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REVIEW: Alzheimer’s Disease: An Exacerbation of Senile Phenoptosis

N. K. Isaev1,2*, E. V. Stelmashook2, E. E. Genrikhs2, M. V. Oborina2, M. R. Kapkaeva2, and V. P. Skulachev1

1Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, 119991 Moscow, Russia; E-mail: isaev@genebee.msu.ru

2Research Center of Neurology, 125367 Moscow, Russia; E-mail: estelmash@mail.ru

* To whom correspondence should be addressed.

Received June 30, 2015; Revision received August 28, 2015
Alzheimer’s disease is characterized by progressive memory loss and cognitive decline accompanied by degeneration of neuronal synapses, massive loss of neurons in the brain, eventually resulting in complete degradation of personality and death. Currently, the cause of the disease is not fully understood, but it is believed that the person’s age is the major risk factor for development of Alzheimer’s disease. People who have survived after cerebral stroke or traumatic brain injury have substantially increased risk of developing Alzheimer’s disease. Social exclusion, low social activity, physical inactivity, poor mental performance, and low level of education are among risk factors for development of this neurodegenerative disease, which is consistent with the concept of phenoptosis (Skulachev, V. P., et al. (1999) Biochemistry (Moscow), 64, 1418-1426; Skulachev, M. V., and Skulachev, V. P. (2014) Biochemistry (Moscow), 79, 977-993) stating that rate of aging is related to psychological and social aspects in human behavior. Here we assumed that Alzheimer’s disease might be considered as an exacerbation of senile phenoptosis. If so, then development of this disease could be slowed using mitochondria-targeted antioxidants due to the accumulated data demonstrating a link between mitochondrial dysfunction and oxidative stress both with normal aging and Alzheimer’s disease.
KEY WORDS: phenoptosis, Alzheimer’s disease, aging, brain, mitochondria-targeted antioxidants, SkQ

DOI: 10.1134/S0006297915120056