The determination of neuroimmunopsychology in psychiatric pathology
Keywords:
Immune system, Depressive disorder, Bipolar disorder, Schizophrenia, Anxiety disorder, Autoimmune, InflammationAbstract
The immune system and central nervous system interact in a process called Neuroimmunopsychia
which is essential for mental health and brain function. This interaction occurs through multiple
pathways, such as humoral, neural, and cellular communication.
Various elements, such as corticosteroids, TH17 cells, cytokines, the complement system,
microglial cells, the blood-brain barrier and the intestinal microbiota, play a significant role in
this interaction. Dysfunction in any of these components can contribute to the development of
neuropsychiatric disorders, such as schizophrenia, autism spectrum disorder, depression, and
Alzheimer’s disease.
Neuroimmunopsychia also has a crucial role in neurological and organic diseases.
Neurodegenerative disorders such as Alzheimer’s disease, multiple sclerosis and Parkinson’s
show neuroinflammation and the involvement of immune cells, such as microglia. Diseases such
as autoimmune encephalitis, epilepsy and their neurobehavioral comorbidities are also linked to
inflammation and immune response. In addition, peripheral tumors can affect the central nervous
system and cause cognitive and affective symptoms, while diseases such as systemic lupus
erythematosus, myasthenia gravis and locked-in syndrome also involve an interaction between
neuroinflammation and the immune system.
Neuroimmunopsychia also plays an important role in bipolar disorder, depressive disorders, and
psychotic disorders. In bipolar disorder, alterations in endolysosomal and autophagy pathways, as
well as in the ubiquitin-proteasome system, have been identified. These pathways are involved in
regulating protein quality and flow, and dysfunction in them has been observed in mood disorders
and neurodegenerative diseases.
In the case of major depressive disorder, the implications of various cytokines on the disease have
been studied, as well as chronic low-grade inflammation and imbalance in pro-inflammatory and
anti-inflammatory responses. The neuroimmunopsyche in these disorders can influence brain
function and contribute to symptoms.
Research has revealed an increasingly obvious connection between psychiatric disorders and
the immune system. The presence of inflammatory mechanisms is relevant in disorders such
as depression, Post-Traumatic Stress Disorder (PTSD), anxiety disorders, addiction and Autism
Spectrum Disorder (ASD), among others.
Systemic inflammation can affect the activity of key neurotransmitters, such as serotonin, and
hormonal changes can contribute to the onset of postpartum mood disorders. Treatments aimed
at reducing inflammation, such as antidepressants and Selective Serotonin Reuptake Inhibitors
(SSRIs), have shown benefits in these disorders. In addition, neuroimmunopsychia may play a role
in addiction and ASD, with inflammation affecting reward processes and neuronal function.
COVID-19 infection has also sparked growing interest in its impact on mental health and the
interaction between the immune system and neuropsychiatric disorders. The SARS-CoV-2 virus
can invade the central nervous system, triggering an inflammatory response in the brain and
contributing to neuroinflammation. This may be related to the development of psychiatric illnesses
such as major depressive disorder, psychosis, and cognitive impairment.
Oxidative stress, another factor implicated in the pathogenesis of COVID-19, can also affect brain
function and neuroinflammation. Obsessive Compulsive Disorder-OCD, related to COVID-19, has
also been studied in relation to neuroimmunopsychics.
In terms of diagnosis and treatment, biomarkers and the use of drugs with anti-inflammatory
properties have been investigated. Inflammatory markers have been associated with psychotic
disorders and depression, and biomarkers such as detection of my RNA and neutrophil-lymphocyte
ratio have been proposed. Psychotropic drugs and neuromodulation therapies have shown anti-
inflammatory effects and benefits on symptoms. In addition, non-pharmacological approaches
such as environmental enrichment and practices such as yoga and meditation have been shown
to reduce levels of pro-inflammatory cytokines and improve symptoms of psychiatric disorders.
