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Query: UMLS:C0025362 (mental retardation)
 15,878 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eugenics, the attempt to improve the genetic quality of the human species by 'better breeding', developed as a worldwide movement between 1900 and 1940. It was particularly prominent in the United States, Britain and Germany, and in those countries was based on the then-new science of Mendelian genetics. Eugenicists developed research programs to determine the degree in which traits such as Huntington's chorea, blindness, deafness, mental retardation (feeblemindedness), intelligence, alcoholism, schizophrenia, manic depression, rebelliousness, nomadism, prostitution and feeble inhibition were genetically determined. Eugenicists were also active in the political arena, lobbying in the United States for immigration restriction and compulsory sterilization laws for those deemed genetically unfit; in Britain they lobbied for incarceration of genetically unfit and in Germany for sterilization and eventually euthanasia. In all these countries one of the major arguments was that of efficiency: that it was inefficient to allow genetic defects to be multiplied and then have to try and deal with the consequences of state care for the offspring. National socialists called genetically defective individuals 'useless eaters' and argued for sterilization or euthanasia on economic grounds. Similar arguments appeared in the United States and Britain as well. At the present time (1997) much research and publicity is being given to claims about a genetic basis for all the same behaviors (alcoholism, manic depression, etc.), again in an economic context--care for people with such diseases is costing too much. There is an important lesson to learn from the past: genetic arguments are put forward to mask the true--social and economic--causes of human behavioral defects.
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PMID:The social and economic origins of genetic determinism: a case history of the American Eugenics Movement, 1900-1940 and its lessons for today. 946 76

Epidemiological studies in Korea on mental illness began about four decades ago by Choi and Yoo. This was followed by more than 25 papers. Interviews by psychiatrists were not randomly selected samples. Consistent diagnostic tools were not used except by Yeon et al. The definition of prevalence was not definite and, therefore, not comparable. The research was confined to major psychoses such as schizophrenia, manic depressive illnesses, mental retardation and epilepsy. Most of the studies were performed in rural areas only. The present study was designed to meet the above described criteria as well as testing the applicability of Diagnostic Interview Schedule-III (DIS-III) in Korea. In order to accomplish those goals the Korean version of DIS-III was constructed and the lifetime prevalence of mental disorders was studied both in urban (Seoul) and rural areas.
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PMID:A nationwide epidemiological study of mental disorders in Korea. 989 67

Mentally retarded children and adolescents not infrequently develop affective disorders, including a pattern of rapid cycling bipolar disorder. From work with nonretarded adults this pattern is known to have a tendency to chronicity and treatment resistance. Among persons with mental retardation, such a pattern is often marked by periods of severe overexcitation and underexcitation, often producing serious caretaking stress. Generally, it has been difficult to make this diagnosis in persons with severe to profound mental retardation and other severe disabilities, and it is probably often missed. However, knowing which questions to ask may facilitate diagnosis. It is our hypothesis that a positive family history of affective disorder in the presence of brain dysfunction increases the risk of rapid cycling affective disorder. Treatment results so far are limited to case reports and open trials. Much more research needs to be done to identify predictors of bipolar disorder and rapid cycling, the extent to which findings from studies of adults without mental retardation apply, and the most effective methods of treatment.
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PMID:Rapid Cycling Disorders in Mentally Retarded Children. 1032 Apr 12

Even clinical neuropsychiatrists who do not focus on mental illness and mental retardation may be intrigued by the subject of mood disorders in persons with Down syndrome. This article reviews the following subjects in persons with Down syndrome: epidemiology of major depression and bipolar disorder; clinical symptoms including "psychotoform," differential diagnosis of mood disorders, comorbid diagnoses, and treatment.
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PMID:Mood Disorders and Down Syndrome. 1032 Apr 14

This report summarizes the findings presented at the Chromosome 4 Workshop of the Sixth World Congress on Psychiatric Genetics (October 1998, Bonn, Germany). Chromosome 4 linkage and association results for several psychiatric phenotypes including bipolar affective disorder, schizophrenia, alcoholism, and mental retardation are reviewed. In bipolar affective disorder, positive linkage results for markers on 4q35 were reported by three independent groups. In addition, findings in bipolar disorder were reported for markers spanning 4p14-16, and of particular interest are the results that coincide with the original Blackwood et al. [1996: Nat Genet 12:427-430] region at 4p16. For schizophrenia, modest positive results were reported for 4q31, as well as for marker D4S2917 at a region of 4q close to the centromere. Chromosome 4 continues to demonstrate interesting results in alcoholism, particularly in the region of the alcohol dehydrogenase gene cluster; however, it is not clear how to interpret the contrast in the susceptibility versus protective loci that are being reported in this region.
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PMID:Chromosome 4 Workshop Summary: Sixth World Congress on Psychiatric Genetics, Bonn, Germany, October 6-10, 1998. 1037 35

The X-chromosome breakpoint in a female patient with a balanced translocation t(X;12)(q24;q15), bipolar affective disorder and mental retardation was mapped within the glutamate receptor 3 (GRIA3) gene by fluorescence in situ hybridization. The GRIA3 cDNA of 5894 bp was cloned, and the gene structure and pattern of expression were determined. The most abundant GRIA3 transcript is composed of 17 exons. An additional 5 exons (2a, 2b, 5a, 5b, and 5c) from the 5' end of the GRIA3 open reading frame were identified by EST analysis (ESTs AI379066 and AA947914). Two new polymorphic microsatellite repeats, (TC)(n=12-26) and (AC)(n=15-19), were identified within GRIA3 5' and 3'UTRs. No mutations were detected in families segregating disorders mapping across GRIA3, one with X-linked bipolar affective disorder (BP) and one with a nonspecific X-linked mental retardation (MRX27). To assess the possibility of the involvement of the GRIA3 gene in familial cases of complex BP, a large set of 373 individuals from 40 pedigrees segregating BP were genotyped using closely linked (DXS1001) and intragenic (DXS1212 and GRIA3 3' UTR (AC)(n))) GRIA3 STR markers. No evidence of linkage was found by parametric Lod score analysis (the highest Lod score was 0. 3 at DXS1212, using the dominant transmission model) or by affected sib-pair analysis.
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PMID:Characterization of the human glutamate receptor subunit 3 gene (GRIA3), a candidate for bipolar disorder and nonspecific X-linked mental retardation. 1064 33

