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The Complex Link between Inflammation and Depression

A special issue of Applied Sciences (ISSN 2076-3417). This special issue belongs to the section "Applied Biosciences and Bioengineering".

Deadline for manuscript submissions: closed (20 August 2022) | Viewed by 3716

Special Issue Editor


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Guest Editor
Department of Epidemiology and Prevention, Istituto Neurologico Mediterraneo IRCCS Neuromed, 86077 Pozzilli, Italy
Interests: molecular psychiatry; statistical genetics; biostatistics; data science

Special Issue Information

Dear Colleagues,

Depression is one of the most prevalent disorders worldwide, representing a heavy medical and social burden for many welfare systems. There are several forms of depression, ranging from mild to severe, based on the psychological domains impaired and on how much it affects every-day life. Major depressive disorder (MDD) represents the most severe stage in this range, with many milder and subclinical forms going undetected, especially in population strata with lower socioeconomic status and reduced access to healthcare service. Depression is comorbid with a number of chronic health conditions, such as cardiovascular disease (CVD), cancer, and diabetes, alongside a number of neuropsychiatric disorders. Depression represents a risk factor for these conditions, although in most cases it may be also a consequence. Moreover, depression often represents one of the first symptoms of common neurodegenerative disorders like Alzheimer’s and Parkinson’s disease. Common biological pathways like low-grade inflammation have been suggested to be at the basis of these links, and to be one of the pathological mechanisms acting in depression. However, many open questions remain in this field, and some aspects of the disease are still scarcely investigated. These include:

  • The directionality of the relation between psychological health and inflammation, which remains unclear: while some data support the hypothesis that inflammation predisposes to depression, others suggest the opposite or even a bi-directional effect between depression and inflammation;
  • A fine-grained picture of the relation between inflammation and specific depressive domains;
  • The influence of lifestyle (e.g., nutrition) and other environmental exposures (e.g., pollution) on the link between depression and inflammation;
  • The contribution of inflammation to treatment-resistant forms of depression and the effect of anti-depressant drugs on inflammatory response;
  • The role of different biomarkers of low-grade inflammation in explaining the link between depression and chronic conditions like CVD, cancer, and type 2 diabetes;
  • The long-hypothesized but yet unclear link between depression and platelets, which represent a sort of “circulating neurons”;
  • The mechanisms which may explain why depression occurs in the prodromal phase of common neurodegenerative disorders;
  • The role of inflammation in psychiatric comorbidities of depression and related traits, such as bipolar disorder, anxiety, suicidality, schizophrenia, and attention deficit hyperactivity disorder (ADHD).

Epidemiological, functional, and genetic/genomic studies attempting to clarify one or more of these aspects are invited to contribute to this Special Issue. Moreover, studies investigating measures and domains related to both depression and inflammation (e.g., association with frailty measures, cognitive performance, or other mental health scales like psychological resilience and quality of life) will be also taken into consideration. Studies using machine learning techniques and bioinformatic tools will be considered a plus, such as those investigating these relations in different ethnicities/ancestries, specific population strata (e.g., elders), or analyzing gender-specific aspects. Reviews on any of the abovementioned topics are also welcome.

Dr. Alessandro Gialluisi
Guest Editor

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. Applied Sciences is an international peer-reviewed open access semimonthly 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 2400 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

  • inflammation
  • depression
  • major depressive disorder
  • depressive symptoms
  • neuropsychiatric disorders
  • neurodegenerative disorders
  • cardiovascular disease
  • diabetes
  • cancer
  • aging
  • gender
  • Parkinson’s disease
  • Alzheimer’s disease
  • anxiety
  • bipolar disorder
  • blood platelets

Published Papers (2 papers)