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about the role of corticosteroids in psychiatric disorders; evidence from animal and clinical studies. J Psychiatr Res. noviembre de 2022;155:363–70. 59.de Bartolomeis A, Barone A, Vellucci L, Mazza B, Austin MC, Iasevoli F, et al. Linking Inflammation, Aberrant Glutamate-Dopamine Interaction, and Post-synaptic Changes: Translational Relevance for Schizophrenia and Antipsychotic Treatment: a Systematic Review. Mol Neurobiol. el 13 de octubre de 2022;59(10):6460–501. 60.Parker SE, Bellingham MC, Woodruff TM. Complement drives circuit modulation in the adult brain. Prog Neurobiol. julio de 2022;214:102282. 61.Reale M, Costantini E, Greig NH. Cytokine Imbalance in Schizophrenia. From Research to Clinic: Potential Implications for Treatment. Front Psychiatry. el 5 de marzo de 2021;12. 62.Chen Z, Huang Y, Wang B, Peng H, Wang X, Wu H, et al. T cells: an emerging cast of roles in bipolar disorder. Transl Psychiatry. el 8 de mayo de 2023;13(1):153. 63.Yeung SSH, Ho YS, Chang RCC. The role of meningeal populations of type II innate lymphoid cells in modulating neuroinflammation in neurodegenerative diseases. Exp Mol Med. el 6 de septiembre de 2021;53(9):1251–67. 64.Borovcanin MM, Vesic K. Breast cancer in schizophrenia could be interleukin-33-mediated. World J Psychiatry. el 19 de noviembre de 2021;11(11):1065–74. 65.Miljevic C, Munjiza-Jovanovic A, Jovanovic T. Impact of Childhood Adversity, as Early Life Distress, on Cytokine Alterations in Schizophrenia. Neuropsychiatr Dis Treat. marzo de 2023;Volume 19:579–86. 66.Harsanyi S, Kupcova I, Danisovic L, Klein M. Selected Biomarkers of Depression: What Are the Effects of Cytokines and Inflammation? Int J Mol Sci. el 29 de diciembre de 2022;24(1):578. 67.Misiak B, Bartoli F, Carrà G, Stańczykiewicz B, Gładka A, Frydecka D, et al. Immune-inflammatory markers and psychosis risk: A systematic review and meta-analysis. Psychoneuroendocrinology. mayo de 2021;127:105200. 68.Welcome MO. Cellular mechanisms and molecular signaling pathways in stress-induced anxiety, depression, and blood–brain barrier inflammation and leakage. Inflammopharmacology. el 24 de junio de 2020;28(3):643–65. 69.Matutino Santos P, Pereira Campos G, Nascimento C. Endo-Lysosomal and Autophagy Pathway and Ubiquitin-Proteasome System in Mood Disorders: A Review Article. Neuropsychiatr Dis Treat. enero de 2023;Volume 19:133–51. 70.Endres D, Maier V, Leypoldt F, Wandinger KP, Lennox B, Pollak TA, et al. Autoantibody-associated psychiatric syndromes: a systematic literature review resulting in 145 cases. Psychol Med. el 7 de abril de 2022;52(6):1135–46. 71.Theoharides TC, Kavalioti M, Tsilioni I. Mast Cells, Stress, Fear and Autism Spectrum Disorder. Int J Mol Sci. el 24 de julio de 2019;20(15):3611. 72.Patlola SR, Donohoe G, McKernan DP. Anti-inflammatory effects of 2nd generation antipsychotics in patients with schizophrenia: A systematic review and meta-analysis. J Psychiatr Res. abril de 2023;160:126–36. 73.Murashko AA, Pavlov KA, Pavlova O V., Gurina OI, Shmukler A. Antibodies against N-Methyl D-Aspartate Receptor in Psychotic Disorders: A Systematic Review. Neuropsychobiology. 2022;81(1):1–18. 74.Ermakov EA, Melamud MM, Buneva VN, Ivanova SA. Immune System Abnormalities in Schizophrenia: An Integrative View and Translational Perspectives. Front Psychiatry. el 25 de abril de 2022;13. 75.Ribarič S. Physical Exercise, a Potential Non-Pharmacological Intervention for Attenuating Neuroinflammation and Cognitive Decline in Alzheimer’s Disease Patients. Int J Mol Sci. el 17 de marzo de 2022;23(6):3245. 76.Smiley CE, Wood SK. Stress- and drug-induced neuroimmune signaling as a therapeutic target for comorbid anxiety and substance use disorders. Pharmacol Ther. noviembre de 2022;239:108212. Scientific & Education Medical Journal / Vol. 10 - N° 3 - 2023, 23-44Vargas et al.
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