Open Science Badges in the Journal of Neurochemistry.

The Open Science Framework (OSF) has the mission to increase openness, integrity, and reproducibility in research. The Journal of Neurochemistry became a signatory of their Transparency and Openness guidelines in 2016, which provides eight modular standards (Citation standards, Data Transparency, Analytic Methods/Code Transparency, Research Materials Transparency, Design and Analysis Transparency, Study Pre-registration, Analysis Plan Transparency, Replication) with increasing levels of stringency. Furthermore, OSF recommends and offers a collection of practices intended to make scientific processes and results more transparent and available in a standardized way for reuse to people outside the research team. It includes making research materials, data, and laboratory procedures freely accessible online to anyone. This editorial announces the decision of the Journal of Neurochemistry to introduce Open Science Badges, maintained by the Open Science Badges Committee and by the Center for Open Science (COS). The Open Science Badges, visual icons placed on publications, certify that an open practice was followed and signal to readers that an author has shared the corresponding research evidence, thus, allowing an independent researcher to understand how to reproduce the procedure.

Gene regulation and genetics in neurochemistry, past to future.

Ask any neuroscientist to name the most profound discoveries in the field in the past 60 years, and at or near the top of the list will be a phenomenon or technique related to genes and their expression. Indeed, our understanding of genetics and gene regulation has ushered in whole new systems of knowledge and new empirical approaches, many of which could not have even been imagined prior to the molecular biology boon of recent decades. Neurochemistry, in the classic sense, intersects with these concepts in the manifestation of neuropeptides, obviously dependent upon the central dogma (the established rules by which DNA sequence is eventually converted into protein primary structure) not only for their conformation but also for their levels and locales of expression. But, expanding these considerations to non-peptide neurotransmitters illustrates how gene regulatory events impact neurochemistry in a much broader sense, extending beyond the neurochemicals that translate electrical signals into chemical ones in the synapse, to also include every aspect of neural development, structure, function, and pathology. From the beginning, the mutability - yet relative stability - of genes and their expression patterns were recognized as potential substrates for some of the most intriguing phenomena in neurobiology - those instances of plasticity required for learning and memory. Near-heretical speculation was offered in the idea that perhaps the very sequence of the genome was altered to encode memories. A fascinating component of the intervening progress includes evidence that the central dogma is not nearly as rigid and consistent as we once thought. And this mutability extends to the potential to manipulate that code for both experimental and clinical purposes. Astonishing progress has been made in the molecular biology of neurochemistry during the 60 years since this journal debuted. Many of the gains in conceptual understanding have been driven by methodological progress, from automated high-throughput sequencing instruments to recombinant-DNA vectors that can convey color-coded genetic modifications in the chromosomes of live adult animals. This review covers the highlights of these advances, both theoretical and technological, along with a brief window into the promising science ahead. This article is part of the 60th Anniversary special issue.

Reflections on 60 years of publication of the Journal of Neurochemistry.

This review reflects on the origins, development, publishing trends, and scientific directions of the Journal of Neurochemistry over its 60 year lifespan as seen by key contributors to the Journal's production. The Journal first appeared in May 1956 with just two issues published in that inaugural year. By 1963, it appeared monthly and, by 2002, 24 hard copy issues were published yearly. In 2014, the Journal became online only. For much of its time, the Journal was managed through two separate editorial offices each with their respective Chief Editor (the 'Western' and 'Eastern' hemispheres). The Journal was restructured to operate through a single editorial office and Editor-in-Chief from 2013. Scientifically, the Journal progressed through distinct scientific eras with the first two decades generally centered around developments in methodology followed by a period when publications delved deeper into underlying mechanisms. By the late 1980s, the Journal had entered the age of genetics and beyond, with an increasing focus on neurodegenerative diseases. Reviews have played a regular part in the success of J Neurochem with focused special and virtual issues being a highlight of recent years. Today, 60 years and onwards, J Neurochem continues to be a leading source of top-quality, original and review articles in neuroscience. We look forward to its continued success at the forefront of neurochemistry in the decades to come. This article celebrates 60 years of publication of Journal of Neurochemistry including personal reminiscences from some of the Chief Editors, past and present, as well as input from some of the key contributors to the Journal over this period. We highlight the scientific, technological, and publishing developments along the way, with reference to key papers published in the Journal. The support of the Journal toward the aims and objectives of the International Society for Neurochemistry (ISN) is also emphasized. This article is part of the 60th Anniversary special issue.

A Learned Society's Perspective on Publishing.

