Trace Elements in Alzheimer's Disease and Dementia: The Current State of Knowledge

Trace Elements in Alzheimer's Disease and Dementia: The Current State of Knowledge

2024 | Magdalena Tyczyńska, Marta Gędek, Adam Brachet, Wojciech Stręk, Jolanta Flieger, Grzegorz Teresiński, Jacek Baj
This review explores the role of trace elements in Alzheimer's disease (AD) and dementia, focusing on their impact on neurodegenerative processes. Trace elements such as zinc, copper, iron, manganese, and selenium are involved in various neurotoxic mechanisms, including oxidative stress, inflammation, and amyloid aggregation. Low zinc levels suppress neurotoxicity caused by β-amyloid, while high levels of copper, iron, and manganese promote α-synuclein aggregation, leading to synaptic dysfunction. Aluminium disrupts metal homeostasis, increasing reactive oxygen species and causing cellular death. Selenium plays a role in ferroptosis, a form of cell death linked to oxidative stress. Iron accumulation is associated with neurodegeneration, and its levels are correlated with cognitive decline. Copper toxicity is linked to AD and Wilson's disease, while magnesium deficiency contributes to neuroinflammation and cognitive decline. Mercury and arsenic also contribute to neurodegeneration through oxidative stress and mitochondrial dysfunction. The review highlights the complex interactions between trace elements and neurodegenerative diseases, suggesting potential therapeutic strategies targeting these elements. The study emphasizes the importance of understanding trace element dynamics in the pathophysiology of neurodegenerative disorders.This review explores the role of trace elements in Alzheimer's disease (AD) and dementia, focusing on their impact on neurodegenerative processes. Trace elements such as zinc, copper, iron, manganese, and selenium are involved in various neurotoxic mechanisms, including oxidative stress, inflammation, and amyloid aggregation. Low zinc levels suppress neurotoxicity caused by β-amyloid, while high levels of copper, iron, and manganese promote α-synuclein aggregation, leading to synaptic dysfunction. Aluminium disrupts metal homeostasis, increasing reactive oxygen species and causing cellular death. Selenium plays a role in ferroptosis, a form of cell death linked to oxidative stress. Iron accumulation is associated with neurodegeneration, and its levels are correlated with cognitive decline. Copper toxicity is linked to AD and Wilson's disease, while magnesium deficiency contributes to neuroinflammation and cognitive decline. Mercury and arsenic also contribute to neurodegeneration through oxidative stress and mitochondrial dysfunction. The review highlights the complex interactions between trace elements and neurodegenerative diseases, suggesting potential therapeutic strategies targeting these elements. The study emphasizes the importance of understanding trace element dynamics in the pathophysiology of neurodegenerative disorders.
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