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Topic: Metal Ions and Oxidative Stress in Neurodegenerative Diseases

A special issue of Neuroimmunology and Neuroinflammation

ISSN 2349-6142 (Online), ISSN 2347-8659 (Print)

Submission deadline: 31 Jul 2021

Guest Editor(s)

  • Dr. Luigi Casella
    Department of Chemistry, University of Pavia, Pavia, Italy.

    Website | E-mail

Special Issue Introduction

Neurodegenerative diseases are caused by a collection of extremely complex processes, involving the interplay of several pathological events, the most common of which include protein misfolding and aggregation, mitochondrial dysfunction, autophagy impairment, oxidative stress, accumulation of toxic metals, and neuroinflammation. The brain has higher energy demand, and hence higher oxygen consumption, to support its higher oxidative metabolic activity, and therefore, it is particularly exposed to oxidative stress risks. The effects of oxidative stress are evident from a number of markers showing that all types of biological molecules, including proteins, lipids and DNA, undergo oxidation or cleavage at functional groups in the diseased brains of deceased patients with, e.g. Alzheimer’s or Parkinson’s disease, or amyotrophic lateral sclerosis. The chemical species usually responsible for these oxidative processes are collectively labeled as “reactive oxygen species” (ROS), as they derive from partial reduction of dioxygen, but it is important to note that ROS formation is systematically promoted by redox active metal ions, particularly Fe and Cu, as well as Mn, which are broadly distributed in the brain. These transition metal ions support a wide range of essential processes, as cofactors of metalloproteins involved in the production of cellular energy and in other key processes, such as myelination and neurotransmitter metabolism, or in synaptic signaling and allosteric regulation. Under normal conditions, the activity and circulation of Fe, Cu, and Mn are kept under control, and several mechanisms allow neuronal cells to repair the oxidative damage induced by ROS and scavenge potentially toxic radical species. In addition, aging is characterized by deficiencies in the regulation of metal ions and their accumulation in the brain. The loss of homeostatic control becomes particularly relevant in neurodegenerative diseases, where the oxidative damage leads to chronic neuroinflammation and pronounced neuronal death. This special issue aims to gather new evidence on the mechanisms inducing oxidative stress, metal ion dyshomeostasis, and proposals of new therapies to reduce the impact of neuroinflammation during aging and diseases.

Outlines of possible topics of interest:
- Molecular mechanisms of oxidative stress in neurodegenerative diseases
- Metal binding to neuropeptides and neuronal proteins
- Protein aggregation by metal ions and oxidative stress
- Metal ion dysregulation as promoter of neuroinflammation
- Metal ion interactions with receptors at synapses
- Pathways of metal ion circulation and signaling
- Metal ion imaging in cells and tissues
- Metal ion transporters and their inhibition
- Molecules for metal ion chelation therapy
- Strategies to mitigate oxidative stress and possible regenerative treatments

Submission Deadline

31 Jul 2021

Submission Information

For Author Instructions, please refer to http://nnjournal.net/pages/view/author_instructions
For Online Submission, please login at https://oaemesas.com/NN/?IssueId=617
Submission Deadline: 31 Jul 2021
Contacts: Orla, Assistant Editor, orla@nnjournal.net

Published Articles

This special issue is now open for submission.
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