The DOI matches its Crossref record; 202 of the 202 references it cites were found in a registry or an index.
Brain metabolic dysfunction at the core of Alzheimer's disease
Open accessAbstract
Growing evidence supports the concept that Alzheimer’s disease (AD) is fundamentally a metabolic disease with molecular and biochemical features that correspond with diabetes mellitus and other peripheral insulin resistance disorders. Brain insulin/IGF resistance and its consequences can readily account for most of the structural and functional abnormalities in AD. However, disease pathogenesis is complicated by the fact that AD can occur as a separate disease process, or arise in association with systemic insulin resistance diseases, including diabetes, obesity, and non-alcoholic fatty liver disease. Whether primary or secondary in origin, brain insulin/IGF resistance initiates a cascade of neurodegeneration that is propagated by metabolic dysfunction, increased oxidative and ER stress, neuro-inflammation, impaired cell survival, and dysregulated lipid metabolism. These injurious processes compromise neuronal and glial functions, reduce neurotransmitter homeostasis, and cause toxic oligomeric pTau and (amyloid beta peptide of amyloid beta precursor protein) AβPP-Aβ fibrils and insoluble aggregates (neurofibrillary tangles and plaques) to accumulate in brain. AD progresses due to: (1) activation of a harmful positive feedback loop that progressively worsens the effects of insulin resistance; and (2) the formation of ROS- and RNS-related lipid, protein, and DNA adducts that permanently damage basic cellular and molecular functions. Epidemiologic data suggest that insulin resistance diseases, including AD, are exposure-related in etiology. Furthermore, experimental and lifestyle trend data suggest chronic low-level nitrosamine exposures are responsible. These concepts offer opportunities to discover and implement new treatments and devise preventive measures to conquer the AD and other insulin resistance disease epidemics.
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“In humans, weight loss sufficient to reduce peripheral insulin resistance improves cognitive performance [122, 123] and enhances neuropsychiatric function [124], and reductions in metabolic indices through Mediterranean diet adherence lowers the risk for AD [125].”
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Role of gut microbiota and nutrients in amyloid formation and pathogenesis of Alzheimer disease
Pistollato, F., Sumalla Cano, S., Elio, I., Masias Vergara, M., Giampieri, F., & Battino, M. (2016) · Nutrition Reviews · doi:10.1093/nutrit/nuw023 · Cited by 496
Melatonin and inflammation-Story of a double-edged blade
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Butterfield, D. A., Di Domenico, F., & Barone, E. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2014.06.010 · Cited by 402
Docosahexaenoic Acid and Cognition throughout the Lifespan
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Metadata
- Authors
- de la Monte, S. M., & Tong, M.
- Venue
- Biochemical Pharmacology
- Publisher
- Elsevier BV
- Published
- 2014-04
- Volume
- 88
- Issue
- 4
- Pages
- 548-559
- ISSN
- 0006-2952 (ISSN-L)
- OpenAlex
- W2005441052
- Cited by
- 461
- References
- 202
- FWCI
- 28.57
- Type
- journal article
- Language
- en
- Open access
- green
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