Journal
NATURE REVIEWS NEUROSCIENCE
Volume 20, Issue 3, Pages 148-160Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41583-019-0132-6
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Funding
- US National Institutes of Health [1R01 AG060056-01]
- National Medical Research Council
- Tan Chin Tuan Centennial Foundation, Singapore
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Alzheimer disease (AD) is a major cause of age-related dementia. We do not fully understand AD aetiology and pathogenesis, but oxidative damage is a key component. The brain mostly uses glucose for energy, but in AD and amnestic mild cognitive impairment glucose metabolism is dramatically decreased, probably owing, at least in part, to oxidative damage to enzymes involved in glycolysis, the tricarboxylic acid cycle and ATP biosynthesis. Consequently, ATP-requiring processes for cognitive function are impaired, and synaptic dysfunction and neuronal death result, with ensuing thinning of key brain areas. We summarize current research on the interplay and sequence of these processes and suggest potential pharmacological interventions to retard AD progression.
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