The presence of maternal antibodies to food and infectious antigens may
confer an increased risk of developing schizophrenia and psychosis in
adult offspring. Complement factor C1q is an immune molecule with
multiple functions including clearance of antigen–antibody complexes
from circulation and mediation of synaptic pruning during fetal brain
development. To determine if maternal C1q was associated with offspring
schizophrenia and psychosis, we evaluated 55 matched case–control
maternal serum pairs from the National Collaborative Perinatal Project.
Sample pairs were composed of mothers whose offspring developed
psychoses as adults and those whose offspring were free from psychiatric
disease. Matching criteria for offspring included birth date, delivery
hospital, race, and gender, with further matching based on mother's age.
IgG markers of C1q, bovine milk casein, egg ovalbumin, and wheat gluten
were measured with enzyme-linked immunosorbent assays. C1q levels were
compared to food antigen IgG and to previously generated data for
C-reactive protein, adenovirus, herpes simplex viruses, influenza
viruses, measles virus, and Toxoplasma gondii. C1q was significantly elevated in case mothers with odds ratios of 2.66–6.31 (conditional logistic regressions, p ≤ 0.008–0.05).
In case mothers only, C1q was significantly correlated with antibodies
to both food and infectious antigens: gluten (R2 = 0.26, p ≤ 0.004), herpes simplex virus type 2 (R2 = 0.21, p ≤ 0.02), and adenovirus (R2 = 0.25, p ≤ 0.006).
In conclusion, exposure to maternal C1q activity during pregnancy may
be a risk factor for the development of schizophrenia and psychosis in
offspring. Prenatal measurement of maternal C1q may be an important and
convergent screening tool to identify potentially deleterious immune
activation from multiple sources.
confer an increased risk of developing schizophrenia and psychosis in
adult offspring. Complement factor C1q is an immune molecule with
multiple functions including clearance of antigen–antibody complexes
from circulation and mediation of synaptic pruning during fetal brain
development. To determine if maternal C1q was associated with offspring
schizophrenia and psychosis, we evaluated 55 matched case–control
maternal serum pairs from the National Collaborative Perinatal Project.
Sample pairs were composed of mothers whose offspring developed
psychoses as adults and those whose offspring were free from psychiatric
disease. Matching criteria for offspring included birth date, delivery
hospital, race, and gender, with further matching based on mother's age.
IgG markers of C1q, bovine milk casein, egg ovalbumin, and wheat gluten
were measured with enzyme-linked immunosorbent assays. C1q levels were
compared to food antigen IgG and to previously generated data for
C-reactive protein, adenovirus, herpes simplex viruses, influenza
viruses, measles virus, and Toxoplasma gondii. C1q was significantly elevated in case mothers with odds ratios of 2.66–6.31 (conditional logistic regressions, p ≤ 0.008–0.05).
In case mothers only, C1q was significantly correlated with antibodies
to both food and infectious antigens: gluten (R2 = 0.26, p ≤ 0.004), herpes simplex virus type 2 (R2 = 0.21, p ≤ 0.02), and adenovirus (R2 = 0.25, p ≤ 0.006).
In conclusion, exposure to maternal C1q activity during pregnancy may
be a risk factor for the development of schizophrenia and psychosis in
offspring. Prenatal measurement of maternal C1q may be an important and
convergent screening tool to identify potentially deleterious immune
activation from multiple sources.
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