Copper in Glucose Intolerance, Cognitive Decline, and Alzheimer's Disease

Rosanna Squitti, Armando J Mendez, Camillo Ricordi, Mariacristina Siotto, Ronald B Goldberg

Research output: Contribution to journalArticle

Abstract

Trace metal dyshomeostasis has been linked to loss of cognitive performance. In particular, a disturbance in the regulation of copper (Cu), characterized by an increase in circulating Cu not bound to ceruloplasmin (non-Cp Cu), is thought to play a role in the development of Alzheimer disease (AD) and other neurodegenerative diseases in the aging population. Non-Cp Cu is redox active and its toxicity is thought to result from its ability to accelerate oxidative stress and advanced glycation endproduct (AGE) formation, leading to extracellular matrix damage in tissues including the brain. Cognitive loss is increasingly recognized to be a feature of type 2 diabetes and the increased AGE formation characteristic of diabetes may play a role in the development of this complication. There also is evidence for copper dyshomeostasis in type 2 diabetes, and therefore this could contribute to the cognitive deterioration associated with this disease. Demonstrating that disturbances of copper homeostasis correlate with an increased rate of cognitive decline in type 2 diabetes patients, and that they correlate with an increased rate of conversion from prediabetes to diabetes would bring almost immediate benefits in the clinical community in terms of treatment efficacy, AD prevention, and cost savings.

Original languageEnglish (US)
JournalAlzheimer Disease and Associated Disorders
DOIs
StateAccepted/In press - Jan 1 2018
Externally publishedYes

Fingerprint

Glucose Intolerance
Type 2 Diabetes Mellitus
Copper
Alzheimer Disease
Prediabetic State
Cost of Illness
Ceruloplasmin
Aptitude
Cost Savings
Neurodegenerative Diseases
Oxidation-Reduction
Extracellular Matrix
Oxidative Stress
Homeostasis
Metals
Brain
Population
Cognitive Dysfunction

Keywords

  • Alzheimer disease
  • cardiovascular risk
  • ceruloplasmin
  • copper
  • diabetes type 2

ASJC Scopus subject areas

  • Clinical Psychology
  • Gerontology
  • Geriatrics and Gerontology
  • Psychiatry and Mental health

Cite this

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title = "Copper in Glucose Intolerance, Cognitive Decline, and Alzheimer's Disease",
abstract = "Trace metal dyshomeostasis has been linked to loss of cognitive performance. In particular, a disturbance in the regulation of copper (Cu), characterized by an increase in circulating Cu not bound to ceruloplasmin (non-Cp Cu), is thought to play a role in the development of Alzheimer disease (AD) and other neurodegenerative diseases in the aging population. Non-Cp Cu is redox active and its toxicity is thought to result from its ability to accelerate oxidative stress and advanced glycation endproduct (AGE) formation, leading to extracellular matrix damage in tissues including the brain. Cognitive loss is increasingly recognized to be a feature of type 2 diabetes and the increased AGE formation characteristic of diabetes may play a role in the development of this complication. There also is evidence for copper dyshomeostasis in type 2 diabetes, and therefore this could contribute to the cognitive deterioration associated with this disease. Demonstrating that disturbances of copper homeostasis correlate with an increased rate of cognitive decline in type 2 diabetes patients, and that they correlate with an increased rate of conversion from prediabetes to diabetes would bring almost immediate benefits in the clinical community in terms of treatment efficacy, AD prevention, and cost savings.",
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