Elevated risk of type 2 diabetes for development of Alzheimer disease: A key role for oxidative stress in brain

Butterfield, D. Allan; Di Domenico, Fabio; Barone, Eugenio

doi:10.1016/j.bbadis.2014.06.010

Cited by 402Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchAdvanced Glycation End Products research

Elevated risk of type 2 diabetes for development of Alzheimer disease: A key role for oxidative stress in brain

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Butterfield, D. Allan, Di Domenico, Fabio, Barone, Eugenio·2014·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

DOI 10.1016/j.bbadis.2014.06.010PMC PMC4125611

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Abstract

Alzheimer disease (AD) is the most common form of dementia among the elderly and is characterized by progressive loss of memory and cognition. Epidemiological data show that the incidence of AD increases with age and doubles every 5 years after 65 years of age. From a neuropathological point of view, amyloid-β-peptide (Aβ) leads to senile plaques, which, together with hyperphosphorylated tau-based neurofibrillary tangles and synapse loss, are the principal pathological hallmarks of AD. Aβ is associated with the formation of reactive oxygen (ROS) and nitrogen (RNS) species, and induces calcium-dependent excitotoxicity, impairment of cellular respiration, and alteration of synaptic functions associated with learning and memory. Oxidative stress was found to be associated with type 2 diabetes mellitus (T2DM), which (i) represents another prevalent disease associated with obesity and often aging, and (ii) is considered to be a risk factor for AD development. T2DM is characterized by high blood glucose levels resulting from increased hepatic glucose production, impaired insulin production and peripheral insulin resistance, which close resemble to the brain insulin resistance observed in AD patients. Furthermore, growing evidence suggests that oxidative stress plays a pivotal role in the development of insulin resistance and vice versa. This review article provides molecular aspects and the pharmacological approaches from both preclinical and clinical data interpreted from the point of view of oxidative stress with the aim of highlighting progresses in this field.

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Glucose metabolism is markedly reduced in Alzheimer disease and amnestic mild cognitive impairment.
“in AD and amnestic mild cognitive impairment (aMCI) glucose metabolism is dramatically decreased”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [9]
Section 3.1.1 (page unavailable) reports PET evidence of reduced cerebral glucose metabolism in Alzheimer disease. It also reports oxidation of metabolic enzymes in amnestic MCI, but does not establish that glucose metabolism is dramatically decreased in that group. (LLM, conf=0.83)
Experimental — accuracy not yet measured
Glucose metabolism is significantly impaired in Alzheimer disease and amnestic mild cognitive impairment brains.
“Yet glucose metabolism in AD and aMCI brains is significantly impaired5–7,9,38.”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [9]
Section 3.1.1 (page not available) states that brain glucose utilization is impaired in Alzheimer disease and reports a reduced cerebral glucose metabolic rate in AD. It also reports oxidation of glucose-metabolism proteins in amnestic MCI, but does not establish that glucose metabolism itself is significantly impaired in those brains. (LLM, conf=0.82)
Experimental — accuracy not yet measured
Oxidative or nitrosative damage to multiple proteins, including synaptic proteins, very likely contributes to memory problems and other cognitive deficits, reduced neuronal ATP availability, and decreased clearance of abnormal proteins in Alzheimer disease.
“In summary, oxidative and/or nitrosative damage to multiple proteins, including synaptic proteins is very likely to contribute to the memory problems and other cognitive deficits, reduced ATP availability in neurons, and decreased clearance of abnormal proteins34, creating a “perfect storm” (or sTORm perhaps!) of detrimental cognitive effects in AD9,34,35,41,42.”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [9]
Section 3.1.1, Protein oxidation (page unavailable), links oxidation of metabolic proteins to reduced ATP production, synaptic dysfunction, and cognitive decline. Section 3 also describes oxidative and nitrosative protein damage. The copy does not establish that the damaged proteins include synaptic proteins or that this damage decreases clearance of abnormal proteins. (LLM, conf=0.85)
Experimental — accuracy not yet measured
Oxidative damage is a central component of Alzheimer disease pathogenesis.
“but oxidative damage is a key component.”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [9]
In preclinical Alzheimer disease and Alzheimer disease brains, oxidative damage to many molecules is elevated.
“In the brains of subjects with PCAD and AD, levels of oxidative damage to a wide range of molecules are increased8–19.”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [9]

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Authors: Butterfield, D. A., Di Domenico, F., & Barone, E.
Affiliations: University of Kentucky (US)
Sapienza University of Rome (IT)
Corresponding author: Butterfield, D. Allan
ORCID: Butterfield, D. Allan
Barone, Eugenio
Venue: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
Publisher: Elsevier BV
Published: 2014-09
Volume: 1842
Issue: 9
Pages: 1693-1706
ISSN: 0925-4439 (ISSN-L)
DOI: 10.1016/j.bbadis.2014.06.010
PMC: PMC4125611
OpenAlex: W1994844104
Cited by: 402
References: 227
Citations by year: 2026: 16 · 2025: 36 · 2024: 37 · 2023: 32 · 2022: 22 · 2021: 37 · 2020: 44 · 2019: 40 · 2018: 39 · 2017: 28 · 2016: 25 · 2015: 41 · 2014: 5
FWCI: 3.87
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 365 d)
doi.org/10.15223/policy-017 (stm-asf)
doi.org/10.15223/policy-037 (stm-asf)
doi.org/10.15223/policy-012 (stm-asf)
doi.org/10.15223/policy-029 (stm-asf)
doi.org/10.15223/policy-004 (stm-asf)
Locations: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
Funders: Research Executive Agency (624341)
National Institutes of Health (AG-05119)
Seventh Framework Programme
FP7 People: Marie-Curie Actions
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 › Clinical Biochemistry › Advanced Glycation End Products research
Keywords: Alzheimer's disease, type 2 diabetes, oxidative stress, brain insulin resistance, amyloid-beta, reactive oxygen species, reactive nitrogen species, excitotoxicity, insulin resistance, neurofibrillary tangles, amyloid plaques, pharmacological approaches
MeSH terms: Alzheimer Disease, Brain, Diabetes Mellitus, Type 2, Humans, Risk Factors, Oxidative Stress, Diabetes Complications

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Elevated risk of type 2 diabetes for development of Alzheimer disease: A key role for oxidative stress in brain

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