Welcome to the Journal of Neurology & Neuromedicine

Manuscript Guidelines

The journal has specific rules to formatting a manuscript that authors should adhere to before shipping their manuscript. These guidelines are primarily intended to make the submission of manuscript quick and easy.    Read More

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Ethics & Disclosures

Journal of Neurology and Neuromedicine is primarily based on values centered on loyalty, commitment, scientific accuracy, and ethics. It has adopted clear and rigorous ethical guidelines for best working practices.    Read More

What happens next to your Submission

Each article we publish benefits from hundreds of hours of work by Chief editors, Sectional editors, Reviewers, Manuscript editors, Proofreaders, Graphics and Web experts, who work to ensure that the manuscript meets our standards.    Read More


Focus & Scope

The overarching goal of the Journal of Neurology and Neuromedicine is to remain as a credible source of neurological sciences based information encompassing a variety of relevant areas such as clinical studies, cellular and molecular studies, disease mechanisms, diagnostic approaches, epidemiology, medical aspects, computational studies and treatment options of the most common neurobiological complexities with an emphasis on research that is genetically, structurally, physiologically and pathophysiologically relevant.

The integral part of our scholarly mission is to ensure the accuracy of journal quality in accord with the highest standards of professional ethics.

“Quality is our Priority.
It is the Foundation of our Publication

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Recent Articles

Vol 3-4 Mini Review

Simulation of Cellular Remodeling: from Cardiac Myofiber to Whole Heart

Ani Amar*

Department of Biomedical Engineering, Faculty of Engineering, Tel Aviv University, Israel

Heart failure is characterized as any heart condition resulting from impairment of the heart’s ability to pump blood, with high prevalence in both aged and diseased hearts. Numerous population-based studies have shown that, in patients with impaired left ventricular systolic function, additional structural and functional cardiovascular abnormalities are often found, making it difficult to understand the underlying pathophysiological processes. Advances in experimental and modeling tools have led to the identification of many cellular mechanisms that contribute to cardiac failure. Still, the mechanism by which cardiac myofiber adaptation ultimately leads to failure remains unclear. Several human cell, tissue, and organ models are used to model heart failure. In this mini review, several available human models are summarized with a focus on the simulation of cellular remodeling: from membrane excitation at the level of the single cell to contraction of the ventricle.

DOI: 10.29245/2572.942X/2018/4.1186 Read More
Vol 3-4 Commentary

Commentary: "Promoting Myelin Repair through In vivo Neuroblast Reprogramming"

Bilal El Waly1, Myriam Cayre1, Pascale Durbec1*

1Aix Marseille University, CNRS, IBDM-UMR 7288, Case 907, Parc Scientifique de Luminy, campus de Luminy, 13288 Marseille, Cedex 09, France

DOI: 10.29245/2572.942X/2018/4.1196 Read More
Vol 3-4 Commentary

Commentary: Alpha-Synuclein Aggregates Cause Calcium Dysregulation by Activating Calcium Pump SERCA

Cristine Betzer1,2, Poul Henning Jensen1,2*

1Danish Research Institute of Translational Neuroscience - DANDRITE, Aarhus University, Denmark

2Department of Biomedicine, Aarhus University, Denmark

DOI: 10.29245/2572.942X/2018/4.1197 Read More
Vol 3-4 Mini Review

A Quantitative View on Naturally Occurring Autoantibodies in Neurodegenerative Diseases

Yannick Kronimus, Richard Dodel*, Sascha Neumann

Department of Geriatrics, University Duisburg-Essen, Germaniastrasse 1-3, 45356 Essen, Germany

Accumulation and aggregation of Beta-Amyloid (Aβ) and Alpha-Synuclein (α-Syn) are considered as central or even causative for the development of Alzheimer’s (AD) and Parkinson’s disease (PD). Therefore, the regulation of these proteins seems to be an essential aspect for prevention and is of central interest in current research aiming to find therapeutic approaches. The human immunological repertoire already contains such a regulatory system. Naturally occurring autoantibodies (nAbs) against the proteins Aβ (nAbs-Aβ) and α-Syn (nAbs-α-Syn) are part of the innate immune system and modulate the metabolism of their specific antigens including protein clearance and inhibition of aggregation. Thus, many researchers hypothesize that in the course of AD and PD, quantitative alterations of nAbs-Aβ and nAbs-α-Syn arise resulting in impaired proteastasis. Such alterations would represent promising, reliable biomarkers and indicate potential approaches for therapeutic strategies. Hence, it is not surprising that many studies dealing with nAbs-Aβ and nAbs-α-Syn titers in AD and PD patients in comparison to control participants are available in the literature. In this mini review, we summarize the current evidence. Furthermore, we critically discuss problems and future requirements for nAbs quantification when a clinical application is the overriding goal.

DOI: 10.29245/2572.942X/2018/4.1189 Read More
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Special Features to Authors

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