myelin-basic-protein and Autistic-Disorder

Accumulating evidence from both human and animal studies show that brain is a target of air pollution. Multiple epidemiological studies have now linked components of air pollution to diagnosis of autism spectrum disorder (ASD), a linkage with plausibility based on the shared mechanisms of inflammation. Additional plausibility appears to be provided by findings from our studies in mice of exposures from postnatal day (PND) 4-7 and 10-13 (human 3rd trimester equivalent), to concentrated ambient ultrafine (UFP) particles, considered the most reactive component of air pollution, at levels consistent with high traffic areas of major U.S. cities and thus highly relevant to human exposures. These exposures, occurring during a period of marked neuro- and gliogenesis, unexpectedly produced a pattern of developmental neurotoxicity notably similar to multiple hypothesized mechanistic underpinnings of ASD, including its greater impact in males. UFP exposures induced inflammation/microglial activation, reductions in size of the corpus callosum (CC) and associated hypomyelination, aberrant white matter development and/or structural integrity with ventriculomegaly (VM), elevated glutamate and excitatory/inhibitory imbalance, increased amygdala astrocytic activation, and repetitive and impulsive behaviors. Collectively, these findings suggest the human 3rd trimester equivalent as a period of potential vulnerability to neurodevelopmental toxicity to UFP, particularly in males, and point to the possibility that UFP air pollution exposure during periods of rapid neuro- and gliogenesis may be a risk factor not only for ASD, but also for other neurodevelopmental disorders that share features with ASD, such as schizophrenia, attention deficit disorder, and periventricular leukomalacia.

Topics: Air Pollution; Animals; Animals, Newborn; Autistic Disorder; Brain; Calcium-Binding Proteins; Corpus Callosum; Dental Impression Materials; Disease Models, Animal; Female; Lateral Ventricles; Male; Mice; Mice, Inbred C57BL; Microfilament Proteins; Myelin Basic Protein; Neurotoxicity Syndromes; Neurotransmitter Agents; Particulate Matter; Silicones

40 infantile autistic patients were studied. They ranged from 6 years to 15 years of age at entry. 22 were cases of classical infantile autism; whereas 18 lacked one or more clinical defects associated with infantile autism ("pseudo-autism"). Of the 22 with classic autism, 21 responded to transfer factor (TF) treatment by gaining at least 2 points in symptoms severity score average (SSSA); and 10 became normal in that they were main-streamed in school and clinical characteristics were fully normalized. Of the 18 remaining, 4 responded to TF, some to other therapies. After cessation of TF therapy, 5 in the autistic group and 3 of the pseudo-autistic group regressed, but they did not drop as low as baseline levels.

Topics: Adolescent; Antibodies; Autistic Disorder; Cell Extracts; Child; Dialysis; Follow-Up Studies; Humans; Lymphocytes; Myelin Basic Protein; Pilot Projects; Transfer Factor

To reveal paired and partial correlations of values of neuro-immuno-test and thrombodynamics test in children with childhood autism and schizophrenia in childhood in a state of exacerbation.. The study used a database of children with childhood autism, obtained by us in 2028-2019. The study included 46 patients with childhood autism (CA) aged 2 to 13 years: median age [Q1; Q3] - 5 years [4; 7], 10 girls (22%) and 36 boys (78%)). The thrombodynamics test (TD) was performed on a T-2 thrombodynamics analyzer according to the manufacturer's instructions.. It was shown that there is a statistically significant positive correlation (R=0.369,. Thus, it was shown that the correlations between the studied parameters of the neuro-immuno-test and the indicators of the thrombodynamics test mutually depend on the other indicators of these tests. This confirms the hypothesis that the immune system and the hemostatic system are two different sides of a single supersystem.. Выявить парные и частные корреляции показателей нейроиммунотеста и теста тромбодинамики (ТД) у детей с аутизмом в состоянии обострения.. В работе была использована база данных детей с детским аутизмом, полученная нами в 2018—2019 гг. В исследование были включены 46 больных в возрасте от 2 до 13 лет: медианный возраст [Q1; Q3] 5 лет [4; 7], 10 (22%) девочек и 36 (78%) мальчиков. Тест ТД проводили на регистраторе тромбодинамики Т-2 согласно инструкции.. Была выявлена статистически значимая положительная корреляционная связь (R=0,369,. Таким образом, было показано, что у детей с аутизмом корреляционные связи между изучаемыми параметрами нейроиммунотеста и показателями ТД взаимно зависят от остальных показателей этих тестов. Это подтверждает гипотезу, что иммунная система и система гемостаза представляют две разные стороны единой суперсистемы.

