Mitochondrial DNA deletions are abundant and cause functional impairment in aged human substantia nigra neurons

By Yevgenya Kraytsberg, E. Kudryavtseva, Ann C. McKee, C. Geula, N. Kowall, K. Khrapko. Nature Genetics, 2006

890 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Clinical Biochemistry, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/9622f4fa6a45155597471306c4c527edd9764334

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. D. C. Chan
2. M. Mouradian
3. V. Dias
4. E. Junn
5. M. Beal
6. Christian Haass
7. S. Jin
8. R. Youle

In Clinical Biochemistry

1. D. C. Chan
2. Hsiuchen Chen
3. R. Youle
4. J. Nunnari
5. Xiongwei Zhu
6. Xinglong Wang
7. M. Beal
8. A. Suomalainen

In Molecular Biology

1. D. C. Chan
2. R. Youle
3. Hsiuchen Chen
4. J. Nunnari
5. A. Suomalainen
6. Xiongwei Zhu
7. Xinglong Wang
8. M. Beal

Citations in the corpus

• PINK1- and Parkin-mediated mitophagy at a glance (2012, background): “Complex 1 deficiency (Mizuno et al., 1989; Parker et al., 1989) and deletions in mitochondrial DNA (Bender et al., 2006; Kraytsberg et al., 2006) have also been identified in subtantia nigral neurons of PD patients.”
• Mitochondrial DNA mutations and human disease. (2010, background): “An exponential accumulation of multiple mtDNA deletions has also been reported in aged postmitotic tissues and individuals with neurodegenerative diseases [91 – 93].”
• Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases (2006, positive): “Moreover, somatic deletions can be clonally expanded in individual neurons, and high levels of such deletions correlate with cytochrome oxidase deficiency on a cell-by-cell basis in the substantia nigra, perhaps contributing to the age dependence of P”
• DNA damage and its links to neurodegeneration (2014, neutral): “Similarly, elevated levels of oxidative lesions and SSBs have been reported in the neurons of ALS patients and damage to mitochondrial DNA has been documented in PD (Bender et al., 2006; Kraytsberg et al., 2006; Martin, 2001).”
• Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, positive): “An age-dependent increase in mtDNA deletions has been found in individual DA neurons dissected from the SNc of post mortem human brain (Bender et al , 2006; Kraytsberg et al , 2006).”
• Mitochondrial Dysfunction in Parkinson's Disease (2011, background): “[126] showed high levels of mtDNA deletions in neurons in the SNpc of PD”
• Mitochondrial fusion is required for mtDNA stability in skeletal muscle and tolerance of mtDNA mutations (2010, positive): “…work, it will be important to address whether mitochondrial fusion plays an analogous protective role against age-associated mtDNA deletions, which similarly cause cellular dysfunction only upon clonal expansion to high levels (Bender et al., 2006; Kraytsberg et al., 2006; Wanagat et al., 2001).”
• Mitochondria: In Sickness and in Health (2012, background): “We provide a current view of how mitochondrial functions impinge on health and disease.”