Dear Colleagues,

Redox-active metals play an important role in regulating various cellular pathways important for normal brain function, participating in processes such as myelination, synthesis and release of neurotransmitters, protein turnover, synthesis of neurotrophic factors, antioxidant defense and many others. The metabolism of these metals is tightly regulated by homeostatic systems, including transmembrane proteins and metallopochaperones, which regulate their absorption, intracellular localization, or excretion. Abnormalities in metal homeostasis are closely related to the onset and progression of neurodegenerative diseases. The proposal was even formulated of developing Redox Neurology as an independent subgroup of Neurology. Metal ion imbalance can induce oxidative stress, promote neuroinflammation, overproduction of amyloid-β, cause tau hyperphosphorylation, as well as mitochondrial and autophagic dysfunctions, which may initiate or intensify the aggregation of pathological forms of proteins and impair synaptic functions; it may also disrupt the function of endoplasmic organelles, causing endoplasmic stress. Changes due to metal ion imbalance can also aggravate abnormal distribution and deposition of metal ions, which can lead to chronic neurodegeneration. In recent years, the influence of redox metals on neurodegenerative diseases has been intensively studied. Despite the advances in knowledge, it is still not clear in which diseases redox active metals play a major or secondary pathogenic role, how redox active metals move from vital functions to playing a key role in pathological processes; what pathogenic mechanisms are involved in tissue damage induced by redox active metals, what protective mechanisms are disturbed in disease states. More knowledge is needed about possible therapeutic intervention strategies to prevent / reduce the pathogenic process caused or exacerbated by redox active metals.

This special issue is dedicated to the latest advances in research into the role of redox active metals in neurodegeneration. The aim is to provide an in-depth understanding of the fundamental role of copper, iron, cadmium, manganese and lesser known trace reactive metals in neurodegenerative brain diseases, and to present the results of experimental and clinical studies on pharmacological interventions to reverse metallic abnormalities that could be useful in treating common neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and other conditions such as stroke, multiple sclerosis, and hereditary diseases. Proposals for new therapeutic approaches to prevent and / or restore neurological changes by targeting any target at any stage of redox-active metal induced or exacerbated processes are welcome.

Prof. Dr. Grażyna Gromadzka
Guest Editor

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