Topics: Anticoagulants; Autistic Disorder; Autoantibodies; Child; Female; Hemostatics; Humans; Male; Myelin Basic Protein; Thrombosis

Polyunsaturated fatty acids (PUFAs) are not only essential for energy production, but they also exhibit a range of immunomodulatory properties that progress through T cell mediated events. Autoimmunity may have a pathogenic role in a subgroup of autistic children. This study is the first to investigate the relationship between serum levels of anti-myelin basic protein (anti-MBP) brain-specific auto-antibodies and reduced plasma levels of PUFAs in autistic children. Plasma levels of PUFAs (including linoleic, alphalinolenic, arachidonic "AA" and docosahexaenoic "DHA" acids) and serum anti-MBP were measured in 80 autistic children, aged between 4 and 12 years, and 80 healthy-matched children. Autistic patients had significantly lower plasma levels of PUFAs than healthy children. On the other hand, ω6/ω3 ratio (AA/DHA) was significantly higher in autistic patients than healthy children. Low plasma DHA, AA, linolenic and linoleic acids were found in 67.5%, 50%, 40% and 35%, respectively of autistic children. On the other hand, 70% of autistic patients had elevated ω6/ω3 ratio. Autistic patients with increased serum levels of anti-MBP auto-antibodies (75%) had significantly lower plasma DHA (P<0.5) and significantly higher ω6/ω3 ratio (P<0.5) than patients who were seronegative for these antibodies. In conclusions, some autistic children have a significant positive association between reduced levels of plasma DHA and increased serum levels of anti-MBP brain-specific auto-antibodies. However, replication studies of larger samples are recommended to validate whether reduced levels of plasma PUFAs are a mere association or have a role in the induction of the production of anti-MBP in some autistic children.

Topics: Autistic Disorder; Autoantibodies; Case-Control Studies; Chi-Square Distribution; Child; Child, Preschool; Cross-Sectional Studies; Docosahexaenoic Acids; Fatty Acids, Unsaturated; Female; Humans; Male; Myelin Basic Protein; Psychiatric Status Rating Scales

Autism is a brain developmental disorder with characteristics of social interaction defects, language and communication dysfunction, and repetitive behavior. Occurrence of autism is continuously increasing, but the cause of autism is not clearly defined. Genetic linkage or environmental factors were proposed as sources for pathogenesis of autism. BTBR T+tf/J (BTBR) mice were reported as an appropriate animal model for autism investigation because of their similarities in behavioral abnormalities with human autistic subjects. The aim of this study was to evaluate expression levels of proteins involved with brain development at fetal stage of BTBR mice. FVB/NJ mice were used as a control strain because of their social behaviors. Level of fetal brain immunoglobulin (Ig) G deposit was also evaluated. Fetal brains were obtained at d 18 of gestational period. Thirty-one and 27 fetuses were obtained from 3 pregnant BTBR and FVB dams, respectively. The level of glial fibrillary acidic protein expression was significantly lower in fetal brains of BTBR than FVB/NJ mice. Expression of brain-derived neurotrophic factor and myelin basic protein was significantly more upregulated in BTBR than in FVB/NJ mice. No significant difference was obtained for nerve growth factor between the two strains. Levels of IgG isotypes deposited in fetal brain of BTBR mice were significantly higher than in FVB mice except for IgG1. Overall, these results suggest that prenatal alterations in expression of various fetal brain proteins may be implicated in aberrant behavioral characteristics of BTBR mice.

