Accumulation of nuclear and mitochondrial DNA damage in the frontal cortex cells of patients with HIV-associated neurocognitive disorders

@article{Zhang2012AccumulationON,
  title={Accumulation of nuclear and mitochondrial DNA damage in the frontal cortex cells of patients with HIV-associated neurocognitive disorders},
  author={Yulin Zhang and Meixia Wang and Hongjun Li and Hong-hai Zhang and Ying Shi and Feili Wei and Dao-jie Liu and Kai Liu and Dexi Chen},
  journal={Brain Research},
  year={2012},
  volume={1458},
  pages={1-11}
}
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References

SHOWING 1-10 OF 53 REFERENCES
Molecular mechanisms of HIV-1 associated neurodegeneration
  • H. Ozdener
  • Biology, Medicine
    Journal of Biosciences
  • 2007
TLDR
Mounting data obtained byin vivo and in vitro experiments suggest that neuronal apoptosis is a major feature of HIV associated dementia (HAD), which can occur in the absence of direct infection of neurons.
Impaired base excision repair and accumulation of oxidative base lesions in CD4+ T cells of HIV-infected patients.
TLDR
The results showed that the HIV-infected patients, particularly those with advanced disease, had increased levels of 8-oxoG in CD4(+) T cells and marked declines in DNA glycosylase activity for the repair of oxidative base lesions in these cells.
Mitochondrial oxidative stress in human hepatoma cells exposed to stavudine.
HIV-1 Vpr Causes Neuronal Apoptosis and In Vivo Neurodegeneration
TLDR
HIV-1 Vpr caused neuronal death through convergent pathogenic mechanisms with ensuing in vivo neurodegeneration, yielding new insights into the mechanisms by which HIV-1 injures the nervous system.
Mitochondrial DNA base excision repair and mitochondrial DNA mutation in human hepatic HuH-7 cells exposed to stavudine.
Genetic and metabolic control of the mitochondrial transmembrane potential and reactive oxygen intermediate production in HIV disease.
TLDR
The genetic and metabolic bases of HIV-induced oxidative stress are delineated, which should lead to development of effective antioxidant therapies in HIV disease.
Evidence of apoptotic cell death in HIV encephalitis.
TLDR
It is demonstrated that at least some neuronal and astrocytic death in HIV infection occurs by apoptosis, and it is hypothesize that apoptotic death of reactiveAstrocytes may be a normal mechanism whereby the brain removes an excess number of astroCytes that have proliferated after certain types of brain injury.
Age related mitochondrial degenerative disorders in humans
TLDR
The potential role of mitochondria and mitochondrial DNA mutations in mitochondrial and neurodegenerative diseases, in particular in PD and in AD, are discussed.
Mechanisms of neuronal injury and death in HIV-1 associated dementia.
TLDR
Recently identified injurious mechanisms potentially contributing to neuronal death in association with HIV-1 disease are reviewed, recent and prospective approaches for therapy and prevention of HAD are discussed and improvements in the control of viral infection in the periphery are discussed.
HIV-1 Tat Activates Neuronal Ryanodine Receptors with Rapid Induction of the Unfolded Protein Response and Mitochondrial Hyperpolarization
TLDR
Data suggest that abnormal RyR signaling mediates the neuronal UPR with failure of mitochondrial energy metabolism, and is a critical locus for the neuropathogenesis of HIV-1 in the CNS.
...
...