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Neuropathological Advances in Brain Disorders from MNS2023

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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 10201

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Special Issue Editors

Prof. Dr. Giuseppe Di Giovanni

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1. Department of Physiology & Biochemistry, Faculty of Medicine and Surgery, University of Malta, Msida, Malta
2. Neuroscience Division, School of Biosciences, Cardiff University, Cardiff, UK
Interests: serotonin; GABA; dopamine; epilepsy; addiction; mood disorders; electrophysiology; habenula; basal ganglia; serotonin2 receptors
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Prof. Dr. Goran Šimić

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Department of Neuroscience, Croatian Institute for Brain Research, University of Zagreb School of Medicine, Šalata 12, HR-10000 Zagreb, Croatia
Interests: chemical neuroanatomy; Alzheimer's disease; tauopathies; spinal muscular atrophy; aging mechanisms

Special Issue Information

Dear Colleagues,

This Special Issue, to be published in IJMS, will comprise some of the best papers presented at the most recent Mediterranean Conference of Neuroscience, held in Dubrovnik, Croatia, in 2022. The Mediterranean Neuroscience Society Meetings provide a forum to discuss modern experimental and interdisciplinary approaches that have led to important novel insights into the pathogenesis and treatment of human central and peripheral nervous system diseases, and to explore new avenues for understanding the brain. This SI will showcase the latest developments in the research in this field, conducted by MNS researchers.

This Special Issue "Bioactive Lipids and Cannabinoids, Key Players in Neuropsychiatric Disorders and Beyond" is co-hosted by Molecules Special Issue.

Prof. Dr. Giuseppe Di Giovanni
Prof. Dr. Goran Šimić
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.

Published Papers (4 papers)

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11 pages, 12787 KiB

Open AccessArticle

Differential Serotonergic Modulation of Synaptic Inputs to the Olfactory Cortex

by Ildikó Piszár and Magor L. Lőrincz

Int. J. Mol. Sci. 2023, 24(3), 1950; https://doi.org/10.3390/ijms24031950 - 19 Jan 2023

Viewed by 1495

Abstract

Serotonin (5-hydroxytriptamine, 5-HT) is an important monoaminergic neuromodulator involved in a variety of physiological and pathological functions. It has been implicated in the regulation of sensory functions at various stages of multiple modalities, but its mechanisms and functions in the olfactory system have remained elusive. Combining electrophysiology, optogenetics and pharmacology, here we show that afferent (feed-forward) pathway-evoked synaptic responses are boosted, whereas feedback responses are suppressed by presynaptic 5-HT_1B receptors in the anterior piriform cortex (aPC) in vitro. Blocking 5-HT_1B receptors also reduces the suppressive effects of serotonergic photostimulation of baseline firing in vivo. We suggest that by regulating the relative weights of synaptic inputs to aPC, 5-HT finely tunes sensory inputs in the olfactory cortex. Full article

(This article belongs to the Special Issue Neuropathological Advances in Brain Disorders from MNS2023)

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28 pages, 4619 KiB

Open AccessArticle

Heavy Metals and Essential Metals Are Associated with Cerebrospinal Fluid Biomarkers of Alzheimer’s Disease

by Mirjana Babić Leko, Matej Mihelčić, Jasna Jurasović, Matea Nikolac Perković, Ena Španić, Ankica Sekovanić, Tatjana Orct, Klara Zubčić, Lea Langer Horvat, Nikolina Pleić, Spomenka Kiđemet-Piskač, Željka Vogrinc, Nela Pivac, Andrea Diana, Fran Borovečki, Patrick R. Hof and Goran Šimić

Int. J. Mol. Sci. 2023, 24(1), 467; https://doi.org/10.3390/ijms24010467 - 27 Dec 2022

Cited by 10 | Viewed by 3246

Abstract

Various metals have been associated with the pathogenesis of Alzheimer’s disease (AD), principally heavy metals that are environmental pollutants (such as As, Cd, Hg, and Pb) and essential metals whose homeostasis is disturbed in AD (such as Cu, Fe, and Zn). Although there is evidence of the involvement of these metals in AD, further research is needed on their mechanisms of toxicity. To further assess the involvement of heavy and essential metals in AD pathogenesis, we compared cerebrospinal fluid (CSF) AD biomarkers to macro- and microelements measured in CSF and plasma. We tested if macro- and microelements’ concentrations (heavy metals (As, Cd, Hg, Ni, Pb, and Tl), essential metals (Na, Mg, K, Ca, Fe, Co, Mn, Cu, Zn, and Mo), essential non-metals (B, P, S, and Se), and other non-essential metals (Al, Ba, Li, and Sr)) are associated with CSF AD biomarkers that reflect pathological changes in the AD brain (amyloid β_1–42, total tau, phosphorylated tau isoforms, NFL, S100B, VILIP-1, YKL-40, PAPP-A, and albumin). We used inductively coupled plasma mass spectroscopy (ICP-MS) to determine macro- and microelements in CSF and plasma, and enzyme-linked immunosorbent assays (ELISA) to determine protein biomarkers of AD in CSF. This study included 193 participants (124 with AD, 50 with mild cognitive impairment, and 19 healthy controls). Simple correlation, as well as machine learning algorithms (redescription mining and principal component analysis (PCA)), demonstrated that levels of heavy metals (As, Cd, Hg, Ni, Pb, and Tl), essential metals (Ca, Co, Cu, Fe, Mg, Mn, Mo, Na, K, and Zn), and essential non-metals (P, S, and Se) are positively associated with CSF phosphorylated tau isoforms, VILIP-1, S100B, NFL, and YKL-40 in AD. Full article