Topics: Animals; Autistic Disorder; Autoantibodies; Behavior, Animal; Brain; Brain-Derived Neurotrophic Factor; Female; Fetal Development; Gene Expression Regulation, Developmental; Germ-Free Life; Glial Fibrillary Acidic Protein; Immunoglobulin G; Mast Cells; Mice, Inbred Strains; Mice, Transgenic; Myelin Basic Protein; Neurogenesis; Neuroglia; Neurons; Pregnancy

Autoantibodies from autistic spectrum disorder (ASD) patients react with multiple proteins expressed in the brain. One such autoantibody targets myelin basic protein (MBP). ASD patients have autoantibodies to MBP of both the IgG and IgA classes in high titers, but no autoantibodies of the IgM class. IgA autoantibodies act as serine proteinases and degrade MBP in vitro. They also induce a decrease in long-term potentiation in the hippocampi of rats either perfused with or previously inoculated with this IgA. Because this class of autoantibody causes myelin sheath destruction in multiple sclerosis (MS), we hypothesized a similar pathological role for them in ASD.

Topics: Adolescent; Animals; Autistic Disorder; Brain; Child; Child, Preschool; Cysteine Proteinase Inhibitors; Dose-Response Relationship, Drug; Female; Hippocampus; Humans; Immunoglobulin A; In Vitro Techniques; Leupeptins; Long-Term Potentiation; Male; Myelin Basic Protein; Patch-Clamp Techniques; Proteolysis; Rats; Rats, Sprague-Dawley; Synaptic Transmission

Alterations in the volume, density, connectivity and functional activation of white matter tracts are reported in some individuals with autism and may contribute to their abnormal behaviors. The BTBR (BTBR T+tf/J) inbred strain of mouse, is used to model facets of autism because they develop low social behaviors, stereotypical and immune changes similar to those found in people with autism. Previously, it was thought a total absence of corpus callosal interhemispheric connective tissues in the BTBR mice may underlie their abnormal behaviors. However, postnatal lesions of the corpus callosum do not precipitate social behavioral problems in other strains of mice suggesting a flaw in this theory. In this study we used digital pathological methods to compare subcortical white matter connective tracts in the BTBR strain of mice with those found in the C57Bl/6 mouse and those reported in a standardized mouse brain atlas. We report, for the first time, a novel connective subcortical interhemispheric bridge of tissue in the posterior, but not anterior, cerebrum of the BTBR mouse. These novel connective tissues are comprised of myelinated fibers, with reduced myelin basic protein levels (MBP) compared to levels in the C57Bl/6 mouse. We used electrophysiological analysis and found increased inter-hemispheric connectivity in the posterior hemispheres of the BTBR strain compared with the anterior hemispheres. The conduction velocity was slower than that reported in normal mice. This study shows there is novel abnormal interhemispheric connectivity in the BTBR strain of mice, which may contribute to their behavioral abnormalities.

Topics: Analysis of Variance; Animals; Autistic Disorder; Brain; Corpus Callosum; Disease Models, Animal; Electroencephalography; Enzyme-Linked Immunosorbent Assay; Female; Functional Laterality; Image Processing, Computer-Assisted; Male; Mice; Mice, Inbred C57BL; Mice, Neurologic Mutants; Microtubule-Associated Proteins; Myelin Basic Protein; Nerve Fibers, Myelinated; Neuroimaging; Spectrum Analysis

The amounts of at least three biochemical factors are more often abnormal in autistic people than neurologically normal ones. They include insulin-like growth factor, anti-myelin basic protein, and serotonin. This may explain why processes initiated in utero which hinder normal neurogenesis, especially myelination, continue after delivery. Quantitation of these parameters may make possible the calculation of an autism index, anticipating at birth which children will ultimately develop overt autism.

Topics: Autistic Disorder; Humans; Infant, Newborn; Myelin Basic Protein; Serotonin; Somatomedins

Etiology of autism has become an area of a significant controversy. Allergy induced autism is an area of research wherein immune responses to some allergens may play a pathogenic role in autism. Allergy may induce the production of brain specific auto-antibodies in a subgroup of autistic children. We are the first to investigate the possible link between allergic manifestations and serum levels of both anti-myelin basic protein (anti-MBP) and anti-myelin associated glycoprotein (anti-MAG) brain-specific auto-antibodies, which were measured by ELISA method, in 42 autistic children in comparison to 42 healthy-matched children. Allergic manifestations (bronchial asthma, atopic dermatitis and/or allergic rhinitis) were found in 47.6% of autistic patients. Increased serum levels of anti-MBP and anti-MAG auto-antibodies were found in 57.1% and 66.7%, respectively of autistic children. In addition, 78.5% of autistic children had increased serum levels of both anti-MBP and/or anti-MAG auto-antibodies. Autistic patients with allergic manifestations had significantly higher serum levels of anti-MBP and anti-MAG auto-antibodies than those without these manifestations (P<0.001 and P=0.001, respectively). In conclusion, allergy may be a contributing factor to the increased serum levels of anti-MBP and anti-MAG auto-antibodies in some autistic children. Indeed, we need to know more about the links between allergy, immune system and brain in autism for finding new therapeutic modalities in autism.

