Is decreased blood plasma concentration of the complement C4B protein associated with attention-deficit hyperactivity disorder?

Full Abstract

OBJECTIVE: The complement system is a group of blood proteins that play an important role in defending against viral and bacterial infections. The objective of this investigation was to study the plasma levels of the C4B protein in attention-deficit hyperactivity disorder (ADHD) in an attempt to associate infections with the development of some cases of this disorder. METHOD: C4B plasma protein levels were studied using an enzyme-linked immunosorbent assay in a group of 23 subjects meeting DSM-III-R criteria for ADHD and a similar number of age- and sex-matched controls. Also studied were parents of the ADHD subjects. RESULTS: C4B plasma levels (157.0 micrograms/mL) in the ADHD subjects were significantly (p < .01) lower than those (239.3 micrograms/mL) in the normal age-matched subjects. Mothers of the ADHD subjects also had significantly lower C4B values compared with mothers of normal children. On the other hand, C4B values in the fathers were not significantly altered. CONCLUSIONS: Decreased C4B levels in ADHD, if replicated, may represent an important marker for ADHD (or a subgroup of ADHD). It also seems plausible that C4B levels are an important etiological factor for ADHD.

Author information

Author/s: Warren, R P (RP); Odell, J D (JD); Warren, W L (WL); Burger, R A (RA); Maciulis, A (A); Torres, A R (AR);

Affiliation: Center for Persons with Disabilities, Utah State University, Logan 84322, USA.

Grants: MH42119 (Agency:NIMH NIH HHS)

Journal and publication information

Publication Type: Journal Article; Research Support, U.S. Gov't, P.H.S.

Journal: Journal of the American Academy of Child and Adolescent Psychiatry (J Am Acad Child Adolesc Psychiatry), published in UNITED STATES. (Language: eng)

Reference: 1995-Aug; vol 34 (issue 8) : pp 1009-14

Dates: Created 1995/10/12; Completed 1995/10/12; Revised 2007/11/14;

PMID: 7665439, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )

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