(This article belongs to the Special Issue Neuropathological Advances in Brain Disorders from MNS2023)

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22 pages, 3573 KiB

Open AccessArticle

The Hippocampal Response to Acute Corticosterone Elevation Is Altered in a Mouse Model for Angelman Syndrome

by Eva M. G. Viho, A. Mattijs Punt, Ben Distel, René Houtman, Jan Kroon, Ype Elgersma and Onno C. Meijer

Int. J. Mol. Sci. 2023, 24(1), 303; https://doi.org/10.3390/ijms24010303 - 24 Dec 2022

Cited by 3 | Viewed by 1954

Abstract

Angelman Syndrome (AS) is a severe neurodevelopmental disorder, caused by the neuronal absence of the ubiquitin protein ligase E3A (UBE3A). UBE3A promotes ubiquitin-mediated protein degradation and functions as a transcriptional coregulator of nuclear hormone receptors, including the glucocorticoid receptor (GR). Previous studies showed anxiety-like behavior and hippocampal-dependent memory disturbances in AS mouse models. Hippocampal GR is an important regulator of the stress response and memory formation, and we therefore investigated whether the absence of UBE3A in AS mice disrupted GR signaling in the hippocampus. We first established a strong cortisol-dependent interaction between the GR ligand binding domain and a UBE3A nuclear receptor box in a high-throughput interaction screen. In vivo, we found that UBE3A-deficient AS mice displayed significantly more variation in circulating corticosterone levels throughout the day compared to wildtypes (WT), with low to undetectable levels of corticosterone at the trough of the circadian cycle. Additionally, we observed an enhanced transcriptomic response in the AS hippocampus following acute corticosterone treatment. Surprisingly, chronic corticosterone treatment showed less contrast between AS and WT mice in the hippocampus and liver transcriptomic responses. This suggests that UBE3A limits the acute stimulation of GR signaling, likely as a member of the GR transcriptional complex. Altogether, these data indicate that AS mice are more sensitive to acute glucocorticoid exposure in the brain compared to WT mice. This suggests that stress responsiveness is altered in AS which could lead to anxiety symptoms. Full article

(This article belongs to the Special Issue Neuropathological Advances in Brain Disorders from MNS2023)

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19 pages, 4613 KiB

Open AccessArticle

Reorganization of the Brain Extracellular Matrix in Hippocampal Sclerosis

by Barbara Sitaš, Mihaela Bobić-Rasonja, Goran Mrak, Sara Trnski, Magdalena Krbot Skorić, Darko Orešković, Vinka Knezović, Željka Petelin Gadže, Zdravko Petanjek, Goran Šimić, Danijela Kolenc and Nataša Jovanov Milošević

Int. J. Mol. Sci. 2022, 23(15), 8197; https://doi.org/10.3390/ijms23158197 - 25 Jul 2022

Cited by 4 | Viewed by 2340

Abstract

The extracellular matrix (ECM) is an important regulator of excitability and synaptic plasticity, especially in its highly condensed form, the perineuronal nets (PNN). In patients with drug-resistant mesial temporal lobe epilepsy (MTLE), hippocampal sclerosis type 1 (HS1) is the most common histopathological finding. This study aimed to evaluate the ECM profile of HS1 in surgically treated drug-resistant patients with MTLE in correlation to clinical findings. Hippocampal sections were immunohistochemically stained for aggrecan, neurocan, versican, chondroitin-sulfate (CS56), fibronectin, Wisteria floribunda agglutinin (WFA), a nuclear neuronal marker (NeuN), parvalbumin (PV), and glial-fibrillary-acidic-protein (GFAP). In HS1, besides the reduced number of neurons and astrogliosis, we found a significantly changed expression pattern of versican, neurocan, aggrecan, WFA-specific glycosylation, and a reduced number of PNNs. Patients with a lower number of epileptic episodes had a less intense diffuse WFA staining in Cornu Ammonis (CA) fields. Our findings suggest that PNN reduction, changed ECM protein, and glycosylation expression pattern in HS1 might be involved in the pathogenesis and persistence of drug-resistant MTLE by contributing to the increase of CA pyramidal neurons’ excitability. This research corroborates the validity of ECM molecules and their modulators as a potential target for the development of new therapeutic approaches to drug-resistant epilepsy. Full article

(This article belongs to the Special Issue Neuropathological Advances in Brain Disorders from MNS2023)

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