Mitochondria-Targeted Antioxidants and Alzheimer’s Disease

Alzheimer’s disease (AD) is a neurodegenerative pathology accompanied by age-related mitochondrial dysfunction which is triggered by β-amyloid (Abeta) and hyperphosphorylated tau protein. Excessive production of mitochondrial reactive oxygen species seems to play a central role in this process. It is known that traumatic brain injury and brain ischemia increase the risk of the incidence of AD. Recently, it has been demonstrated that mitochondria-targeted antioxidants can reduce the toxic effects of Abeta, which is elevated in brains due to traumatic injury and ischemia. The same antioxidant therapy decreased the neurologic deficit caused by these pathologic conditions. It was also shown that mitochondria-targeted antioxidants rescue hippocampal long-term potentiation, a neuronal model of memory that is impaired by Abeta. The geroprotective effect of such antioxidants is accompanied by retardation, termination, and in some cases reversal of the development of many typical traits of aging. We suggest that mitochondria-targeted antioxidants have a high potential for reducing the risk of AD onset and might alleviate the consequences of developed AD.