Abstract
Alzheimer’s disease is a progressive neurodegenerative disorder that eventually leads the affected patients to die. The appearance of senile plaques in the brains of Alzheimer’s patients is known as a main symptom of this disease. The plaques consist of different components, and according to numerous reports, their main components include beta-amyloid peptide and transition metals such as copper. In this disease, metal dyshomeostasis leads the number of copper ions to simultaneously increase in the plaques and decrease in neurons. Copper ions are essential for proper brain functioning, and one of the possible mechanisms of neuronal death in Alzheimer’s disease is the copper depletion of neurons. However, the reason for the copper depletion is as yet unknown. Based on the available evidence, we suggest two possible reasons: the first is copper released from neurons (along with beta-amyloid peptides), which is deposited outside the neurons, and the second is the uptake of copper ions by activated microglia.
Highlights
Copper in the gut is mainly absorbed by copper transporter 1 (CTR1) [25], and by divalent metal transporter 1 (DMT1) to a lesser extent [26,27]
Findings on the NLRP3 inflammasome (NACHT, LRR, and PYD domains-containing protein 3) can be considered as additional evidence demonstrating the involvement of copper in the activity of microglia
Inflammasome activation is important in neuroinflammation induced by microglia [119], and it has been indicated that Aβ oligomers can activate NLRP3 inflammasomes in microglia [120,121]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Beyond describing the processes of copper content dysregulation in the bloodstream (recently reviewed in [5]), it remains unclear why the concentration and distribution of copper in the brains of AD patients change, though a number of attempts have been made to interpret this complex phenomenon (reviewed in [9]). Determining how this happens may significantly contribute toward finding appropriate methods for intervening in the progression of the disease and identifying its starting point [23,24]. We compile and discuss the latest results available on one aspect of the complex puzzle of copper imbalance in AD—the brain copper deficiency
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