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Molecular Signals and Genetic Regulations of Neurological Disorders 2.0
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Molecular Signals and Genetic Regulations of Neurological Disorders 2.0

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 November 2023) | Viewed by 5325

Special Issue Editors

Dr. Emanuele Rocco Villani

E-Mail Website
Guest Editor
1. UOC Geriatra - Disturbi Cognitivi e Demenze, Dipartimento di Cure Primarie. AUSL Modena, 41012 Modena, Italy
2. Department of Geriatrics, Fondazione Policlinico Universitario A. Gemelli IRCCS, Università Cattolica Sacro Cuore, 00168 Rome, Italy
Interests: modifiable lifestyle factors and plasma biomarkers of Alzheimer’s disease
Special Issues, Collections and Topics in MDPI journals
Dr. Emanuele Marzetti

E-Mail Website
Guest Editor
Department of Geriatrics and Orthopedics, Università Cattolica del Sacro Cuore, 00168 Rome, Italy
Interests: geriatrics; sarcopenia; frailty; geriatric syndromes; geroscience; biomarkers; mitochondrial dysfunction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Intra- and extracellular molecular signaling play a major role in modulating the genetic and epigenetic regulation of cellular growth, differentiation mechanisms, and vice versa. Moreover, the proteins that make up an organism (proteome) are constantly changing and are intricately linked to neurological diseases. A growing body of research data strongly suggests that imbalances in the abovementioned mechanisms and genetic abnormalities are at the basis of the development of several neurological disorders. Thus, the scope of this Special Issue is to cover the molecular signaling and genetic regulation of neurological disorders, particularly regarding the development and progression of the most prevalent neurological disorders, which are causes of cognitive impairment, movement disorders, cerebrovascular diseases, and brain cancer. We are also interested in discussing neurological disorders such as Down’s syndrome, since it shows some molecular similarity with Alzheimer’s disease, and repeat expansion diseases.

Dr. Emanuele Rocco Villani
Dr. Emanuele Marzetti
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

  • mTOR pathways
  • Alzheimer’s disease, aging, biomarkers, cognitive decline, cytokines, metabolomics, neuroinflammation
  • Parkinson’s disease
  • cerebrovascular diseases, CADASIL, HTR1A
  • mitochondrial dysfunction, mitochondrial quality control, mitochondrial-lysosomal axis, mitophagy, mtDNA
  • proteomics
  • exosomes
  • extracellular vesicles
  • chromosome 21 trisomy, Down’s syndrome, DYRK1-A

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Published Papers (2 papers)

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Research

17 pages, 4000 KiB  
Article
βPix Guanine Nucleotide Exchange Factor Regulates Regeneration of Injured Peripheral Axons
by Yewon Jeon, Yoon Kyung Shin, Hwigyeong Kim, Yun Young Choi, Minjae Kang, Younghee Kwon, Yongcheol Cho, Sung Wook Chi and Jung Eun Shin
Int. J. Mol. Sci. 2023, 24(18), 14357; https://doi.org/10.3390/ijms241814357 - 20 Sep 2023
Cited by 1 | Viewed by 1402
Abstract
Axon regeneration is essential for successful recovery after peripheral nerve injury. Although growth cone reformation and axonal extension are crucial steps in axonal regeneration, the regulatory mechanisms underlying these dynamic processes are poorly understood. Here, we identify βPix (Arhgef7), the guanine nucleotide exchange [...] Read more.
Axon regeneration is essential for successful recovery after peripheral nerve injury. Although growth cone reformation and axonal extension are crucial steps in axonal regeneration, the regulatory mechanisms underlying these dynamic processes are poorly understood. Here, we identify βPix (Arhgef7), the guanine nucleotide exchange factor for Rac1 GTPase, as a regulator of axonal regeneration. After sciatic nerve injury in mice, the expression levels of βPix increase significantly in nerve segments containing regenerating axons. In regrowing axons, βPix is localized in the peripheral domain of the growth cone. Using βPix neuronal isoform knockout (NIKO) mice in which the neuronal isoforms of βPix are specifically removed, we demonstrate that βPix promotes neurite outgrowth in cultured dorsal root ganglion neurons and in vivo axon regeneration after sciatic nerve crush injury. Activation of cJun and STAT3 in the cell bodies is not affected in βPix NIKO mice, supporting the local action of βPix in regenerating axons. Finally, inhibiting Src, a kinase previously identified as an activator of the βPix neuronal isoform, causes axon outgrowth defects in vitro, like those found in the βPix NIKO neurons. Altogether, these data indicate that βPix plays an important role in axonal regrowth during peripheral nerve regeneration. Full article
(This article belongs to the Special Issue Molecular Signals and Genetic Regulations of Neurological Disorders 2.0)
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19 pages, 1812 KiB  
Article
Simultaneous Antagonism at H3R/D2R/D3R Reduces Autism-like Self-Grooming and Aggressive Behaviors by Mitigating MAPK Activation in Mice
by Nermin Eissa, Mohamed Al Awad, Shilu Deepa Thomas, Karthikkumar Venkatachalam, Petrilla Jayaprakash, Sicheng Zhong, Holger Stark and Bassem Sadek
Int. J. Mol. Sci. 2023, 24(1), 526; https://doi.org/10.3390/ijms24010526 - 28 Dec 2022
Cited by 7 | Viewed by 3020
Abstract
Dysregulation in brain neurotransmitters underlies several neuropsychiatric disorders, e.g., autism spectrum disorder (ASD). Also, abnormalities in the extracellular-signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) pathway pave the way for neuroinflammation, neurodegeneration, and altered learning phenotype in ASD. Therefore, the effects of chronic systemic administration [...] Read more.
Dysregulation in brain neurotransmitters underlies several neuropsychiatric disorders, e.g., autism spectrum disorder (ASD). Also, abnormalities in the extracellular-signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) pathway pave the way for neuroinflammation, neurodegeneration, and altered learning phenotype in ASD. Therefore, the effects of chronic systemic administration of the multiple-targeting antagonist ST-713 at the histamine H3 receptor (H3R) and dopamine D2/D3 receptors (D2/D3R) on repetitive self-grooming, aggressive behaviors, and abnormalities in the MAPK pathway in BTBR T + Itpr3tf/J (BTBR) mice were assessed. The results showed that ST-713 (2.5, 5, and 10 mg/kg, i.p.) mitigated repetitive self-grooming and aggression in BTBR mice (all p < 0.05), and the ameliorative effects of the most promising dose of ST-713 (5 mg/kg, i.p.) on behaviors were completely abrogated by co-administration of the H3R agonist (R)-α-methylhistamine or the anticholinergic drug scopolamine. Moreover, the elevated levels of several MAPK pathway proteins and induced proinflammatory markers such as tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), and IL-6 were significantly suppressed following chronic administration of ST-713 (5 mg/kg, i.p.) (all p < 0.01). Furthermore, ST-713 significantly increased the levels of histamine and dopamine in hippocampal tissue of treated BTBR mice (all p < 0.01). The current observations signify the potential role of such multiple-targeting compounds, e.g., ST-713, in multifactorial neurodevelopmental disorders such as ASD. Full article
(This article belongs to the Special Issue Molecular Signals and Genetic Regulations of Neurological Disorders 2.0)
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