Copper in glucose intolerance, cognitive decline, and Alzheimer disease

Rosanna Squitti, Armando Mendez, Camillo Ricordi, Mariacristina Siotto, Ron Goldberg

Research output: Contribution to journalReview article

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)
Pages (from-to)77-85
Number of pages9
JournalAlzheimer disease and associated disorders
Volume33
Issue number1
DOIs
StatePublished - Jan 1 2019

Keywords

  • Alzheimer disease
  • Cardiovascular risk
  • Ceruloplasmin
  • Copper
  • Diabetes type 2

ASJC Scopus subject areas

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

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