Scientific journals that are owned by a learned society, like the Journal of Neurochemistry (JNC), which is owned by the International Society for Neurochemistry (ISN), benefit the scientific community in that a large proportion of the income is returned to support the scientific mission of the Society. The income generated by the JNC enables the ISN to organize conferences as a platform for members and non-members alike to share their research, supporting researchers particularly in developing countries by travel grants and other funds, and promoting education in student schools. These direct benefits and initiatives for ISN members and non-members distinguish a society journal from pure commerce. However, the world of scholarly publishing is changing rapidly. Open access models have challenged the business model of traditional journal subscription and hence provided free access to publicly funded scientific research. In these models, the manuscript authors pay a publication cost after peer review and acceptance of the manuscript. Over the last decade, numerous new open access journals have been launched and traditional subscription journals have started to offer open access (hybrid journals). However, open access journals follow the general scheme that, of all participating parties, the publisher receives the highest financial benefit. The income is generated by researchers whose positions and research are mostly financed by taxpayers' or funders' money, and by reviewers and editors, who frequently are not reimbursed. Last but not least, the authors pay for the publication of their work after a rigorous and sometimes painful review process. JNC itself has an open access option, at a significantly reduced cost for Society members as an additional benefit. This article provides first-hand insights from two former Editors-in-Chief, Kunihiko Suzuki and Leslie Iversen, about the history of JNC's ownership and about the difficulties and battles fought along the way to its current success and reputation. Scientific journals that are owned by a learned society, like the Journal of Neurochemistry (JNC) which is owned by the International Society for Neurochemistry (ISN), benefit the scientific community in that a large proportion of the income is returned to support the scientific mission of the Society. The income generated by the JNC enables the ISN to organize conferences as a platform for members and non-members alike to share their research, supporting researchers particularly in developing countries by travel grants and other funds, and to promote education in student schools. These direct benefits and initiatives for ISN members and non-members distinguish a society journal from pure commerce. However, the world of scholarly publishing is changing rapidly. Open access models have challenged the business model of traditional journal subscription and hence provide free access to publicly funded scientific research. In these models, the manuscript authors pay a publication cost after peer review and acceptance of the manuscript. Over the last decade, numerous new open access journals have been launched and traditional subscription journals have started to offer open access (hybrid journals). However, open access journals pertain to the general scheme that, of all participating parties, the publisher receives the highest financial benefit. The income is generated by researchers whose positions and research are mostly financed by tax payers' or funders' money, reviewers and editors, who frequently are not reimbursed. Last but not least, the authors pay for the publication of their work after a rigorous and sometimes painful review process. JNC itself has an open access option, at a significantly reduced cost for Society members as an additional benefit. This article provides first-hand insights from a long-standing Editor-in-Chief, Kunihiko Suzuki, about the history of JNC's ownership and about difficulties and battles fought on the way to its current success and reputation today. This article is part of the 60th Anniversary special issue.

'From past to future' - deciphering the molecular basis of Alzheimer's disease through the pages of the Journal of Neurochemistry.

The Journal of Neurochemistry has made significant contributions to unraveling the molecular basis for Alzheimer's disease during its 60-year history. To mark its 60th anniversary, this review describes the association between the journal and Alzheimer's disease research - from the early years when Alzheimer's disease was a minor topic in the journal through to the molecular era in the mid-1980s. This coincided with a number of the highly cited Alzheimer's disease studies which described fundamental aspects of the neurochemistry of Alzheimer's disease and encompassed the themes of oxidative stress and post-translational modifications, cholinergic system, tau, purification of Aß, defining the Aß toxic species, mechanism of amyloid precursor protein processing, and the development of diagnostics and therapeutics. The Journal of Neurochemistry has made significant contributions toward unraveling the molecular, cellular and pathological basis of Alzheimer's disease through its 60 years. This article is part of the 60th Anniversary special issue.

Fármacos glutamatérgicos en tratamiento de la esquizofrenia / Glutamatergic drugs for schizophrenia treatment

Actualmente se considera que tanto los síntomas positivos como en negativos de la esquizofrenia podrían deberse a una hipofunción glutamatérgica que tendría como consecuencia la alteración de la actividad de la neurotransmisión dopaminérgica. Concretamente, podría haber una disminución de la señalización glutamatérgica a nivel de los receptores NMDA, pero los agonistas directos de estos receptores no tienen utilidad clínica por ser inespecíficos y sus muchos efectos indeseables. Dados los problemas de falta de eficacia o de efectos secundarios que presentan los fármacos que actúan directamentesobre los receptores ionotrópicos y mGlu2-3, se han ensayado otros que actúan por otros mecanismos, especialmente indirectos, como es la administración co-agonistas de los receptores NMDA (glicina o D-serina), inhibidores del transportador de la glicina (sarcosina, Bitopertin), AMPAkinas (CX-516) y agonistas de los receptores mGlu5. Sin embargo, a pesar de los constantes fracasos, el enfoque glutamatérgico en el tratamiento de la esquizofrenia no está agotado y es necesario revisar todos los aspectos teóricos que relacionan estos mecanismos neuroquímicos con la compleja sintomatología esta patología hasta que logremos moléculas que sean realmente eficaces y que tengan un perfil de efectos secundarios aceptable

