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State-of-the-Art Molecular Neurobiology in USA

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 4986

Special Issue Editors


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Guest Editor
Science & Technology Center, Hill′s Pet Nutrition, Inc., Topeka, KS 66617, USA
Interests: inflammation; immunology; renal; brain; cognition
Independent Researcher, New York, NY 10021, USA
Interests: neurological diseases; pathophysiology; therapeutics; animal models; molecular mechanisms; drug development; mitochondria; biomarker; posttranslational modification; transcription factor; gut-brain axis; Huntington’s disease; Parkinson’s disease; Alzheimer’s disease
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Special Issue Information

Dear Colleagues, 

This Special Issue aims to provide a comprehensive overview of recent advances in molecular Neurobiology in USA by inviting contributions from USA research Institutes/laboratories that consolidate our understanding of this area. Topics include, but are not limited to, the following:

  • Neurobiology
  • Neurochemistry
  • Neurology
  • Neuropathology
  • Neurophysiology
  • Neuropharmacology
  • Neurogenetics
  • Neuro Oncology
  • Aging Neuroscience
  • Disorders of Brain and Mind

Dr. Kiran Panickar
Dr. Ashu Johri
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neurobiology
  • neurochemistry
  • neurology
  • neuropathology
  • neurophysiology
  • neuropharmacology
  • neurogenetics
  • neuro oncology
  • aging neuroscience
  • neurodegeneration

Published Papers (2 papers)

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Research

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15 pages, 2152 KiB  
Article
Renin-Angiotensin System in Huntington′s Disease: Evidence from Animal Models and Human Patients
by Lucas M. Kangussu, Natalia P. Rocha, Priscila A. C. Valadão, Thatiane C. G. Machado, Kívia B. Soares, Julliane V. Joviano-Santos, Leigh B. Latham, Gabriela D. Colpo, Ana Flávia Almeida-Santos, Erin Furr Stimming, Ana Cristina Simões e Silva, Antônio L. Teixeira, Aline Silva Miranda and Cristina Guatimosim
Int. J. Mol. Sci. 2022, 23(14), 7686; https://doi.org/10.3390/ijms23147686 - 12 Jul 2022
Cited by 2 | Viewed by 1424
Abstract
The Renin-Angiotensin System (RAS) is expressed in the central nervous system and has important functions that go beyond blood pressure regulation. Clinical and experimental studies have suggested that alterations in the brain RAS contribute to the development and progression of neurodegenerative diseases. However, [...] Read more.
The Renin-Angiotensin System (RAS) is expressed in the central nervous system and has important functions that go beyond blood pressure regulation. Clinical and experimental studies have suggested that alterations in the brain RAS contribute to the development and progression of neurodegenerative diseases. However, there is limited information regarding the involvement of RAS components in Huntington’s disease (HD). Herein, we used the HD murine model, (BACHD), as well as samples from patients with HD to investigate the role of both the classical and alternative axes of RAS in HD pathophysiology. BACHD mice displayed worse motor performance in different behavioral tests alongside a decrease in the levels and activity of the components of the RAS alternative axis ACE2, Ang-(1-7), and Mas receptors in the striatum, prefrontal cortex, and hippocampus. BACHD mice also displayed a significant increase in mRNA expression of the AT1 receptor, a component of the RAS classical arm, in these key brain regions. Moreover, patients with manifest HD presented higher plasma levels of Ang-(1-7). No significant changes were found in the levels of ACE, ACE2, and Ang II. Our findings provided the first evidence that an imbalance in the RAS classical and counter-regulatory arms may play a role in HD pathophysiology. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in USA)
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Review

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19 pages, 751 KiB  
Review
Maternal and Neonatal Polyunsaturated Fatty Acid Intake and Risk of Neurodevelopmental Impairment in Premature Infants
by Rory J. Heath, Susanna Klevebro and Thomas R. Wood
Int. J. Mol. Sci. 2022, 23(2), 700; https://doi.org/10.3390/ijms23020700 - 9 Jan 2022
Cited by 15 | Viewed by 2880
Abstract
The N3 and N6 long chain polyunsaturated fatty acids (LCPUFA) docosahexaenoic acid (DHA) and arachidonic acid (AA) are essential for proper neurodevelopment in early life. These fatty acids are passed from mother to infant via the placenta, accreting into fetal tissues such as [...] Read more.
The N3 and N6 long chain polyunsaturated fatty acids (LCPUFA) docosahexaenoic acid (DHA) and arachidonic acid (AA) are essential for proper neurodevelopment in early life. These fatty acids are passed from mother to infant via the placenta, accreting into fetal tissues such as brain and adipose tissue. Placental transfer of LCPUFA is highest in the final trimester, but this transfer is abruptly severed with premature birth. As such, efforts have been made to supplement the post-natal feed of premature infants with LCPUFA to improve neurodevelopmental outcomes. This narrative review analyzes the current body of evidence pertinent to neurodevelopmental outcomes after LCPUFA supplementation in prematurely born infants, which was identified via the reference lists of systematic and narrative reviews and PubMed search engine results. This review finds that, while the evidence is weakened by heterogeneity, it may be seen that feed comprising 0.3% DHA and 0.6% AA is associated with more positive neurodevelopmental outcomes than LCPUFA-deplete feed. While no new RCTs have been performed since the most recent Cochrane meta-analysis in 2016, this narrative review provides a wider commentary; the wider effects of LCPUFA supplementation in prematurely born infants, the physiology of LCPUFA accretion into preterm tissues, and the physiological effects of LCPUFA that affect neurodevelopment. We also discuss the roles of maternal LCPUFA status as a modifiable factor affecting the risk of preterm birth and infant neurodevelopmental outcomes. To better understand the role of LCPUFAs in infant neurodevelopment, future study designs must consider absolute and relative availabilities of all LCPUFA species and incorporate the LCPUFA status of both mother and infant in pre- and postnatal periods. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in USA)
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