These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Increased complement classical and mannan-binding lectin pathway activities in schizophrenia.
    Author: Mayilyan KR, Arnold JN, Presanis JS, Soghoyan AF, Sim RB.
    Journal: Neurosci Lett; 2006 Sep 01; 404(3):336-41. PubMed ID: 16860475.
    Abstract:
    Schizophrenia is a severe mental disorder, with worldwide prevalence of 1-1.5%. Immunological research in schizophrenia indicates that infectious or autoimmune processes might play a role in the etiopathogenesis. The complement system is a major mediator of innate immune defence against infection and contributes to many functions of the immune system including inflammation, opsonization and cell lysis. Mannan-binding lectin (MBL) activates the complement system via the lectin pathway. Inherited MBL deficiency, common in most human populations, predisposes to infectious and autoimmune diseases. We measured total complement activity (CH50), C4 activity (C4 CH50), MBL level and the activities of MBL-associated serine proteases, MASP-1 and MASP-2 in sera of 45 schizophrenic patients and in 62 healthy volunteers. We found that schizophrenic patients and healthy volunteers have statistically similar MBL levels and MASP-1 activity. However, MBL-bound MASP-2 activity and therefore MBL and MASP-2-mediated complement activation capacity is increased in schizophrenic patients compared with healthy volunteers (P<0.01). The increase was accompanied by increased CH50 (P<0.02) and C4 CH50 (P<0.02). Our results support the idea that complement system alterations may be involved in schizophrenia.
    [Abstract] [Full Text] [Related] [New Search]