Oxidative metabolism deficiencies in brains of patients with Alzheimer's disease
Abstract
Glucose metabolism in the brain has an important influence on many normal cellular processes. It contributes to the synthesis of acetylcholine, glutamate, aspartate, gamma-aminobutyric acid, glycine, and ATP production (the driving force behind almost all cellular and molecular activity). Neuronal glucose metabolism is controlled antagonistically by insulin and cortisol. Desensitization of the neuronal insulin receptor causes abnormalities in oxidative energy metabolism. During normal aging, the cerebral energy pool is slightly diminished, but its level increases after stressful events. In age-related sporadic late-onset dementia of the Alzheimer type (SDAT), glucose metabolism and formation of cellular energy are severely reduced. Desensitization of the neuronal insulin receptor seems to be an early event in the pathogenesis or even etiology of SDAT causing disturbances in oxidative glucose metabolism and energy failure in insulin-sensitive brain structures. These abnormalities appear to induce a cascade of disturbances that leads to abnormal APP processing and amyloid formation, membrane damage, and neuronal death.
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Alterations in glucose metabolism and mitochondrial energetics occur along with accumulation of oxidative damage before the cardinal signs of Alzheimer's disease pathogenesis in the brains of transgenic animal models and patients.
“Extensive evidence indicates that alterations in glucose metabolism and mitochondrial energetics occur along with the accumulation of oxidative damage before the cardinal signs of AD pathogenesis in the brains of transgenic animal models and patients (Hoyer, 1996; Hirai et al., 2001; Rinaldi et al., 2003; Butterfield et al., 2006; Lin and Beal, 2006; Sultana et al., 2006a,b; Mosconi et al., 2008a;”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Hoyer, 1996
Mitochondrial dysfunction and oxidative stress contribute to the progression of Alzheimer's disease.
“Considerable evidence suggests that mitochondrial dysfunction and oxidative stress contribute to the progression of Alzheimer’s disease (AD).”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Hoyer, 1996
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- Authors
- Hoyer, S.
- Affiliations
- Heidelberg University (DE)
- Corresponding author
- Hoyer, S.
- ORCID
- Hoyer, S.
- Venue
- Acta Neurologica Scandinavica
- Publisher
- Hindawi Limited
- Published
- 1996-04
- Volume
- 94
- Issue
- S165
- Pages
- 18-24
- ISSN
- 0001-6314 (ISSN-L)
- OpenAlex
- W2124687316
- Cited by
- 88
- References
- 5
- Citations by year
- 2026: 1 · 2023: 1 · 2022: 1 · 2021: 2 · 2020: 1 · 2019: 3 · 2018: 3 · 2017: 1 · 2016: 8 · 2015: 2 · 2014: 3 · 2013: 5 · 2012: 1
- FWCI
- 1.54
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Acta Neurologica Scandinavica (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- Alzheimer's disease, oxidative metabolism, brain glucose metabolism, insulin resistance, cortisol, neuronal energy metabolism, late-onset dementia, APP processing, amyloid fibril formation, neuronal cell death, membrane damage, aging
- MeSH terms
- Alzheimer Disease, Brain, Glucose, Humans
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