Version 1
: Received: 16 September 2024 / Approved: 17 September 2024 / Online: 17 September 2024 (08:43:37 CEST)
How to cite:
Sabalic, A.; Mei, V.; Solinas, G.; Madeddu, R. The Role of Copper in Alzheimer’s Disease Etiopathogenesis: An Updated Systematic Review. Preprints2024, 2024091280. https://doi.org/10.20944/preprints202409.1280.v1
Sabalic, A.; Mei, V.; Solinas, G.; Madeddu, R. The Role of Copper in Alzheimer’s Disease Etiopathogenesis: An Updated Systematic Review. Preprints 2024, 2024091280. https://doi.org/10.20944/preprints202409.1280.v1
Sabalic, A.; Mei, V.; Solinas, G.; Madeddu, R. The Role of Copper in Alzheimer’s Disease Etiopathogenesis: An Updated Systematic Review. Preprints2024, 2024091280. https://doi.org/10.20944/preprints202409.1280.v1
APA Style
Sabalic, A., Mei, V., Solinas, G., & Madeddu, R. (2024). The Role of Copper in Alzheimer’s Disease Etiopathogenesis: An Updated Systematic Review. Preprints. https://doi.org/10.20944/preprints202409.1280.v1
Chicago/Turabian Style
Sabalic, A., Giuliana Solinas and Roberto Madeddu. 2024 "The Role of Copper in Alzheimer’s Disease Etiopathogenesis: An Updated Systematic Review" Preprints. https://doi.org/10.20944/preprints202409.1280.v1
Abstract
Background: Alzheimer's disease (AD) is the most common cause of dementia and cognitive decline in the elderly. Although the etiology of AD is unknow, the increase of amyloid precursor protein (APP) leads to the toxic aggregation of Aβ plaques. Several factors such as hypertension, diabetes, dyslipidemia, smoking, hormonal changes, and metal exposure could increase the risk of developing AD.
In this review, we will examine the role of copper (Cu) in the pathophysiology of AD, as well as the mechanisms involved in neurotoxicity and cognitive decline.
Methods: This review was conducted in accordance with PRISMA guidelines. We performed a comprehensive literature analysis of the last ten years on AD and Cu. Only late-onset Alzheimer’s disease was considered; therefore, only studies on elderly people of both sexes were included.
Results: A total of seven articles were picked for this review, three studies focused on non-ceruloplasmin bound Copper (non-Cp-Cu) and four on ceruloplasmin bound Copper (Cp-Cu). The results showed higher Cu concentrations in patients compared to healthy controls.
Conclusion: Elevated concentrations of Cu may contribute to the progression of AD, potentially interacting with ATP7B mutations, oxidative stress, and amyloid-β plaques. Future research is needed to provide more robust evidence and better characterize the relationships between AD and Cu.
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
