Molecular markers associated with cognitive impairment in centenarians

Tinna Stevnsner, Ines Sanchez-Roman*

*Corresponding author af dette arbejde

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisLederpeer review

Abstract

Aging is strongly associated with cognitive decline and degenerative diseases. Therefore, unravelling the basic mechanisms of aging is essential to improve the quality of life of older people. Among others, mitochondrial dysfunction and genomic instability have been con-sidered key hallmarks of aging, and these deficiencies seem to play important roles in age associated cognitive decline [1]. Mitochondrial bioenergetic deterioration together with reactive oxygen species (ROS) induced mitochondrial DNA damage have been shown to accumulate with aging [2]. DNA repair pathways, which are involved in maintaining genomic stability, also seem to change with aging. Most oxidative DNA lesions are repaired by the Base Excision Repair (BER) pathway, in which the major endonuclease at the limiting step is AP endonuclease 1 (APE1), which has also been linked to cognitive decline [3]. Mitochondrial function and DNA repair activity are affected by nicotinamide adenine dinucleotide (NAD) depletion, which is also observed with aging. NAD is an essential co-enzyme involved in mitochondrial health and functions as a cofactor for the DNA repair protein poly (ADP-ribose) polymerase 1 (PARP-1) [4]. Another factor that has been shown to decline with aging and be reduced in neurodegenerative diseases is brain derived neurotrophic factor (BDNF). Importantly, BDNF has been shown to enhance neuronal DNA repair by stimulating APE1 expression and activity [5].

OriginalsprogEngelsk
TidsskriftAging
Vol/bind14
Nummer10
Sider (fra-til)4191-4192
Antal sider2
ISSN1945-4589
DOI
StatusUdgivet - maj 2022

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