Disruption of Mitochondrial-associated ER membranes by HIV-1 tat protein contributes to premature brain aging.
Sterling P ArjonaCharles N S AllenMaryline SanterreScott GrossJonathan SoboloffRosemarie BoozeBassel E SawayaPublished in: CNS neuroscience & therapeutics (2022)
These results suggest that Tat disrupts the MAM, through the induction of PTPIP51 phosphorylation, leading to ROS accumulation, mitochondrial stress, and altered movement. Hence, we concluded that interfering in the MAM-associated cellular pathways contributes to spatial memory impairment and premature brain aging often observed in HIV-1-infected patients.
Keyphrases
- hiv infected patients
- antiretroviral therapy
- hiv infected
- resting state
- oxidative stress
- hiv positive
- human immunodeficiency virus
- white matter
- hiv aids
- functional connectivity
- dna damage
- hepatitis c virus
- cell death
- cerebral ischemia
- working memory
- hiv testing
- multiple sclerosis
- breast cancer cells
- binding protein
- small molecule
- amino acid
- protein protein
- estrogen receptor
- south africa
- endoplasmic reticulum