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18 pages, 1215 KiB  
Article
The Association of Preoperative Depression, and C-Reactive Protein Levels with a Postoperative Length of Stay in Patients Undergoing Coronary Artery Bypass Grafting
by Stjepan Ivankovic, Vedran Coric, Frane Paic, Alma Mihaljevic Peles, Tomo Svagusa, Viktor Kalamar, Mate Petricevic and Bojan Biocina
Appl. Sci. 2022, 12(20), 10201; https://doi.org/10.3390/app122010201 - 11 Oct 2022
Cited by 1 | Viewed by 1377
Abstract
This study aimed to explore the role of preoperative and postoperative C-reactive protein (CRP) levels in mediating the association between the preoperative depression symptoms and postoperative length of stay in patients undergoing coronary artery bypass grafting (CABG). Preoperative depression symptoms of 212 elective [...] Read more.
This study aimed to explore the role of preoperative and postoperative C-reactive protein (CRP) levels in mediating the association between the preoperative depression symptoms and postoperative length of stay in patients undergoing coronary artery bypass grafting (CABG). Preoperative depression symptoms of 212 elective CABG patients were measured using the Beck Depression Inventory (BDI-II). The patient’s demographic and clinical parameters were collected from medical records prior to surgery. Patients were followed up during their in-hospital stay to measure early (1–3 days post-surgery) and persistent (4–6 days post-surgery) CRP response to CABG surgery. The higher persistent CRP response was significantly (p < 0.001) associated with a longer postoperative hospital stay. The binary logistic regression analysis confirmed the association of persistent CRP change with prolonged hospital stay (OR = 1.017, 95% CI = 1.005–1.029, p = 0.009). However, when the gender subgroups were analyzed separately, that remained significant (OR = 1.016, 95% CI = 1.004–1.028, p = 0.005) only for the male subgroup. There was no significant association between elevated BDI-II depression scores and longer postoperative hospital stay. Additionally, no significant influence of BDI-II scores on preoperative or postoperative CRP levels, or vice versa, was detected. Further work is needed to explore the extent and pathways through which depression might influence the postoperative recovery of CABG patients. Full article
(This article belongs to the Special Issue The Complex Link between Inflammation and Depression)
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12 pages, 6639 KiB  
Brief Report
Genomic Overlap between Platelet Parameters Variability and Age at Onset of Parkinson Disease
by Alfonsina Tirozzi, Roberta Parisi, Chiara Cerletti, Maria Benedetta Donati, Giovanni de Gaetano, Licia Iacoviello and Alessandro Gialluisi
Appl. Sci. 2021, 11(15), 6927; https://doi.org/10.3390/app11156927 - 28 Jul 2021
Cited by 5 | Viewed by 1489
Abstract
With the increasing burden of common neurodegenerative disorders and their long-hypothesized link with platelet biology, genomic approaches have been recently used to investigate the presence of a shared genetic basis between neurodegenerative risk and platelet parameters, reporting a significant though moderate genetic correlation [...] Read more.
With the increasing burden of common neurodegenerative disorders and their long-hypothesized link with platelet biology, genomic approaches have been recently used to investigate the presence of a shared genetic basis between neurodegenerative risk and platelet parameters, reporting a significant though moderate genetic correlation between Parkinson Disease (PD) risk and platelet distribution width, an index of platelet size variability. Here, we investigated the genetic overlap of platelet parameters with an endophenotype of PD, age-at-onset (PD-AAO). First, we applied a Linkage Disequilibrium (LD)-score regression to the summary statistics of a large independent Genome Wide Association Study (GWAS) previously conducted, to estimate the co-heritability based on common genetic variants. Then, we analyzed multitrait single-variant associations to identify novel loci associated with both PD-AAO and mean platelet volume (MPV). Finally, we performed gene and gene-set enrichment analyses of these associations. We observed a statistically significant genetic correlation between MPV and PD-AAO (rg (SE) = −0.215 (0.082); p = 0.009). The multitrait analysis revealed eight novel variants associated with PD-AAO and 33 with MPV. The genes most significantly enriched for associations with PD-AAO included ARHGEF3 (Rho Guanine Nucleotide Exchange Factor 3), previously associated with depression, and KALRN (Kalirin RhoGEF Kinase), encoding a PINK1 interactor previously implicated in schizophrenia, Alzheimer Disease and PD itself. Interestingly, these genes were also identified in the analysis of MPV. The most significant gene-set enrichments shared between MPV and PD-AAO were observed for coagulation- and megakaryopoiesis-related pathways. These findings provide novel hints into the common genetic basis of PD endophenotypes, platelet biology and its neuropsychiatric comorbidities, paving the way for investigating common underlying mechanisms. Full article
(This article belongs to the Special Issue The Complex Link between Inflammation and Depression)
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