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Query: UMLS:C0004352 (autism)
 32,579 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inbred MRL, NZB and BXSB strains of mice spontaneously develop a systemic, lupus-like autoimmune disease. The progress of autoimmunity is accompanied with a cascade of behavioral changes, most consistently observed in tasks reflective of emotional reactivity and the two-way avoidance learning task. Given the possibility that behavioral alterations may reflect a detrimental consequence of autoimmune-inflammatory processes and/or an adaptive response to chronic malaise, they are tentatively labeled as autoimmunity-associated behavioral syndrome (AABS). It is hypothesized that neuroactive immune factors (pro-inflammatory cytokines, brain-reactive antibodies) together with endocrine mediators (corticotropin-releasing factor, glucocorticoids) participate in the etiology of AABS. Since AABS develops natively, and has a considerable face and predictive validity, and since the principal pathway to autoimmunity is known, AABS may be a useful model for the study of CNS involvement in human autoimmune diseases and by extension, for testing autoimmune hypotheses of several mental disorders (major depression, schizophrenia, Alzheimer's disease, autism and AIDS-related dementia).
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PMID:Neurobehavioral alterations in autoimmune mice. 916 68

The pterins, neopterin and biopterin, occur naturally in body fluids including urine. It is well established that increased neopterin levels are associated with activation of the cellular immune system and that reduced biopterins are essential for neurotransmitter synthesis. It has been suggested that some autistic children may be suffering from an autoimmune disorder. To investigate this further we performed high performance liquid chromatography analyses of urinary pterins in a group of pre-school autistic children, their siblings and age-matched control children. Both urinary neopterin and biopterin were raised in the autistic children compared to controls and the siblings showed intermediate values. This supports the possible involvement of cell-mediated immunity in the aetiology of autism.
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PMID:Urinary levels of neopterin and biopterin in autism. 950 5

The question of a connection between vaccination and autoimmune illness (or phenomena) is surrounded by controversy. A heated debate is going on regarding the causality between vaccines, such as measles and anti-hepatitis B virus (HBV), and multiple sclerosis (MS). Brain antibodies as well as clinical symptoms have been found in patients vaccinated against those diseases. Other autoimmune illnesses have been associated with vaccinations. Tetanus toxoid, influenza vaccines, polio vaccine, and others, have been related to phenomena ranging from autoantibodies production to full-blown illness (such as rheumatoid arthritis (RA)). Conflicting data exists regarding also the connection between autism and vaccination with measles vaccine. So far only one controlled study of an experimental animal model has been published, in which the possible causal relation between vaccines and autoimmune findings has been examined: in healthy puppies immunized with a variety of commonly given vaccines, a variety of autoantibodies have been documented but no frank autoimmune illness was recorded. The findings could also represent a polyclonal activation (adjuvant reaction). The mechanism (or mechanisms) of autoimmune reactions following immunization has not yet been elucidated. One of the possibilities is molecular mimicry; when a structural similarity exists between some viral antigen (or other component of the vaccine) and a self-antigen. This similarity may be the trigger to the autoimmune reaction. Other possible mechanisms are discussed. Even though the data regarding the relation between vaccination and autoimmune disease is conflicting, it seems that some autoimmune phenomena are clearly related to immunization (e.g. Guillain-Barre syndrome). The issue of the risk of vaccination remains a philosophical one, since to date the advantages of this policy have not been refuted, while the risk for autoimmune disease has not been irrevocably proved. We discuss the pros and cons of this issue (although the temporal relationship (i.e. always 2-3 months following immunization) is impressive).
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PMID:Vaccination and autoimmunity-'vaccinosis': a dangerous liaison? 1064 10

We report a child who developed autoimmune lymphoproliferative syndrome (ALPS) secondary to a heterozygous dominant negative mutation in the death domain of the Fas receptor. Previously developmentally normal, he had symptoms of autism with rapid regression in developmental milestones coincident with the onset of lymphoproliferation and autoimmune hemolytic anemia. Low-dose steroid therapy induced early and complete remission in the ALPS phenotype. There was subjective improvement, followed by objective improvement in speech and developmental milestones. We propose that autism may be part of the autoimmune disease spectrum of ALPS in this child, and this case represents a novel manifestation and target organ involvement in this disease.
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PMID:Response to steroid therapy in autism secondary to autoimmune lymphoproliferative syndrome. 1080 86

