Relation of ASC and IL-1beta with neurocognitive parameters in patients with Obsessive-Compulsive Disorder

Discussion: Our results indicate that some aspects of neurocognitive impairment in patients with OCD might be related to neuroinflammatory processes, with implications for our understanding of the pathogenesis of OCD.

📌 3 Key Takeaways

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Objective & Hypothesis:Objective: It is now well accepted that inflammatory processes play a role in the etiopathogenesis of psychiatric disorders.

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Key Findings & Data:NLRP3 inflammasome, which is formed by the combination of NLRP3, ASC and Caspase-1 proteins, and its activator NEK7, takes part in these processes.

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Conclusion & Impact:Discussion: Our results indicate that some aspects of neurocognitive impairment in patients with OCD might be related to neuroinflammatory processes, with implications for our understanding of the pathogenesis of OCD.

🔬Design:Research Article

📍Scope:Comprehensive Sample

⚙️Variables:Domain Parameters

Abstract

Objective: It is now well accepted that inflammatory processes play a role in the etiopathogenesis of psychiatric disorders. NLRP3 inflammasome, which is formed by the combination of NLRP3, ASC and Caspase-1 proteins, and its activator NEK7, takes part in these processes. In this study, we aimed to investigate the relationship between inflammatory markers (i.e. IL-1β, IL-18, NLRP3 inflammasome protein levels) and cognitive functions in patients with obsessive compulsive disorder (OCD). Method: Forty-two patients between the ages of 18-45 who were diagnosed with OCD were included in the study. Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-I), Yale-Brown Obsessive Compulsive Scale (Y-BOCS), and Hamilton Depression Scale (HAMD) were used for clinical evaluations. In order to evaluate cognitive functions, Trail Making Test (TMT), Berg Card Sorting Test and Category Fluency Test were applied. IL- 1β and IL-18 cytokine levels were determined by the ELISA method; measurement of the protein amounts of NLRP3, Caspase-1, ASC and NEK7 were performed by Western blotting. Results: Serum IL-1beta was negatively correlated with TMT (B-A) (rs=-.36, p= 0.019). Similarly, ASC was negatively correlated with TMT-B and TMT (B-A) (rs=-.38, p= 0.03; rs=-0.36, p = 0.04, respectively). However, no statistically significant relationship was found between other inflammatory parameters (NLRP3, Caspase-1, and IL-18) and neurocognitive tests. Discussion: Our results indicate that some aspects of neurocognitive impairment in patients with OCD might be related to neuroinflammatory processes, with implications for our understanding of the pathogenesis of OCD.

Özet

Amaç: İnflamatuar süreçlerin psikiyatrik bozuklukların etyopatogenezinde rol oynadığı yaygın kabul görmektedir. Bu süreçlerde NLRP3, ASC ve Caspase-1 proteinlerinin bir araya gelmesiyle ve NEK7'nin aktivasyonuyla oluşan NLRP3 inflamatuarı yer almaktadır. Bu çalışmada obsesif kompulsif bozukluk (OKB) hastalarında inflamatuar belirteçler (ör: IL-1β, IL-18, NLRP3 inflamatuar protein düzeyleri) ile bilişsel işlevler arasındaki ilişkinin araştırılması amaçlanmıştır. Yöntem: OKB tanısı almış 18-45 yaş arası kırk-iki hasta çalışmaya dahil edilmiştir. Klinik değerlendirmeler için DSM-IV Eksen I. Bozuklukları için Yapılandırılmış Psikiyatrik Görüşme Formu (SCID-I), Yale Brown Obsesyon Kompulsiyon Ölçeği (Y-BOCS) ve Hamilton Depresyon Ölçeği (HAM-D) kullanılmıştır. Bilişsel işlevleri değerlendirmek için İz Sürme Testi (TMT), Berg Kart Eşleme Testi ve Kategori Akıcılık Testi uygulanmıştır. IL-1β ve IL-18 sitokin seviyeleri ELISA yöntemi ile belirlenirken NLRP3, Kaspaz-1, ASC ve NEK7'nin protein miktarlarının ölçümü Western blot yöntemi ile gerçekleştirilmiştir. Bulgular: Serum IL-1beta seviyeleri, TMT (B-A) ile negatif korelasyon göstermiştir (rs=-.36, p= 0.019). Benzer şekilde ASC, TMT-B ve TMT (B-A) ile negatif korelasyon göstermiştir (sırasıyla rs=-.38, p=0.03; rs=-0.36, p=0.04). Ancak diğer inflamatuar parametreler (NLRP3, Caspase-1 ve IL-18) ile nörobilişsel testler arasında istatistiksel olarak anlamlı bir ilişki bulunamamıştır. Sonuç: Elde ettiğimiz sonuçlar, OKB'li hastalarda nörobilişsel bozulmanın bazı yönlerinin nöroinflamatuar süreçlerle ilişkili olabileceğine işaret etmektedir ve bu bulgu OKB patogenezinin anlaşılmasına katkı sağlayabilir.

