative stress, including mitochondrial DNA damage, have been implicated in all three diseases—AD, PD, and AMD (12, 17, 98, 165).”
From Unraveling a Multifactorial Late-Onset Disease: From Genetic Susceptibility to Disease Mechanisms for Age-Related Macular Degeneration (2009) · cites this paper as [98]
In the citing paper
“Numerous studies have demonstrated a central role of mitochondria and energy homeostasis in the pathogenesis of aging-associated neurodegenerative diseases (98, 157, 166).”
From Unraveling a Multifactorial Late-Onset Disease: From Genetic Susceptibility to Disease Mechanisms for Age-Related Macular Degeneration (2009) · cites this paper as [98]
In the citing paper
“Much evidence suggests a role for mitochondrial dysfunction in the pathophysiology of PD, a common age-associated neurodegenerative disease characterized by progressive degeneration of the nigrostriatal dopamine (DA) pathway and presence of the intraneuronal protein inclusions (Lewy bodies)1-3.”
From Mitochondrial Approaches for Neuroprotection (2008) · cites this paper as [2]
In the citing paper
“Several different pathogenic mechanisms have been identified in the CNS and peripheral tissues during the disease course in ALS, but mitochondrial and bioenergetic defects are implicated widely in ALS pathogenesis2.”
From Mitochondrial Approaches for Neuroprotection (2008) · cites this paper as [2]
In the citing paper
“These studies provide compelling evidence for a role of PGC-1α in the pathogenesis of neurodegenerative diseases, and thus it is a promising therapeutic target for neurodegenerative disorders2, 72.”
From Mitochondrial Approaches for Neuroprotection (2008) · cites this paper as [2]
In the citing paper
“Second, high cellular ROS levels are associated with cancer, diabetes, inflammatory diseases, ischemia-related diseases, and neurodegeneration, and are thus commonly thought to contribute to human pathologies and aging 80–83.”
From Mitochondrial reactive oxygen species regulate cellular signaling and dictate biological outcomes (2010) · cites this paper as [81]
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Metadata
- Authors
- Lin, M. T., & Beal, M. F.
- Affiliations
- Cornell University (US)
- Corresponding author
- Beal, M. Flint
- ORCID
- Beal, M. Flint
- Venue
- Nature
- Published
- 2006-10
- Volume
- 443
- Issue
- 7113
- Pages
- 787-795
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2152165298
- Cited by
- 6,455
- References
- 103
- Citations by year
- 2026: 266 · 2025: 386 · 2024: 393 · 2023: 362 · 2022: 408 · 2021: 454 · 2020: 412 · 2019: 366 · 2018: 450 · 2017: 373 · 2016: 356 · 2015: 326 · 2014: 290 · 2013: 296 · 2012: 293
- FWCI
- 13.10
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- American Federation for Aging Research
- National Institutes of Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial dysfunction, oxidative stress, neurodegenerative diseases, aging, mitochondrial DNA mutations, cell death, energy metabolism, free radicals, pathogenesis, mitochondrial-targeted therapy
- MeSH terms
- Aging, Animals, Humans, Mitochondria, Apoptosis, Oxidative Stress, Neurodegenerative Diseases
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