Topics: Autistic Disorder; Autoantibodies; Biomarkers; Brain; Child; Cross-Sectional Studies; Female; Follow-Up Studies; Humans; Hypersensitivity; Male; Myelin Basic Protein; Myelin-Associated Glycoprotein

One of the most consistent biological findings in autism is the elevated blood serotonin levels. Immune abnormalities, including autoimmunity with production of brain specific auto-antibodies, are also commonly observed in this disorder. Hyperserotonemia may be one of the contributing factors to autoimmunity in some patients with autism through the reduction of T-helper (Th) 1-type cytokines. We are the first to investigate the possible role of hyperserotonemia in the induction of autoimmunity, as indicated by serum anti-myelin-basic protein (anti-MBP) auto-antibodies, in autism.. Serum levels of serotonin and anti-MBP auto-antibodies were measured, by ELISA, in 50 autistic patients, aged between 5 and 12 years, and 30 healthy-matched children.. Autistic children had significantly higher serum levels of serotonin and anti-MBP auto-antibodies than healthy children (P < 0.001 and P < 0.001, respectively). Increased serum levels of serotonin and anti-MBP auto-antibodies were found in 92% and 80%, respectively of autistic patients. Patients with severe autism had significantly higher serum serotonin levels than children with mild to moderate autism (P < 0.001). Serum serotonin levels had no significant correlations with serum levels of anti-MBP auto-antibodies in autistic patients (P = 0.39).. Hyperserotonemia may not be one of the contributing factors to the increased frequency of serum anti-MBP auto-antibodies in some autistic children. These data should be treated with caution until further investigations are performed. However, inclusion of serum serotonin levels as a correlate may be useful in other future immune studies in autism to help unravel the long-standing mystery of hyperserotonemia and its possible role in the pathophysiology of this disorder.

Topics: Animals; Autistic Disorder; Autoantibodies; Case-Control Studies; Child; Child, Preschool; Female; Humans; Myelin Basic Protein; Serotonin; Severity of Illness Index

Autism is a heterogeneous group of life-long neurologic problems that begin in childhood. Success in efforts to understand and treat autism has been mostly elusive. The role of autoimmunity in autism has gained recognition both for associated systemic autoimmune disease and the presence of brain autoantibodies in autistic children and their family members. There is an acknowledged genetic susceptibility to autism--most notably allotypes of complement C4. C4 defects are associated with several autoimmune diseases and also confer susceptibility to mycobacterial infections. Mycobacterium avium ss. paratuberculosis (MAP) causes an enteric inflammatory disease in ruminant animals (Johne's disease) and is the putative cause of the very similar Crohn's disease in humans. Humans are widely exposed to MAP in food and water. MAP has been also linked to ulcerative colitis, irritable bowel syndrome, sarcoidosis, Blau syndrome, autoimmune (Type 1) diabetes, Hashimoto's thyroiditis and multiple sclerosis. Environmental agents are thought to trigger autism in the genetically at risk. Molecular mimicry is the proposed mechanism by which MAP is thought to trigger autoantibodies. Autoantibodies to brain myelin basic protein (MBP) is a common feature of autism. This article considers the subset of autoimmunity-related autism patients and postulates that MAP, through molecular mimicry to its heat shock protein HSP65, triggers autism by stimulating antibodies that cross react with myelin basic protein (MBP).