It is accepted that both positive and negative symptoms of schizophrenia may be due to hypofunction of glutamatergic pathways leading to altered dopaminergic neurotransmission activity. Specifically, there may be diminished glutamatergic signaling at the level of the NMDA receptors, but direct receptor agonists have no clinical utility due to their nonspecific actions and undesirable side effects. Given the problems of ineffectiveness or side effects of drugs that act directly on ionotropic and metabotropicmGlu2-3 receptors, clinical trials have been conducted with other drugs that have other mechanisms of action, especially indirect mechanisms, such as the co-administration of NMDA agonists (glycine or D-serine), glycine transporter inhibitors (sarcosine bitopertin), ampakines (CX-516), andmGlu5 receptor agonists. However, despite repeated failures, the glutamatergic approach to the treatment of schizophrenia has not been exhausted and all theoretical aspects that relate these complex neurochemical mechanisms with symptoms of schizophrenia should be reviewed until we find truly effective molecules with an acceptable side effect profile

Esquizofrenia y cultura moderna: razones de la locura / Schizophrenia and modern culture: reasons for insanity

Después de señalar la incertidumbre y confusión a la que ha llevado la investigación neurobiológica de la esquizofrenia, como muestran y reconocen revisiones recientes, se ofrecen siete razones para su reconsideración como un trastorno del yo más que del cerebro. La primera razón empieza por concebir la esquizofrenia como un trastorno del yo, en la perspectiva de la fenomenología actual. La segunda relaciona el hecho de su origen reciente (a partir de 1750) con la particular configuración del yo moderno y la gran transformación de la comunidad en la sociedad de los individuos (industrialización, urbanización). La tercera hace hincapié en la afinidad entre esquizofrenia y adolescencia, una edad crítica en la formación del yo, que empezó a ser problemática a finales del siglo xviii. La cuarta es el mejor pronóstico de la esquizofrenia en los países en desarrollo, respecto de los desarrollados, lo que probablemente tiene que ver con el proceso de modernización (que todavía conserva estructuras comunitarias en los países menos desarrollados). La quinta es la alta incidencia de esquizofrenia entre emigrantes, como hecho a explicar en términos de un modelo socioevolutivo. La sexta revisa la leyenda genética de la esquizofrenia, cómo la epigenética devuelve el protagonismo al ambiente. La séptima y última razón se refiere a la reconsideración de la terapia psicológica como posible tratamiento de elección y no meramente adjunto a la medicación, sabido que para los pacientes es más importante la química interpersonal que la neuroquímica (AU)

After pointing out the uncertainty and confusion to which neurobiological research has led schizophrenia, as shown and acknowledged in recent reviews, we offer seven reasons for reconsidering schizophrenia a disorder of the self, rather than of the brain. The first reason starts out conceiving schizophrenia as a disorder of the self, in the perspective of current phenomenology. The second relates the fact of its recent origin (as of 1750) with the particular configuration of the modern self and with the great transformation of the community into a society of individuals (industrialization, urbanization). The third reason emphasizes the affinity between schizophrenia and adolescence, a critical age in the formation of the self, which started to be problematic at the end of the 18th century. The fourth is the better prognosis of schizophrenia in developing countries, in comparison to developed countries, which probably has to do with the process of modernization (which still maintains community structures in less developed countries). The fifth is the high incidence of schizophrenia among immigrants, as a fact to be explained in terms of a socioevolutionary model. The sixth reason reviews the genetic legend of schizophrenia, and how epigenetics gives protagonism back to the environment. The seventh and last reason refers to the reconsideration of psychological therapy as the possible treatment of choice and not merely an adjunct to medication, as it is known that, for patients, interpersonal chemistry is more important than neurochemistry (AU)

[Neurophysiological, neurochemical, autonomous and chronobiological basics of sleep medicine].

The review discusses various mechanisms of the rapidly growing problem of Sleep Medicine. The "Sleep-wakefulness" cycle is a continuum of different functional states and the diseases that these states might prompt to manifest themselves in various ways. In these cases, we must say that change produces the conditions of disease manifestation rather than the disease itself. The paper describes the dynamics of the autonomous parameters during sleep, emphasizes the role and importance of chronobiological aspects of the "sleep-wakefulness" cycle. The holographic principle of the operation I sleep cycle is described which persists even in the cerebral stroke. From the standpoint of neurochemistry, modern hypnotics and drugs of the nearest future can be divided into 2 groups: proS (pro sleep)--for sleeping, and antiW (anti-wakefulness)--vs. wakefulness.