Cognitive function plays a pivotal role in assessing an individual’s quality of life. This research aimed to investigate how azelaic acid (AzA), a natural dicarboxylic acid with antioxidant and anti-inflammatory properties, affects aluminium chloride (AlCl3)-induced behavioural changes and biochemical alterations in the hippocampus of rats.

Thirty-two male Wistar rats divided into four groups received distilled water, AzA 50 mg/kg, AlCl3 100 mg/kg and AzA plus AlCl3, respectively, by oral gavage for 6 weeks. Behavioural changes were evaluated using open-field maze, elevated plus maze, novel object recognition (NOR), passive avoidance task, and Morris water maze (MWM) tests. Also, malondialdehyde (MDA), carbonyl protein, tumour necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), nuclear factor-kappa B (NF-κB), C/EBP homologous protein (CHOP), glycogen synthase kinase-3 beta (GSK-3β), brain-derived neurotrophic factor (BDNF) and acetylcholinesterase (AChE) activity were examined.

AzA significantly affected AlCl3-provoked anxiety-like behaviours and learning and memory impairments. It also reduced the toxic effect of AlCl3 on MDA, carbonyl protein, TNF-α, IL-1β, NF-κB and GSK-3β status; however, its beneficial effects on AlCl3-induced changes of CHOP, BDNF and AChE activity were not significant.

These findings disclosed that AzA could improve behavioural and cognitive function and almost limit the oxidative stress and neuroinflammation caused by AlCl3.

Inflammation is increasingly recognised as a fundamental component of the pathophysiology of major depressive disorder (MDD), with a variety of inflammatory biomarkers playing pivotal roles. These markers are closely linked to both the severity of symptoms and the responsiveness to treatments in MDD.

This scoping review aims to explore the scientific literature investigating the complex relationships between inflammatory biomarkers and depression, by identifying new studies and critical issues in current research.

Following the PRISMA Extension for Scoping Reviews guidelines, we systematically searched databases including PubMed, Scopus, PsycINFO, Open Grey and Cochrane Library. Our search focused on articles published from 1 January 2020 to 1 May 2024. We included studies evaluating inflammatory biomarkers in adult patients with MDD, utilising observational and randomised controlled trial designs, and review studies.

Our analysis examined 44 studies on the complex interplay between inflammation and its multiple effects on MDD. Significant associations between specific inflammatory biomarkers and depression severity were found, requiring cautious interpretation. We also highlight several methodological limitations in the current studies, which warrant caution in directly applying these findings to clinical practice. However, identified methodologies show potential for using these biomarkers as diagnostic tools or therapeutic targets, including anti-inflammatory interventions.

The findings emphasise the need for sophisticated, integrative research to understand inflammation's role in MDD. Future studies should identify specific biomarker panels for diagnosing depression and bridging peripheral biomarker measurements with central neuroinflammatory processes, leading to better diagnostic and treatment strategies.

To investigate the effects of cannabidiol (CBD) on emotional and cognitive symptoms in rats with intra-nigral 6-hydroxydopamine (6-OHDA) lesions.

Adult male Wistar rats received bilateral intranigral 6-OHDA infusions and were tested in a battery of behavioural paradigms to evaluate non-motor symptoms. The brains were obtained to evaluate the effects of CBD on hippocampal neurogenesis.

6-OHDA-lesioned rats exhibited memory impairments and despair-like behaviour in the novelty-suppressed feeding test and forced swim test, respectively. The animals also exhibited dopaminergic neuronal loss in the substantia nigra pars compacta (SNpc), striatum, and ventral tegmental area and a reduction of hippocampal neurogenesis. CBD decreased dopaminergic neuronal loss in the SNpc, reduced the mortality rate and decreased neuroinflammation in 6-OHDA-lesioned rats. In parallel, CBD prevented memory impairments and attenuated despair-like behaviour that were induced by bilateral intranigral 6-OHDA lesions. Repeated treatment with CBD favoured the neuronal maturation of newborn neurons in the hippocampus in Parkinsonian rats.

The present findings suggest a potential beneficial effect of CBD on non-motor symptoms induced by intra-nigral 6-OHDA infusion in rats.

The s100b inflammatory protein is involved in schizophrenia pathophysiology. We aim at studying the evolution of the s100b serum levels in acutely relapsed paranoid schizophrenia patients at three different time points (admission, discharge and 3 months after hospital discharge 3MAHD).

Twenty-three paranoid schizophrenia inpatients meeting DSM-IV criteria participated in the research. Twenty-three healthy subjects matched by age, gender and season acted as the control group. Psychopathology was measured with the Positive and Negative Syndrome Scale (PANSS). Serum s100b levels were determined at 12:00 and 24:00 h with an enzyme-linked immunoassay kit.

Patients had significant higher serum s100b levels at admission and discharge (12:00 h) than the group of healthy subjects. At admission and discharge, s100b serum levels at 24 h had decreased compared to the 24:00 h s100b levels of the healthy subjects. At 3MAHD patients and healthy subjects had similar levels of serum s100b protein. Positive and negative PANSS scores decreased significantly between admission and discharge. Positive and negative PANSS scores decreased between discharge and 3MAHD, but these changes had no statistical significance.

Our study confirms that the acute inflammatory response produced in acutely relapsed patients is reversed after 3 month of hospital discharge. The variations of serum s100b concentrations when the patients suffer from an acute relapse may be a useful predictor of disease evolution.

Suicide is the second leading cause of death (8.5% of all deaths) in adolescents. The search for neurobiological markers of suicidal behavior seems to be highly actual. Such markers may include quantitative EEG parameters and signs of neuroinflammation that plays an important role in the pathogenesis of various mental disorders.

