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Biomolecules
Special Issues
Converging Pathophysiologies of Psychiatric and Neurodegenerative Disorders
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Converging Pathophysiologies of Psychiatric and Neurodegenerative Disorders

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 January 2021) | Viewed by 8097

Special Issue Editors

Prof. Dr. Giulio Pasinetti

E-Mail Website
Guest Editor
Icahn School of Medicine at Mount Sinai, New York, NY, USA
Interests: inflammation; inflammasome; beta-amyloid; Tau; microglia; apoptosis; caspase; Alzheimer’s disease; Parkinson’s disease; amyotrophic lateral sclerosis; frontotemporal dementia; traumatic brain injury; polyphenols; bioavailability; drug discovery
Special Issues, Collections and Topics in MDPI journals
Dr. Kyle J. Trageser

E-Mail Website
Guest Editor
Icahn School of Medicine at Mount Sinai, New York, NY, USA
Interests: inflammation; inflammasome; microglia; neurodegeneration; amyotrophic lateral sclerosis; frontotemporal dementia; Alzheimer’s Disease; drug discovery

Special Issue Information

Dear Colleagues,

Commonalities in the etiopathogenesis of psychiatric and neurodegenerative disorders have become of interest both in determining the driving mechanisms of these varied diseases, as well as for the creation of new therapeutic strategies. Projections of the incidence of neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, amyotrophic lateral sclerosis, and Huntington’s disease, suggest that 1 in 5 adults over the age of 65 will be affected by 2030, as the population ages. Furthermore, as of 2018, 1 in 5 adults experienced a psychiatric disorder. Neuroinflammation has been shown among a wide range of mood disorders, personality disorders, as well as neurodegenerative diseases. The elevation of pro-inflammatory markers has been demonstrated in vivo through a variety of animal models and human studies both peripherally, as well as in the central nervous system. Morphological changes including synaptic dysfunction and glial activation and proliferation are also present across these disorders. The physiological impacts of chronic stress may additionally contribute to these inflammatory and morphological changes. Newly designed therapeutics and treatment strategies may leverage these commonalities.

For this Special Issue of Biomolecules, "Converging Pathophysiologies of Psychiatric and Neurodegenerative Disorders”, the submission of review and primary research articles considering the nexus of pathologies in these disorders, with an emphasis on mechanisms, biomarkers, and treatments is encouraged.

Dr. Giulio Pasinetti
Dr. Kyle J. Trageser
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. Biomolecules 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 2700 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

  • neuroinflammation
  • neurodegeneration
  • Alzheimer’s Disease
  • Parkinson’s Disease
  • microglia
  • inflammation
  • synaptic plasticity

Published Papers (2 papers)

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Research

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15 pages, 1516 KiB  
Article
Contactin-1 Is Reduced in Cerebrospinal Fluid of Parkinson’s Disease Patients and Is Present within Lewy Bodies
by Madhurima Chatterjee, Inger van Steenoven, Evelien Huisman, Linda Oosterveld, Henk Berendse, Wiesje M. van der Flier, Marta Del Campo, Afina W. Lemstra, Wilma D. J. van de Berg and Charlotte E. Teunissen
Biomolecules 2020, 10(8), 1177; https://doi.org/10.3390/biom10081177 - 12 Aug 2020
Cited by 12 | Viewed by 3201
Abstract
Synaptic degeneration is an early phenomenon in Parkinson’s disease (PD) pathogenesis. We aimed to investigate whether levels of synaptic proteins contactin-1 and contactin-2 in cerebrospinal fluid (CSF) of PD patients are reduced compared to dementia with Lewy bodies (DLB) patients and controls and [...] Read more.
Synaptic degeneration is an early phenomenon in Parkinson’s disease (PD) pathogenesis. We aimed to investigate whether levels of synaptic proteins contactin-1 and contactin-2 in cerebrospinal fluid (CSF) of PD patients are reduced compared to dementia with Lewy bodies (DLB) patients and controls and to evaluate their relationship with α-synuclein aggregation. Contactin-1 and -2 were measured in CSF from PD patients (n = 58), DLB patients (n = 72) and age-matched controls (n = 90). Contactin concentration differences between diagnostic groups were assessed by general linear models adjusted for age and sex. Contactin immunoreactivity was characterized in postmortem substantia nigra, hippocampus and entorhinal cortex tissue of PD patients (n = 4) and controls (n = 4), and its relation to α-syn aggregation was evaluated using confocal laser scanning microscopy. Contactin-1 levels were lower in PD patients (42 (36–49) pg/mL) compared to controls (52 (44–58) pg/mL, p = 0.003) and DLB patients (56 (46–67) pg/mL, p = 0.001). Contactin-2 levels were similar across all diagnostic groups. Within the PD patient group, contactin-1 correlated with t-α-syn, tTau and pTau (r = 0.30–0.50, p < 0.05), whereas contactin-2 only correlated with t-α-syn (r = 0.34, p = 0.03). Contactin-1 and -2 were observed within nigral and cortical Lewy bodies and clustered within bulgy Lewy neurites in PD brains. A decrease in CSF contactin-1 may reflect synaptic degeneration underlying Lewy body pathology in PD. Full article
(This article belongs to the Special Issue Converging Pathophysiologies of Psychiatric and Neurodegenerative Disorders)
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Review

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9 pages, 569 KiB  
Review
SIRT1 and SIRT2 Modulators: Potential Anti-Inflammatory Treatment for Depression?
by Yuqing Zhang, Shailendra Anoopkumar-Dukie and Andrew Keith Davey
Biomolecules 2021, 11(3), 353; https://doi.org/10.3390/biom11030353 - 25 Feb 2021
Cited by 14 | Viewed by 3872
Abstract
Depression is a psychiatric disorder that has a significant health burden on patients and their families. Unfortunately, the current antidepressant medications that mainly target monoamine neurotransmitters have limited efficacy. Recent evidence has indicated that neuroinflammation participates in the genesis and development of depression, [...] Read more.
Depression is a psychiatric disorder that has a significant health burden on patients and their families. Unfortunately, the current antidepressant medications that mainly target monoamine neurotransmitters have limited efficacy. Recent evidence has indicated that neuroinflammation participates in the genesis and development of depression, and interacts with other factors involved in depression. Therefore, exploring effective anti-inflammatory medications could be beneficial for the development of new treatment options for depression. Sirtuins are a unique class of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases, which have seven members that can affect multiple downstream targets by deacetylation activity. Among these seven members, SIRT1 and SIRT2 have been shown to participate in the pathophysiology of inflammation in numerous studies. Thus, in this short article, we review the association of SIRT1 and SIRT2 activity and depression, and evidence of the effects of SIRT1 and SIRT2 modulators on inflammation in vitro and depressive-like behaviours in vivo. Full article
(This article belongs to the Special Issue Converging Pathophysiologies of Psychiatric and Neurodegenerative Disorders)
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