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Cite This Article

TETİK, M., AYKAÇ, C., KURUOĞLU, A., EKİNCİ, B., YARAŞ, T., UZGAN, B. Ö., AKGÜL, Ö., ALKIN, T. (2022). Relation of ASC and IL-1beta with neurocognitive parameters in patients with Obsessive-Compulsive Disorder. Klinik Psikiyatri Dergisi, Cilt: 25 - Sayı: 1, 75–83. https://ajindex.com/articles/573783

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References (11)

Ruscio AM, Stein DJ, Chiu WT, Kessler RC. The epidemiology of obsessivecompulsive disorder in the National Comorbidity Survey Replication. Mol. Psychiatry 2010
DOI: 10.1038/mp.2008.94 2. Pauls DL, Abramovitch A, Rauch SL, Geller DA. Obsessive– compulsive disorder: an integrative genetic and neurobiological perspective. Nat. Rev. Neurosci 2014
DOI: 10.1038/nrn3746 3. Cosco TD, Pillinger T, Emam H, Solmi M, Budhdeo S, Prina AM, Maes M, Stein DJ, Stubbs B, Carvalho AF. Immune aberrations in obsessive-compulsive disorder: a systematic review and meta-analysis. Mol. Neurobiol 2019
DOI: 10.1007/s12035-018- 1409-x 4. Kim HK, Andreazza AC, Elmi N, Chen W, Young LT. Nodlike receptor pyrin containing 3 (NLRP3) in the post-mortem frontal cortex from patients with bipolar disorder: a potential mediator between mitochondria and immune-activation. J. Psychiatr. Res 2016
DOI: 10.1016/j.jpsychires.2015.10.015 5. Alcocer-Gómez E, de Miguel M, Casas-Barquero N, Núñez- Vasco J, Sánchez-Alcazar JA, Fernández-Rodríguez A, Cordero MD. NLRP3 inflammasome is activated in mononuclear blood cells from patients with major depressive disorder. Brain Behav. Immun 2014
DOI: 10.1016/j.bbi.2013.10.017 6. Kaufmann FN, Costa AP, Ghisleni G, Diaz AP, Rodrigues ALS, Peluffo H, Kaster MP. NLRP3 inflammasome-driven pathways in depression: clinical and preclinical findings. Brain Behav. Immun 2017
DOI: 10.1016/j.bbi.2013.10.017 7. Mao Z, Liu C, Ji S, Yang Q, Ye H, Han H, Xue Z. The NLRP3 inflammasome is involved in the pathogenesis of Parkinson’s disease in rats. Neurochem. Res 2017
DOI: 10.1007/s11064-017-2185-0 8. Saresella M, Piancone F, Marventano I, Zoppis M, Hernis A, Zanette M, Trabattoni D, Chiappedi M, Ghezzo A, Canevini MP, la Rosa F, Esposito S, Clerici M. Multiple inflammasome complexes are activated in autistic spectrum disorders. Brain Behav. Immun 2016
DOI: 10.1016/j.bbi.2016.03.009 9. Frank MG, Weber MD, Watkins LR, Maier SF. Stressinduced neuroinflammatory priming: a liability factor in the etiology of psychiatric disorders. Neurobiol. Stress 2016
DOI: 10.1016/j.ynstr.2015.12.004 10. Zheng D, Liwinski T, Elinav E. Inflammasome activation and regulation: toward a better understanding of complex mechanisms. Cell Discov 2020
DOI: 10.1038/s41421-020- 0167-x 11. He Y, Hara H, Núñez G. Mechanism and regulation of NLRP3 inflammasome activation. Trends Bioche