Cytochrome c oxidase defects of the human substantia nigra in normal aging
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Ultradeep mapping of neuronal mitochondrial deletions in Parkinson's disease
2018, Neurobiology of AgingCitation Excerpt :Somatic mitochondrial DNA (mtDNA) mutations accumulate in postmitotic cell populations with increasing age and, if high enough levels are reached, can cause dysfunction of the respiratory chain (Bua et al., 2006; Itoh et al., 1996; Sciacco et al., 1994).
Species-specific lifespans: Can it be a lottery based on the mode of mitochondrial DNA replication?
2016, Mechanisms of Ageing and DevelopmentMitochondrial DNA mutations in neurodegeneration
2015, Biochimica et Biophysica Acta - BioenergeticsCitation Excerpt :A further analysis by combining data from 10 previous PD studies also showed independent protective effects for haplogroups J, K and T, and an increased risk of disease for super-haplogroup HV (p = 3.63 × 10− 3, OR = 1.112), though the mechanism remains unclear [105]. The observation of a mosaic pattern of respiratory chain deficiency in human PD post-mortem brain tissue [107] further supported the hypothesis that mitochondrial DNA mutations may be implicated in respiratory chain impairment in PD. In 2006 Bender et al. confirmed that PD patients had a greater proportion of COX deficient neurons in the substantia nigra than controls (~ 3% vs 1%, p = 0.003) [3], and although mtDNA deletion levels in both PD and controls was high in SN tissue homogenates (52.3% ± 9.3% vs 43.3% ± 9.3%) this did not reach statistical significance (p = 0.06).
Ageing and Parkinson's disease: Why is advancing age the biggest risk factor?
2014, Ageing Research ReviewsCitation Excerpt :Respiratory deficiency can be defined as a decline in the activity of complex IV which can be visualised in tissue using the COX/SDH assay. Bender et al. report that approximately 3% of SN neurons are COX deficient in patients with PD compared to 1% in age matched controls, while other studies have reported up to 30% COX deficiency in some cases (Bender et al., 2006; Itoh et al., 1996; Kraytsberg et al., 2006). Furthermore, Elson et al. predicted that 1–4% of post mitotic cells in 80–120 year olds would be COX deficient and that this accumulation would begin from the age of 60 (Elson et al., 2001).
Mitochondrial-nuclear epistasis: Implications for human aging and longevity
2011, Ageing Research ReviewsConvergent evidence for abnormal striatal synaptic plasticity in dystonia
2010, Neurobiology of DiseaseCitation Excerpt :DA's influence in dystonia is varied, complex, and sometimes paradoxical. Despite some SNc DA cell loss with normal aging (Cruz-Sanchez et al., 1997; Itoh et al., 1996) and unlike Parkinson's disease, there is historically no evidence for abnormal cellular degeneration of nigral DA cells in dystonia. Nevertheless, reduced striatal DA (Perlmutter et al., 1997b; Tabbal et al., 2006), or more commonly a general DA dysfunction (Augood et al., 2004, 1999; Breakefield et al., 2008; Perlmutter and Mink, 2004), have been suggested as factors in dystonia (see also Wichmann (2008) for a recent review).