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Pharmaceuticals
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Stress, Neurotransmitters and Neurodegeneration
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Stress, Neurotransmitters and Neurodegeneration

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 6497

Special Issue Editors

Prof. Dr. Stefano Puglisi-Allegra

E-Mail Website
Guest Editor
Department of Psychology, Sapienza University of Rome, 00185 Roma, Italy
Interests: neural mechanisms of learning and memory, emotion and motivation, with particular emphasis on neurotransmission and neuroplasticity in mesocorticolimbic and mesocorticostriatal systems; preclinical models of psychopathologies such as stress, addiction, and depression; translational models of Phenylketonuria to envisage new therapeutic devices
Prof. Dr. Francesco Fornai

E-Mail Website
Guest Editor
Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, 56124 Pisa, Italy
Interests: neuroanatomy; neuroscience; neurodegeneration; methamphetamine; autophagy; movement disorders; substances of abuse; morphology; ultrastructure
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Stress is a consequence of challenges to the organism produced by events known as stressors, which are usually unpredictable and uncontrollable stimuli or conditions. These external or internal stimuli promote classic stress responses aimed at adaptation according to physiological and/or psychological compensation. Stress-associated adaptive changes may increase the resistance to pathological outcomes, thus either favoring resilience, in the best-case scenario, or causing dysfunctional coping that increases the “allostatic load” and leads to disease.

In mammals, including humans, brain neurotransmitters are crucial in promoting adaptive or maladaptive stress-induced neural adjustments.

Recent evidence has shown that psychological stress can have deleterious effects on neurodegenerative disease progression in preclinical animal models. This strongly suggests that in humans, life events should be taken into account to improve resilience, reduce stress, and protect against neurodegeneration.

Research on the neural circuitry that regulates behavioral and hormonal stress responses has highlighted the involvement of a plethora of brain regions and neurotransmitter systems in dysfunctions related to neuropsychiatric diseases and neurodegeneration.

Neurotransmitters and hormones are therefore the priority target of drug therapies aimed at sustaining resilience and protecting against the deleterious effects of stress on the nervous system.

This Special Issue aims at bringing together studies on stress-induced brain dysfunctions in order to uncover new avenues for neuropharmacological treatments to sustain resilience and coping ability and to protect against neurodegeneration in the central nervous system, focusing on neurotransmission, inflammation, vascularity, and autophagy.

Submissions of original research articles, reviews are invited. Studies on both human and animal models, as well as their respective state-of-the-art experimental applications, are welcome.

Prof. Dr. Stefano Puglisi-Allegra
Prof. Dr. Francesco Fornai
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. Pharmaceuticals is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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

  • Psychological stress
  • Neurotransmission
  • Hormones
  • Neurotrophins
  • Resilience
  • Coping
  • Stress vulnerability
  • Inflammation
  • Microglia
  • Autophagy
  • Neurovascular system
  • Neuroprotection
  • Covid-19 stress
  • Post-Traumatic Stress Disorder (PTDS)

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Published Papers (2 papers)