Topics: Antibodies, Bacterial; Autistic Disorder; Autoimmunity; Bacterial Proteins; Chaperonin 60; Cross Reactions; Humans; Models, Immunological; Molecular Mimicry; Mycobacterium avium subsp. paratuberculosis; Myelin Basic Protein

Autoantibodies to central nervous system antigens, such as myelin basic protein (MBP), may play a role in autism. We measured autoantibody titers to MBP in children with autism, both classic onset and regressive onset forms, controls (healthy age- and gender-matched) and individuals with Tourette syndrome via enzyme-linked immunosorbent assays. We found a significant difference in autoantibody titers to MBP, not accounted for by age or medication, between Tourette and classic autism (both significantly lower) when compared to regressive autism, but not when compared to controls. Autoantibody responses against MBP are unlikely to play a pathogenic role in autism.

Topics: Autistic Disorder; Autoantibodies; Axons; Blotting, Western; Brain; Child; Child, Preschool; Enzyme-Linked Immunosorbent Assay; Female; Histones; Humans; Male; Myelin Basic Protein; Myelin Sheath; Reference Values; Tourette Syndrome

Serum antibodies in 100 mothers of children with autistic disorder (MCAD) were compared to 100 age-matched mothers with unaffected children (MUC) using as antigenic substrates human and rodent fetal and adult brain tissues, GFAP, and MBP. MCAD had significantly more individuals with Western immunoblot bands at 36 kDa in human fetal and rodent embryonic brain tissue. The density of bands was greater in fetal brain at 61 kDa. MCAD plus developmental regression had greater reactivity against human fetal brain at 36 and 39 kDa. Data support a possible complex association between genetic/metabolic/environmental factors and the placental transfer of maternal antibodies in autism.

Topics: Adult; Aged; Animals; Antibodies, Heterophile; Autistic Disorder; Autoantibodies; Birth Order; Brain; Brain-Derived Neurotrophic Factor; Female; Glial Fibrillary Acidic Protein; Humans; Immunoglobulin G; Isoantibodies; Isoantigens; Male; Maternal-Fetal Exchange; Middle Aged; Mothers; Myelin Basic Protein; Nerve Tissue Proteins; Neurons; Parity; Pregnancy; Rats; Species Specificity

Brain derived neurotrophic factor (BDNF) elevation in newborn sera predicts intellectual/social developmental abnormalities. Other autoantibodies (AAs) to endothelial cells (ECs) and myelin basic protein (MBP) are also elevated in some children. We tested relationships between BDNF, BDNF AAs, and other AAs in children with these disorders.. BDNF levels and IgG/IgM autoantibodies to BDNF, ECs, MBP, and histones were measured in children with autism, childhood disintegrative disorder (CDD), pervasive developmental delay-not otherwise specified (PDD-nos), acquired epilepsy, Landau-Kleffner syndrome (LKS); healthy children (HC), and children with non-neurological illnesses (NNI).. Mean BDNF levels were elevated in children with autism and CDD, (p < or = 0.0002) compared to HC or NNI. Mean IgG and IgM BDNF AAs were elevated in children with autism, CDD and epilepsy (p < or = 0.0005) compared to HC but not to NNI. Mean IgM AA EC titers detected by immunocytochemistry were higher in autism, PDD-NOS, epilepsy, and LKS (p < or = 0.005) compared to HC and NNI. While mean ELISA IgG EC AAs were higher in autism and PPD-NOS (p < 0.005) compared to HC but not NNI, ELISA IgM EC AAs were higher in children with autism, CDD, PDD-NOS, and epilepsy compared to both HC and NNI (p < 0.0005). Mean anti-MBP IgG and IgM titers were higher in all study groups (p < 0.005) except for LKS compared to both HC and NNI.. Children with developmental disorders and epilepsy have higher AAs to several neural antigens compared to controls. The presence of both BDNF AAs and elevated BDNF levels in some children with autism and CDD suggests a previously unrecognized interaction between the immune system and BDNF.

