The current molecular understanding of Alzheimer’s disease (AD) has still not resulted
in successful interventions. Mitochondrial dysfunction of the AD brain is currently
emerging as a hallmark of this disease. One mitochondrial function often affected in AD is
oxidative phosphorylation responsible for ATP production, but also for production of reactive
oxygen species (ROS) and for the de novo synthesis of pyrimidines. This paper reviews the
role of mitochondrial produced ROS and pyrimidines in the aetiology of AD and their proposed
role in oxidative degeneration of macromolecules, synthesis of essential phospholipids
and maintenance of mitochondrial viability in the AD brain.
Keywords: Mitochondria, DNA repair, dNTP pools, Nucleotide metabolism, Brain.
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