Vaccinations are invaluable in protection from a wide variety of diseases that can cause substantial morbidity and mortality. Although a rare complication of vaccination, autoimmune disorders represent one of these morbidities. Recently, widespread public concern has arisen from case reports suggesting that--similar to what has been observed after natural viral infections--there might be an association between specific immunizations and autoimmune diseases. Herein we address the biological plausibility of such a connection, focusing particularly on the examples of hepatitis B, rubella, and measles-mumps-rubella (MMR) vaccinations, and the autoimmune diseases they are potentially associated with. Our review of the available data suggests that, for the general population, the risk: benefit ratio is overwhelmingly in favor of vaccinations. However, the possibility cannot be ruled out that, in genetically susceptible individuals, vaccination can result in the unmasking of an autoimmune disease triggered by the immunization. We also critically examine the existing data suggesting a link between immunization against MMR and autism, and briefly discuss the controversial evidence pointing to a possible relationship between mercury exposure from vaccines and autistic disorders. There is a continued urgent need for rigorously designed and executed studies addressing these potential associations, although the use of vaccinations remains a critical public health tool for protection against infectious disease.
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PMID:Vaccines, viruses, and voodoo. 1253 Jan 14

Searching for a mechanism underlying autoimmunity in autism, we postulated that gliadin peptides, heat shock protein 60 (HSP-60), and streptokinase (SK) bind to different peptidases resulting in autoantibody production against these components. We assessed this hypothesis in patients with autism and in those with mixed connective tissue diseases. Associated with antigliadin and anti-HSP antibodies, children with autism and patients with autoimmune disease developed anti-dipeptidylpeptidase I (DPP I), anti-dipeptidylpeptidase IV (DPP IV [or CD26]) and anti-aminopeptidase N (CD13) autoantibodies. A significant percentage of autoimmune and autistic sera were associated with elevated immunoglobulin G (IgG), IgM, or IgA antibodies against three peptidases, gliadin, and HSP-60. These antibodies are specific, since immune absorption demonstrated that only specific antigens (e.g., DPP IV absorption of anti-DPP IV), significantly reduced IgG, IgM, and IgA antibody levels. For direct demonstration of SK, HSP-60, and gliadin peptide binding to DPP IV, microtiter wells coated with DPP IV were reacted with SK, HSP-60, and gliadin. They were then reacted with anti-DPP IV or anti-SK, anti-HSP, and antigliadin antibodies. Adding SK, HSP-60, and gliadin peptides to DPP IV resulted in 27 to 43% inhibition of the DPP IV-anti-DPP IV reaction, but DPP IV-positive peptides caused 18 to 20% enhancement of antigen-antibody reactions. We propose that (i) superantigens (e.g., SK and HSP-60) and dietary proteins (e.g., gliadin peptides) in individuals with predisposing HLA molecules bind to aminopeptidases and (ii) they induce autoantibodies to peptides and tissue antigens. Dysfunctional membrane peptidases and autoantibody production may result in neuroimmune dysregulation and autoimmunity.
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PMID:Heat shock protein and gliadin peptide promote development of peptidase antibodies in children with autism and patients with autoimmune disease. 1513 76

The developing brain is uniquely susceptible to the neurotoxic hazard posed by mercurials. Host differences in maturation, metabolism, nutrition, sex, and autoimmunity influence outcomes. How population-based variability affects the safety of the ethylmercury-containing vaccine preservative, thimerosal, is unknown. Reported increases in the prevalence of autism, a highly heritable neuropsychiatric condition, are intensifying public focus on environmental exposures such as thimerosal. Immune profiles and family history in autism are frequently consistent with autoimmunity. We hypothesized that autoimmune propensity influences outcomes in mice following thimerosal challenges that mimic routine childhood immunizations. Autoimmune disease-sensitive SJL/J mice showed growth delay; reduced locomotion; exaggerated response to novelty; and densely packed, hyperchromic hippocampal neurons with altered glutamate receptors and transporters. Strains resistant to autoimmunity, C57BL/6J and BALB/cJ, were not susceptible. These findings implicate genetic influences and provide a model for investigating thimerosal-related neurotoxicity.
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PMID:Neurotoxic effects of postnatal thimerosal are mouse strain dependent. 1518 8