Topics: Antibodies, Antinuclear; Autistic Disorder; Autoantibodies; Brain-Derived Neurotrophic Factor; Cells, Cultured; Cerebral Cortex; Child; Child, Preschool; Cohort Studies; Endothelial Cells; Enzyme-Linked Immunosorbent Assay; Epilepsy; Female; Histones; Humans; Immunoglobulin G; Immunoglobulin M; Immunohistochemistry; Landau-Kleffner Syndrome; Male; Myelin Basic Protein; Nervous System; Umbilical Veins

The hypothesis of an immune dysfunction in autism spectrum disorders has previously been put forward without, however, compelling evidence of a direct relation to its etiology or pathogenesis. To further understand if autoimmunity could play a significant role in autism, we analyzed autoantibody repertoires to brain tissue extract in the plasma of 171 autism children, their parents, and 54 controls, by quantitative immunoblotting. Multiparametric analysis revealed significant differences between patients and controls, and showed that one single reactivity in Section 32 of the blot had the most power to discriminate between these samples. Family correlation coefficients and heritability estimates did not provide any evidence that this reactivity was genetically determined. While the molecular weight of the target protein suggested that it might be an isoform of Myelin Basic Protein (MBP), inhibition assays with human MBP argued against this hypothesis. The study evidences the widespread occurrence of autoreactivities to brain tissue in autism patients, which may represent the immune system's neuroprotective response to a previous brain injury occurred during neurodevelopment. The molecular identification of the target protein in Section 32 will contribute to the understanding of the role of immune responses against brain antigens in autistic patients.

Topics: Adolescent; Autistic Disorder; Autoantibodies; Blotting, Western; Brain; Child; Child, Preschool; Female; Humans; Male; Myelin Basic Protein; Nuclear Family

We measured autoantibodies against nine different neuron-specific antigens and three cross-reactive peptides in the sera of autistic subjects and healthy controls by means of enzyme-linked immunosorbent assay (ELISA) testing. The antigens were myelin basic protein (MBP), myelin-associated glycoprotein (MAG), ganglioside (GM1), sulfatide (SULF), chondroitin sulfate (CONSO4), myelin oligodendrocyte glycoprotein (MOG), alpha,beta-crystallin (alpha,beta-CRYS), neurofilament proteins (NAFP), tubulin and three cross-reactive peptides, Chlamydia pneumoniae (CPP), streptococcal M protein (STM6P) and milk butyrophilin (BTN). Autistic children showed the highest levels of IgG, IgM and IgA antibodies against all neurologic antigens as well as the three cross-reactive peptides. These antibodies are specific because immune absorption demonstrated that only neuron-specific antigens or their cross-reactive epitopes could significantly reduce antibody levels. These antibodies may have been synthesized as a result of an alteration in the blood-brain barrier. This barrier promotes access of preexisting T-cells and central nervous system antigens to immunocompetent cells, which may start a vicious cycle. These results suggest a mechanism by which bacterial infections and milk antigens may modulate autoimmune responses in autism.

Topics: Antigens; Antigens, Bacterial; Autistic Disorder; Autoimmune Diseases of the Nervous System; Bacterial Infections; Bacterial Outer Membrane Proteins; Butyrophilins; Carrier Proteins; Child; Child, Preschool; Chlamydophila pneumoniae; Cross Reactions; Encephalitis; Female; Humans; Immunoglobulin A; Immunoglobulin G; Immunoglobulin M; Male; Membrane Glycoproteins; Milk Hypersensitivity; Myelin Basic Protein; Myelin Proteins; Myelin-Associated Glycoprotein; Myelin-Oligodendrocyte Glycoprotein; Neurons; Neurotoxins; Streptococcus

Several preparations of MMR vaccines and their progenitor monovalent vaccine bulks produced by two different manufacturers were examined serologically for the presence of chicken myelin basic protein (MBP) residues. The products were challenged against several commercial preparations of anti-hMBP antisera that reacted positively with the control MBP preparations of human and chicken origins. There was no evidence of the presence of MBP components in MMR vaccines or their progenitor vaccine bulks as shown by the reactivity profiles of the antibody preparations against control and test antigens.

