OBM Neurobiology is an international peer-reviewed Open Access journal published quarterly online by LIDSEN Publishing Inc. By design, the scope of OBM Neurobiology is broad, so as to reflect the multidisciplinary nature of the field of Neurobiology that interfaces biology with the fundamental and clinical neurosciences. As such, OBM Neurobiology embraces rigorous multidisciplinary investigations into the form and function of neurons and glia that make up the nervous system, either individually or in ensemble, in health or disease. OBM Neurobiology welcomes original contributions that employ a combination of molecular, cellular, systems and behavioral approaches to report novel neuroanatomical, neuropharmacological, neurophysiological and neurobehavioral findings related to the following aspects of the nervous system: Signal Transduction and Neurotransmission; Neural Circuits and Systems Neurobiology; Nervous System Development and Aging; Neurobiology of Nervous System Diseases (e.g., Developmental Brain Disorders; Neurodegenerative Disorders).

OBM Neurobiology publishes research articles, technical reports and invited topical reviews. Although the OBM Neurobiology Editorial Board encourages authors to be succinct, there is no restriction on the length of the papers. Authors should present their results in as much detail as possible, as reviewers are encouraged to emphasize scientific rigor and reproducibility.

Archiving: full-text archived in CLOCKSS.

Rapid publication: manuscripts are undertaken in 11.8 days from acceptance to publication (median values for papers published in this journal in the second half of 2021, 1-2 days of FREE language polishing time is also included in this period).

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Special Issue

Metals and Neurodegeneration

Submission Deadline: December 31, 2021 (Open) Submit Now

Guest Editor

Joy Mitra, PhD

Research Associate, Department of Neurosurgery, Center for Neuroregeneration, The Houston Methodist Research Institute, Houston, TX, United States

Website | E-Mail

Research interests: Immunohistochemistry; In Situ Hybridization; Neuronal Differentiation; Immunofluorescence; Gene Expression; PCR

About This Topic

Metals play crucial roles in maintaining the normal physiological functions in human body. While metals are essentially required by the body’s immune response and other defense mechanisms against external and internal damaging insults. However, slight variation from the normal physiological concentration of metals, especially pro-oxidant transition metals, has been shown to play roles in disease causing patho-mechanisms by affecting the body’s overall metal homoeostasis. Decades of research has shown the implication of pro-oxidant metal dyshomoeostasis in almost all types neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis and so on. Notably, studies have shown that essential trace metals like zinc, iron etc., which are important for normal brain cell functioning, become toxic under the diseased condition, hence called ‘double-edged sword’, by inducing oxidative genome damage, cell membrane disruption, mitochondrial pathology and the most importantly facilitating pathogenic protein aggregate formation in neurons, leading to irreversible neuronal death by metal-associated death mechanism. Emerging findings have also highlighted the pro-oxidant metals’ role in developing post-stroke neuropathological complications and chronic dementia. Besides these negative impacts, metals play crucial roles in relaying electrical signals across the neuronal synapses and associated nerve cells, acting as co-factor for protein activity and as transcription factor as well. Although, recent investigations have been gradually shedding light on the feedback loop mechanism linking cellular stress levels and metal-induced toxicities, however, there is no effective therapeutic strategy to chelate out the disease-causing metal selectively and precisely from the affected cellular compartment only. Keeping these facts into account, it is of utmost importance to revisit the specific roles of metals in brain functions, understand the underlying cause which initiates metal dyshomeostasis, and how these conditions influence the alteration in neuronal gene expressions and inhibit the genome repair processes. In this special issue we will focus on the following aspects highlighting multifaceted roles of metal dyshomoeostasis in various neuropsychiatric and neurodegenerative disorders:

1) Introduction.

2) Role of metals in neuronal gene expressions and brain functions (motor and cognitive)

3) Metals in protective mechanisms in brain.

4) Metals in genome repair processes.

5) Involvement of pro-oxidant metals in neuropsychiatric, neurodegenerative and stroke pathologies.

6) Metal chelation therapy and its limitations.

7) Concluding assessment and suggestions for much needed improvements in chelation therapy.