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Research

19 pages, 3358 KiB  
Article
Inhibition of 11β-HSD1 Ameliorates Cognition and Molecular Detrimental Changes after Chronic Mild Stress in SAMP8 Mice
by Dolors Puigoriol-Illamola, Júlia Companys-Alemany, Kris McGuire, Natalie Z. M. Homer, Rosana Leiva, Santiago Vázquez, Damian J. Mole, Christian Griñán-Ferré and Mercè Pallàs
Pharmaceuticals 2021, 14(10), 1040; https://doi.org/10.3390/ph14101040 - 13 Oct 2021
Cited by 4 | Viewed by 3021
Abstract
Impaired glucocorticoid (GC) signaling is a significant factor in aging, stress, and neurodegenerative diseases such as Alzheimer’s disease. Therefore, the study of GC-mediated stress responses to chronic moderately stressful situations, which occur in daily life, is of huge interest for the design of [...] Read more.
Impaired glucocorticoid (GC) signaling is a significant factor in aging, stress, and neurodegenerative diseases such as Alzheimer’s disease. Therefore, the study of GC-mediated stress responses to chronic moderately stressful situations, which occur in daily life, is of huge interest for the design of pharmacological strategies toward the prevention of neurodegeneration. To address this issue, SAMP8 mice were exposed to the chronic mild stress (CMS) paradigm for 4 weeks and treated with RL-118, an 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) inhibitor. The inhibition of this enzyme is linked with a reduction in GC levels and cognitive improvement, while CMS exposure has been associated with reduced cognitive performance. The aim of this project was to assess whether RL-118 treatment could reverse the deleterious effects of CMS on cognition and behavioral abilities and to evaluate the molecular mechanisms that compromise healthy aging in SAMP8 mice. First, we confirmed the target engagement between RL-118 and 11β-HSD1. Additionally, we showed that DNA methylation, hydroxymethylation, and histone phosphorylation were decreased by CMS induction, and increased by RL-118 treatment. In addition, CMS exposure caused the accumulation of reactive oxygen species (ROS)-induced damage and increased pro-oxidant enzymes—as well as pro-inflammatory mediators—through the NF-κB pathway and astrogliosis markers, such as GFAP. Of note, these modifications were reversed by 11β-HSD1 inhibition. Remarkably, although CMS altered mTORC1 signaling, autophagy was increased in the SAMP8 RL-118-treated mice. We also showed an increase in amyloidogenic processes and a decrease in synaptic plasticity and neuronal remodeling markers in mice under CMS, which were consequently modified by RL-118 treatment. In conclusion, 11β-HSD1 inhibition through RL-118 ameliorated the detrimental effects induced by CMS, including epigenetic and cognitive disturbances, indicating that GC-excess attenuation shows potential as a therapeutic strategy for age-related cognitive decline and AD. Full article
(This article belongs to the Special Issue Stress, Neurotransmitters and Neurodegeneration)
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25 pages, 17333 KiB  
Article
Inhibition of Autophagy In Vivo Extends Methamphetamine Toxicity to Mesencephalic Cell Bodies
by Michela Ferrucci, Francesca Biagioni, Carla L. Busceti, Chiara Vidoni, Roberta Castino, Ciro Isidoro, Larisa Ryskalin, Alessandro Frati, Stefano Puglisi-Allegra and Francesco Fornai
Pharmaceuticals 2021, 14(10), 1003; https://doi.org/10.3390/ph14101003 - 29 Sep 2021
Cited by 5 | Viewed by 2395
Abstract
Methamphetamine (METH) is a widely abused psychostimulant and a stress-inducing compound, which leads to neurotoxicity for nigrostriatal dopamine (DA) terminals in rodents and primates including humans. In vitro studies indicate that autophagy is a strong modulator of METH toxicity. In detail, suppressing autophagy [...] Read more.
Methamphetamine (METH) is a widely abused psychostimulant and a stress-inducing compound, which leads to neurotoxicity for nigrostriatal dopamine (DA) terminals in rodents and primates including humans. In vitro studies indicate that autophagy is a strong modulator of METH toxicity. In detail, suppressing autophagy increases METH toxicity, while stimulating autophagy prevents METH-induced toxicity in cell cultures. In the present study, the role of autophagy was investigated in vivo. In the whole brain, METH alone destroys meso-striatal DA axon terminals, while fairly sparing DA cell bodies within substantia nigra pars compacta (SNpc). No damage to either cell bodies or axons from ventral tegmental area (VTA) is currently documented. According to the hypothesis that ongoing autophagy prevents METH-induced DA toxicity, we tested whether systemic injection of autophagy inhibitors such as asparagine (ASN, 1000 mg/Kg) or glutamine (GLN, 1000 mg/Kg), may extend METH toxicity to DA cell bodies, both within SNpc and VTA, where autophagy was found to be inhibited. When METH (5 mg/Kg × 4, 2 h apart) was administered to C57Bl/6 mice following ASN or GLN, a frank loss of cell bodies takes place within SNpc and a loss of both axons and cell bodies of VTA neurons is documented. These data indicate that, ongoing autophagy protects DA neurons and determines the refractoriness of cell bodies to METH-induced toxicity. Full article
(This article belongs to the Special Issue Stress, Neurotransmitters and Neurodegeneration)
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