Genome investigations of autism, attention deficit hyperactivity disorder (ADHD), and dyslexia suggest possible genetic overlap. Atypical cerebral asymmetry (ACA), the absence of the left hemisphere dominance for language, may be a shared phenotype due to genes located in regions of overlap. A binomal test is used to evaluate whether linked regions overlap more than expected by chance for 15 genome-wide scans in autism, ADHD, and dyslexia. Significant evidence of linkage overlap (P = 10(-7)) is seen for autism, ADHD, and dyslexia for seven chromosomal regions (2p11-12, 5p13, 7q22-33, 9q33-34, 13q22, 16p13, and 17p11-q11). Linkage analysis of ACA and molecular markers for 270 sibling pairs with ADHD is conducted using the Haseman-Elston statistic. Linkage analysis supports ACA as a shared phenotype with risk genes located on 9q33-34 or 16p13 (P < 0.004). Further support stems from the overlap of these regions in schizophrenia, bipolar illness, specific language impairment (SLI), and handedness, all traits associated with ACA. Autism, ADHD, and dyslexia share regions of linkage overlap and ACA may be a shared phenotype for such genes similar to HLA in autoimmune disease. Because ACA is associated with certain aspects of creativity, such risk genes may also be enhancer genes for creativity.
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PMID:Toward localizing genes underlying cerebral asymmetry and mental health. 1580 84

Historically, immunological research in psychiatry was based on empirical findings and early epidemiological studies indicating a possible relationship between psychiatric symptoms and acute infectious diseases. However, aetiopathological explanations for psychiatric disorders are no longer closely related to acute infection. Nevertheless, immune hypotheses have been discussed in schizophrenia, affective disorders and infantile autism in the last decades. Although the variability between the results of the epidemiological studies conducted to date is strikingly high, there is still some evidence that the immune system might play a role in the aetiopathogenesis of these three psychiatric diseases, at least in subgroups of patients. In anxiety disorders immunological research is still very much in its infancy, and the few and inconsistent data of immune changes in these patients are believed to reflect the influence of short- or long-term stress exposure. Nevertheless, there are also some hints raising the possibility that autoimmune mechanisms could interrupt neurotransmission, which would be of significance in certain patients with anxiety and panic disorders. Drug and alcohol (ethanol) dependence are not believed to be primarily influenced by an immunological aetiology. On the other hand, immune reactions due to different drugs of abuse and alcohol may directly or indirectly influence the course of concomitant somatic diseases. In different organic brain disorders the underlying somatic disease is defined as a primary immune or autoimmune disorder, for instance HIV infection or systemic lupus erythematosus (SLE). For other neurodegenerative disorders, such as Alzheimer's disease, immunoaetiopathological mechanisms are supported by experimental and clinical studies. Treatment strategies based on immune mechanisms have been investigated in patients with schizophrenia and affective disorders. Furthermore, some antipsychotics and most antidepressants are known to have direct or indirect effects on the immune system. Different immunotherapies have been used in autism, including transfer factor, pentoxifylline, intravenous immunoglobulins and corticosteroids. Immunosuppressive and/or immunomodulating agents are well established methods for treating the neuropsychiatric sequelae of immune or autoimmune disorders, for example AIDS and SLE. Therapeutic approaches in Alzheimer's disease also apply immunological methods such as strategies of active/passive immunisation and NSAIDs. Considering the comprehensive interactive network between mind and body, future research should focus on approaches linking targets of the different involved systems.
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PMID:Immunological aetiology of major psychiatric disorders: evidence and therapeutic implications. 1603 89

A multicenter study of 308 children with Autism Spectrum Disorder (ASD) was conducted through the Collaborative Programs of Excellence in Autism (CPEA), sponsored by the National Institute of Child Health and Human Development, to compare the family history of autoimmune disorders in children with ASD with and without a history of regression. A history of regression was determined from the results of the Autism Diagnostic Interview-Revised (ADI-R). Family history of autoimmune disorders was obtained by telephone interview. Regression was significantly associated with a family history of autoimmune disorders (adjusted OR=1.89; 95% CI: 1.17, 3.10). The only specific autoimmune disorder found to be associated with regression was autoimmune thyroid disease (adjusted OR=2.09; 95% CI: 1.28, 3.41).
J Autism Dev Disord 2006 Apr
PMID:Familial autoimmune thyroid disease as a risk factor for regression in children with Autism Spectrum Disorder: a CPEA Study. 1659 35


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