Neuroinflammation and psychiatric illness

Najjar, Souhel; Pearlman, Daniel M; Alper, Kenneth; Najjar, Amanda; Devinsky, Orrin

doi:10.1186/1742-2094-10-43

Cited by 733Tryptophan and brain disordersNeuroinflammation and Neurodegeneration MechanismsStress Responses and Cortisol

Neuroinflammation and psychiatric illness

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Najjar, Souhel, Pearlman, Daniel M, Alper, Kenneth, Najjar, Amanda, Devinsky, Orrin·2013·Journal of Neuroinflammation

DOI 10.1186/1742-2094-10-43PMC PMC3626880

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Abstract

Multiple lines of evidence support the pathogenic role of neuroinflammation in psychiatric illness. While systemic autoimmune diseases are well-documented causes of neuropsychiatric disorders, synaptic autoimmune encephalitides with psychotic symptoms often go under-recognized. Parallel to the link between psychiatric symptoms and autoimmunity in autoimmune diseases, neuroimmunological abnormalities occur in classical psychiatric disorders (for example, major depressive, bipolar, schizophrenia, and obsessive-compulsive disorders). Investigations into the pathophysiology of these conditions traditionally stressed dysregulation of the glutamatergic and monoaminergic systems, but the mechanisms causing these neurotransmitter abnormalities remained elusive. We review the link between autoimmunity and neuropsychiatric disorders, and the human and experimental evidence supporting the pathogenic role of neuroinflammation in selected classical psychiatric disorders. Understanding how psychosocial, genetic, immunological and neurotransmitter systems interact can reveal pathogenic clues and help target new preventive and symptomatic therapies.

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Glucocorticoid desensitization dampens the immune system's response to cortisol, leading to elevated peripheral pro-inflammatory factors (TNF, IL-17, IL-1β, IL-6) and sustained neuroinflammation marked by chronic microglial and astrocyte activation.
“This desensitization dampens the immune system’s response to cortisol, ultimately leading to elevated peripheral pro-inflammatory factors (e.g., TNF, IL-17, IL-1β, IL-6) and sustained neuroinflammation, marked by chronic microglial and astrocyte activation [29,31,32,33,34].”
From Comparative Analysis of HPA-Axis Dysregulation and Dynamic Molecular Mechanisms in Acute Versus Chronic Social Defeat Stress (2025) · cites this paper as [32]
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Various neurological and psychiatric diseases have been associated with neuroinflammation in some post-mortem studies.
“As various neurological and psychiatric diseases have been associated with neuroinflammation in some post-mortem studies,183, 184, 185”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [184]
The Review section ('Psychiatric disorders associated with innate inflammation'; page unavailable) reports post-mortem evidence of inflammatory changes in depression, bipolar disorder, and schizophrenia, while noting mixed findings. The passages support the psychiatric-disease portion, but do not establish the claim about neurological diseases in post-mortem studies. (LLM, conf=0.84)
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The interaction between innate and adaptive immune systems and neurotransmitters emerged as a mechanism underpinning mood disorders, psychosis, and anxiety disorders.
“The interaction between innate and adaptive immune systems and neurotransmitters emerged as a mechanism underpinning mood disorders, psychosis, and anxiety disorders (Najjar et al., 2013).”
From Anxiety and depression in COVID-19 survivors: role of inflammatory and clinical predictors (2020) · cites this paper as Najjar et al., 2013

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Najjar S Pearlman D Devinsky O Najjar A Nadkarni S Butler T Zagzag D Neuropsychiatric autoimmune encephalitis with negative VGKC-complex, NMDAR, and GAD autoantibodies: a case report and literature review, forthcoming Cogn Behav Neurol in press 23538571
Rodríguez AD González PA García MJ de la Rosa A Vargas M Marrero F Circadian variations in proinflammatory cytokine concentrations in acute myocardial infarction Rev Esp Cardiol 2003 56 555 560 12783730

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JOURNAL OF NEUROINFLAMMATION REVIEW Open Access
Illness, P., Najjar, S., Pearlman, D. M., Alper, K., Najjar, A., & Devinsky, O. (2014)
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Authors: Najjar, S., Pearlman, D. M., Alper, K., Najjar, A., & Devinsky, O.
Affiliations: NYU Langone Health (US)
Dartmouth Institute for Health Policy and Clinical Practice (US)
Corresponding author: Najjar, Souhel
ORCID: Najjar, Souhel
Pearlman, Daniel M
Alper, Kenneth
Devinsky, Orrin
Venue: Journal of Neuroinflammation
Publisher: Springer Science and Business Media LLC
Published: 2013-04-01
Volume: 10
Issue: 1
Pages: 43-43
ISSN: 1742-2094 (ISSN-L)
DOI: 10.1186/1742-2094-10-43
PMC: PMC3626880
OpenAlex: W2097086441
Cited by: 733
References: 265
Citations by year: 2026: 28 · 2025: 59 · 2024: 73 · 2023: 56 · 2022: 74 · 2021: 65 · 2020: 54 · 2019: 57 · 2018: 67 · 2017: 54 · 2016: 53 · 2015: 46 · 2014: 36 · 2013: 10
FWCI: 3.15
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/2.0 (unspecified)
Locations: Journal of Neuroinflammation (publishedVersion, cc-by)
Europe PMC (PubMed Central) (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
Topics: Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords: neuroinflammation, mental illness, autoimmunity, psychosis, major depressive disorder, bipolar disorder, schizophrenia, obsessive-compulsive disorder, glutamatergic system, monoaminergic systems, neurotransmitter dysregulation, neuroimmunology
MeSH terms: Animals, Autoimmune Diseases, Mental Disorders, Humans, Inflammation, Autoimmunity

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