Topics: Albumins; Animals; Antibody Specificity; Antigen-Antibody Reactions; Autistic Disorder; Autoimmunity; Chemistry, Pharmaceutical; Chickens; Cross Reactions; Enzyme-Linked Immunosorbent Assay; Humans; Measles-Mumps-Rubella Vaccine; Myelin Basic Protein; Safety

Considering an autoimmunity and autism connection, brain autoantibodies to myelin basic protein (anti-MBP) and neuron-axon filament protein (anti-NAFP) have been found in autistic children. In this current study, we examined associations between virus serology and autoantibody by simultaneous analysis of measles virus antibody (measles-IgG), human herpesvirus-6 antibody (HHV-6-IgG), anti-MBP, and anti-NAFP. We found that measles-IgG and HHV-6-IgG titers were moderately higher in autistic children but they did not significantly differ from normal controls. Moreover, we found that a vast majority of virus serology-positive autistic sera was also positive for brain autoantibody: (i) 90% of measles-IgG-positive autistic sera was also positive for anti-MBP; (ii) 73% of measles-IgG-positive autistic sera was also positive for anti-NAFP; (iii) 84% of HHV-6-IgG-positive autistic sera was also positive for anti-MBP; and (iv) 72% of HHV-6-IgG-positive autistic sera was also positive for anti-NAFP. This study is the first to report an association between virus serology and brain autoantibody in autism; it supports the hypothesis that a virus-induced autoimmune response may play a causal role in autism.

Topics: Adult; Antibodies, Viral; Autistic Disorder; Autoantibodies; Brain; Child; Child, Preschool; Herpesvirus 6, Human; Humans; Immunoblotting; Immunoglobulin G; Measles virus; Middle Aged; Myelin Basic Protein; Nerve Tissue Proteins

Based on a possible pathological relationship of autoimmunity to autism, antibodies reactive with myelin basic protein (anti-MBP) were investigated in the sera of autistic children. Using a screening serum dilution of 1:400 in the protein-immunoblotting technique, approximately 58% (19 of 33) sera of autistic children (< or = 10 years of age) were found to be positive for anti-MBP. This result in autistics was significantly (p < or = .0001) different from the controls (8 of 88 or only 9% positive), which included age-matched children with normal health, idiopathic mental retardation (MR) and Down syndrome (DS), and normal adults of 20 to 40 years of age. Since autism is a syndrome of unknown etiology, it is possible that anti-MBP antibodies are associated with the development of autistic behavior.

Topics: Adult; Age Factors; Antibody Specificity; Autistic Disorder; Autoantibodies; Autoimmune Diseases; Child; Child, Preschool; Double-Blind Method; Down Syndrome; Female; Humans; Infant; Intellectual Disability; Male; Myelin Basic Protein; Nerve Tissue Proteins

This study examined the linkage between elevated blood serotonin in autism and the presence of circulating autoantibodies against the serotonin 5HT1A receptor. Information was also obtained on the diagnostic and receptor specificity of these autoantibodies. Blood serotonin was measured as was inhibition of serotonin binding to human cortical membranes by antibody-rich fractions of blood from controls and from patients with childhood autism, schizophrenia, obsessive-compulsive disorder, Tourette's, and multiple sclerosis. The results showed elevated blood serotonin was not closely related to inhibition of serotonin binding by antibody-rich blood fractions. Inhibition of binding was highest for patients with multiple sclerosis and was not specific to the 5HT1A receptor as currently defined. Although inhibition was not specific to autism, the data were insufficient to establish if people with autism differed from normal controls on this measure.

Topics: Adolescent; Adult; Autistic Disorder; Autoantibodies; Binding, Competitive; Child; Child, Preschool; Female; Frontal Lobe; Humans; Immunoglobulin G; Male; Middle Aged; Multiple Sclerosis; Myelin Basic Protein; Obsessive-Compulsive Disorder; Receptors, Serotonin; Schizophrenia, Childhood; Serotonin; Tourette Syndrome

Topics: Autistic Disorder; Autoimmune Diseases; Humans; Myelin Basic Protein; Receptors, Serotonin; Serotonin

Cell-mediated immune response to human myelin basic protein was studied by the macrophage migration inhibition factor test in 17 autistic patients and a control group of 11 patients suffering from other mental diseases included in the differential diagnosis of the syndrome of autism. Of the 17 autistic patients, 13 demonstrated inhibition of macrophage migration, whereas none of the nonautistic patients showed such a response. The results indicate the existence of a cell-mediated immune response to brain tissue in the syndrome of autism.

Topics: Adolescent; Adult; Autistic Disorder; Brain; Cell Migration Inhibition; Child; Female; Humans; Intellectual Disability; Macrophage Migration-Inhibitory Factors; Macrophages; Male; Myelin Basic Protein; Schizophrenia, Childhood