Neuro-immune crosstalk in depressive symptoms of multiple sclerosis

Depressive disorders can occur in up to 50% of people with multiple sclerosis in their lifetime. If left untreated, comorbid major depressive disorders may not spontaneously remit and is associated with an increased morbidity and mortality. Conversely, epidemiological evidence supports increased psy...

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Vydané v:Neurobiology of disease Ročník 177; s. 106005
Hlavní autori: Wang, Chao, Zhou, Yulin, Feinstein, Anthony
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States Elsevier Inc 01.02.2023
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Abstract Depressive disorders can occur in up to 50% of people with multiple sclerosis in their lifetime. If left untreated, comorbid major depressive disorders may not spontaneously remit and is associated with an increased morbidity and mortality. Conversely, epidemiological evidence supports increased psychiatric visit as a significant prodromal event prior to diagnosis of MS. Are there common molecular pathways that contribute to the co-development of MS and psychiatric illnesses? We discuss immune cells that are dysregulated in MS and how such dysregulation can induce or protect against depressive symptoms. This is not meant to be a comprehensive review of all molecular pathways but rather a framework to guide future investigations of immune responses in depressed versus euthymic people with MS. Currently, there is weak evidence supporting the use of antidepressant medication in comorbid MS patients. It is our hope that by better understanding the neuroimmune crosstalk in the context of depression in MS, we can enhance the potential for future therapeutic options. •People with MS are 2–3 times more likely to develop MDD compared to the general popualtion.•Depression and MS share certain key immune system changes,•There is equivocal evidence supporting the effectiveness of antidepressant medication in MS-related depression.•Selected Disease Modifying Therapies may improve depression in people with MS.
AbstractList Depressive disorders can occur in up to 50% of people with multiple sclerosis in their lifetime. If left untreated, comorbid major depressive disorders may not spontaneously remit and is associated with an increased morbidity and mortality. Conversely, epidemiological evidence supports increased psychiatric visit as a significant prodromal event prior to diagnosis of MS. Are there common molecular pathways that contribute to the co-development of MS and psychiatric illnesses? We discuss immune cells that are dysregulated in MS and how such dysregulation can induce or protect against depressive symptoms. This is not meant to be a comprehensive review of all molecular pathways but rather a framework to guide future investigations of immune responses in depressed versus euthymic people with MS. Currently, there is weak evidence supporting the use of antidepressant medication in comorbid MS patients. It is our hope that by better understanding the neuroimmune crosstalk in the context of depression in MS, we can enhance the potential for future therapeutic options.
Depressive disorders can occur in up to 50% of people with multiple sclerosis in their lifetime. If left untreated, comorbid major depressive disorders may not spontaneously remit and is associated with an increased morbidity and mortality. Conversely, epidemiological evidence supports increased psychiatric visit as a significant prodromal event prior to diagnosis of MS. Are there common molecular pathways that contribute to the co-development of MS and psychiatric illnesses? We discuss immune cells that are dysregulated in MS and how such dysregulation can induce or protect against depressive symptoms. This is not meant to be a comprehensive review of all molecular pathways but rather a framework to guide future investigations of immune responses in depressed versus euthymic people with MS. Currently, there is weak evidence supporting the use of antidepressant medication in comorbid MS patients. It is our hope that by better understanding the neuroimmune crosstalk in the context of depression in MS, we can enhance the potential for future therapeutic options. •People with MS are 2–3 times more likely to develop MDD compared to the general popualtion.•Depression and MS share certain key immune system changes,•There is equivocal evidence supporting the effectiveness of antidepressant medication in MS-related depression.•Selected Disease Modifying Therapies may improve depression in people with MS.
Depressive disorders can occur in up to 50% of people with multiple sclerosis in their lifetime. If left untreated, comorbid major depressive disorders may not spontaneously remit and is associated with an increased morbidity and mortality. Conversely, epidemiological evidence supports increased psychiatric visit as a significant prodromal event prior to diagnosis of MS. Are there common molecular pathways that contribute to the co-development of MS and psychiatric illnesses? We discuss immune cells that are dysregulated in MS and how such dysregulation can induce or protect against depressive symptoms. This is not meant to be a comprehensive review of all molecular pathways but rather a framework to guide future investigations of immune responses in depressed versus euthymic people with MS. Currently, there is weak evidence supporting the use of antidepressant medication in comorbid MS patients. It is our hope that by better understanding the neuroimmune crosstalk in the context of depression in MS, we can enhance the potential for future therapeutic options.Depressive disorders can occur in up to 50% of people with multiple sclerosis in their lifetime. If left untreated, comorbid major depressive disorders may not spontaneously remit and is associated with an increased morbidity and mortality. Conversely, epidemiological evidence supports increased psychiatric visit as a significant prodromal event prior to diagnosis of MS. Are there common molecular pathways that contribute to the co-development of MS and psychiatric illnesses? We discuss immune cells that are dysregulated in MS and how such dysregulation can induce or protect against depressive symptoms. This is not meant to be a comprehensive review of all molecular pathways but rather a framework to guide future investigations of immune responses in depressed versus euthymic people with MS. Currently, there is weak evidence supporting the use of antidepressant medication in comorbid MS patients. It is our hope that by better understanding the neuroimmune crosstalk in the context of depression in MS, we can enhance the potential for future therapeutic options.
ArticleNumber 106005
Author Wang, Chao
Zhou, Yulin
Feinstein, Anthony
Author_xml – sequence: 1
  givenname: Chao
  surname: Wang
  fullname: Wang, Chao
  organization: Biological Sciences Platform, Sunnybrook Research Institute, Toronto, ON, Canada
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  givenname: Yulin
  surname: Zhou
  fullname: Zhou, Yulin
  organization: Biological Sciences Platform, Sunnybrook Research Institute, Toronto, ON, Canada
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  givenname: Anthony
  surname: Feinstein
  fullname: Feinstein, Anthony
  email: ant.feinstein@utoronto.ca
  organization: Department of Psychiatry, Sunnybrook Health Sciences Centre and University of Toronto, Toronto, ON, Canada
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Keywords Depression
Multiple sclerosis
Neuroimmune crosstalk
Adaptive and innate immune responses
Comorbidity
Demyelination
Language English
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Snippet Depressive disorders can occur in up to 50% of people with multiple sclerosis in their lifetime. If left untreated, comorbid major depressive disorders may not...
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SubjectTerms Adaptive and innate immune responses
Antidepressive Agents - therapeutic use
Comorbidity
Demyelination
Depression
Depressive Disorder, Major - drug therapy
Depressive Disorder, Major - epidemiology
Depressive Disorder, Major - psychology
Humans
Multiple sclerosis
Multiple Sclerosis - complications
Multiple Sclerosis - drug therapy
Neuroimmune crosstalk
Title Neuro-immune crosstalk in depressive symptoms of multiple sclerosis
URI https://www.clinicalkey.com/#!/content/1-s2.0-S0969996123000190
https://dx.doi.org/10.1016/j.nbd.2023.106005
https://www.ncbi.nlm.nih.gov/pubmed/36680805
https://www.proquest.com/docview/2768240218
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Volume 177
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