The aim of the study was to reveal the relationships between pre-treatment clinical, EEG, and neuroimmunological parameters in depressive adolescents with suicidal attempts in their history.

35 female depressive patients (all right-handed, age 16–25, mean 18,7±2.9 years old) were enrolled in the study. Total HDRS-17 scores varied from 13 to 43 (mean 27,7±8.1). Multichannel resting EEG was recorded with spectral power (SP) measurements in narrow frequency sub-bands. Functional activities of leukocyte elastase (LE) and of its antagonist α1-proteinase inhibitor (α1-PI), as neuroinflammation markers, were measured in the blood plasma. Leukocyte/inhibitory index (LII=LE/α1-PI) was calculated. Spearman’s correlations between clinical, EEG, and neuroimmunological parameters were analyzed.

Sum of anxiety cluster of HDRS-17 scale (items 9, 10, 11) correlated positively (p<0.02) with LE and α1-PI values, as well as with theta1 (4-6 Hz) and theta2 (6-8 Hz) SP in EEG leads of the right hemisphere. In turn, α1-PI values correlated negatively and LII values correlated positively with alpha3 (11-13 Hz) SP in majority of EEG leads.

The data obtained confirm the contribution of neuroinflammation to clinical conditions, especially to anxiety level, and to EEG pattern in depressive female adolescents with suicidal attempts. The study supported by RBRF grant No.20-013-00129a.

No significant relationships.

Schizophrenia affects approximately 1% of the world population, having a devastating impact not only in patients but in all society. As a result, it has been subject of extensive investigation and the presence of certain genes was associated with an increased risk of developing schizophrenia. However, the presence of these genes is not sufficient, therefore, other factors are necessarily involved.Observation of the association between schizophrenia and inflammatory states of the Central Nervous System led to the hypothesis that a dysfunction of the immune system may play a central role in this process.

In this work we intend to make a brief review of the existing literature related to the immunological theory of schizophrenia.

A bibliographic research was conducted in Medline library using the following terms: “schizophrenia and immune system”; “schizophrenia and inflammation” and “schizophrenia and neuroinflammation”.

The survey results reveal increasing evidence of the key role of the immune system in schizophrenia. Several studies show benefits of treatment with anti-inflammatory drugs in patients at an early stage of the disease. In the same way, it was verified that pro and anti-inflammatory cytokines influence glutamatergic transmission and tryptophan metabolism. Furthermore, the decrease in microglial activity appears to have a beneficial effect on schizophrenia.

Future will say if neuroimmunology mechanisms are primary or a secondary consequence in Schizophrenia. Recent discoveries in this area are encouraging and open the possibility of new therapeutic targets and new therapeutic approaches to this disease.

No significant relationships.

The mild encephalitis (ME) hypothesis of severe mental disorders, ME to be caused by infections, autoimmunity , toxicity and trauma ( Bechter 2001, updated Bechter 2013), is now emergingly supported from neuroimaging and CSF and postmorten findings.

Review about the present status of ME hypothesis and autoimmune psychosis and remainig challenges to assess and categorize mild neuroinflammation.

expert review

Autoimmune Encephalitis presenting with exclusive psychiatric symptoms and all cases of Autoimmune Psychosis (international consensus criteria in Pollak et al, Lancet Psychiatry, 2020) match the proposed ME criteria ( Bechter 2001 & 2013). Majority of these cases of an autoimmune type of ME are well treatable with immune modulatory treatments. It remained unclear, whether CNS antibodies are causal or contributive by shaping the observed clinical syndrome. The increasing evidence of mild neuroinflammation present in considerable subgroup of schizophrenia or psychosis spectrum cases from ongoing clinical studies, including CSF ( Bechter et al 2010, Endres et al 2018, 2020, aso.) and neuroimaging plus the observed clinical improvement with immune modulytory therapies, strongly support ME hypothesis, potentialy even in considerably larger subgroup of SMDs,supported by brain biopsy (Najjar et al ,several papers) and post mortem studies (Bogerts et al group ,Weickert et al group, several papers).

Beyond ME even more refined categories of mild neuroinflammation, including parainflammation ( proposed by Medzhitov 2008) and neuroprogression ( proposed by Berk et al 2010/11) need to be considered in further research on the possible role of mild neuroinflammation in SMDs (Bechter 2020, Frontiers Psychiatry).

No significant relationships.

Autism spectrum disorder (ASD) is a common neurodevelopmental disorder. Its underlying causes and pathophysiologies remain unclear. Recent data support the potential involvement of neuroinflammation in the onset of this disorder.

The aim of our study was to investigate the potential link between ASD and inflammatory mediators.

This descriptive study was conducted among ASD outpatients followed-up at the child and adolescent psychiatry department in the Military Hospital of Instruction of Tunis. Blood samples were collected for inflammatory cytokines dosage, notably the interleukin 1β (IL-1β), interleukin 6 (IL-6) and the Tumor Necrosis Factor α (TNF-α) immunodosage.

Twenty-four patients were included in this study, aged between four and ten years old (mean age= 6,55 years; minimum=4; maximum=10 years). Our sample was mainly represented by male patients (95,6%). TNF-α plasmatic levels were high (>5pg/mL) among all of our sample with a mean of 11,6 pg/mL (minimum= 6,87; maximum=17,7 pg/mL; standard deviation= 3,52 pg/mL), suggesting abnormal peripheral blood mononuclear cells response. However, IL-1β and IL-6 plasmatic levels were relatively normal.

An immune response dysregulation was detected in our sample. Multiple clinical and experimental studies investigated the implication of inflammatory cytokines in neurodevelopmental disruption. Their results, however, remain controversial and limited by small samples. Further studies need to be done in order to investigate the neuroimmunological factors linked with ASD.