Abstract
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.
Keywords
Oxidative stressDementiaGlycolysisOxidative phosphorylationDiseaseCitric acid cycleNeurodegenerationNeuroscienceAlzheimer's diseaseCarbohydrate metabolismPathogenesisBiologyBrain damageMedicineMetabolismBiochemistryInternal medicine
MeSH Terms
Alzheimer DiseaseAnimalsBrainDisease ProgressionGlucose IntoleranceGlycolysisHumansOxidative Stress
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Publication Info
- Year
- 2019
- Type
- review
- Volume
- 20
- Issue
- 3
- Pages
- 148-160
- Citations
- 1685
- Access
- Closed
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Cite This
D. Allan Butterfield,
Barry Halliwell
(2019).
Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease.
Nature reviews. Neuroscience
, 20
(3)
, 148-160.
https://doi.org/10.1038/s41583-019-0132-6
Identifiers
- DOI
- 10.1038/s41583-019-0132-6
- PMID
- 30737462
- PMCID
- PMC9382875