Five patients with a fragile site at 16q22-23 and neuropsychiatric disorders are reported. Three of five had Tourette disorder, three had mental retardation, two had bipolar disorder, and one had autistic disorder. During our attempts to study the fragile sites in more detail we were unable to reproduce the fragile sites found several years earlier. The potential relationship between the fragile sites and the neuropsychiatric disorders in these patients is discussed. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:69-73, 2000.
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PMID:Peek-a-boo fragile site at 16d associated with Tourette syndrome, bipolar disorder, autistic disorder, and mental retardation. 1089 28

Family and adoption studies indicate that genetic factors play a role in the development of many psychiatric disorders. A variable number of possible interacting genes predisposing to the diseases is likely. The genetic dissection has been hampered by genetic complexity as well as by difficulties in defining the phenotypes. Genetic mapping efforts using sib pairs, twins and individual large families has revealed preliminary or tentative evidence for susceptibility loci for a number of psychiatric disorders. Illnesses include the prion disease familial fatal insomnia (FFI), alcoholism, anorexia nervosa, autism, bipolar affective disorder, dyslexia, enuresis nocturnal, epilepsia, obsessive-compulsive disorders (OCD), schizophrenia, as well as the dementias, Alzheimer's disease and frontal lobe dementia, and mental retardation. The genes and proteins related to the newly discovered transmitter in the central nervous system, nitric oxide (NO), and its genes and proteins are also reviewed. The number of mapped human genes now exceeds 30,000 of the estimated total number of 60,000 to 100,000 genes. This rapid development will facilitate gene mapping, as well as efforts to isolate and identify the genes responsible for symptom susceptibility in many of the etiologically unclear psychiatric diseases with complex genetic origin.
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PMID:[Mental disease a heritage. New genetic knowledge can reveal "public diseases" such as autism, dyslexia, alcoholism, anorexia, schizophrenia]. 1070 80

Depression is a relatively common health issue in children and adolescents. Different pathogenetic factors are implied: genetic, biological, psychological and environmental. The core symptoms of depression are the same for children, adolescents and adults but the prominence of characteristic symptoms changes with age. The clinical picture of depression according to age level is described in different types of mood disorders (major depressive disorder, dysthymia, bipolar disorder) and in mental retardation. Over half of the youths with depression have comorbid conditions: anxiety disorders, other mood disorders, attention deficit/hyperactivity disorder, and conduct disorders. Different factors affect the natural course and risk of suicide. Assessment procedures of depression and comorbid conditions include a psychiatric evaluation of the depressed subject and his family, structured interviews and specific rating scales. A comprehensive treatment strategy, psychoeducational, psychotherapeutic and psychopharmacological, is proposed.
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PMID:Depressive disorder in children and adolescents. 1072 95

New hopes for cloning susceptibility genes for schizophrenia and bipolar affective disorder followed the discovery of a novel type of DNA mutation, namely unstable DNA. One class of unstable DNA, trinucleotide repeat expansion, is the causal mutation in myotonic dystrophy, fragile X mental retardation, Huntington disease and a number of other rare Mendelian neurological disorders. This finding has led researchers in psychiatric genetics to search for unstable DNA sites as susceptibility factors for schizophrenia and bipolar affective disorder. Increased severity and decreased age at onset of disease in successive generations, known as genetic anticipation, was reported for undifferentiated psychiatric diseases and for myotonic dystrophy early in the twentieth century, but was initially dismissed as the consequence of ascertainment bias. Because unstable DNA was demonstrated to be a molecular substrate for genetic anticipation in the majority of trinucleotide repeat diseases including myotonic dystrophy, many recent studies looking for genetic anticipation have been performed for schizophrenia and bipolar affective disorder with surprisingly consistent positive results. These studies are reviewed, with particular emphasis placed on relevant sampling and statistical considerations, and concerns are raised regarding the interpretation of such studies. In parallel, molecular genetic investigations looking for evidence of trinucleotide repeat expansion in both schizophrenia and bipolar disorder are reviewed. Initial studies of genome-wide trinucleotide repeats using the repeat expansion detection technique suggested possible association of large CAG/CTG repeat tracts with schizophrenia and bipolar affective disorder. More recently, three loci have been identified that contain large, unstable CAG/CTG repeats that occur frequently in the population and seem to account for the majority of large products identified using the repeat expansion detection method. These repeats localize to an intron in transcription factor gene SEF2-1B at 18q21, a site named ERDA1 on 17q21 with no associated coding region, and the 3' end of a gene on 13q21, SCA8, that is believed to be responsible for a form of spinocerebellar ataxia. At present no strong evidence exists that large repeat alleles at either SEF2-1B or ERDA1 are involved in the etiology of schizophrenia or bipolar disorder. Preliminary evidence suggests that large repeat alleles at SCA8 that are non-penetrant for ataxia may be a susceptibility factor for major psychosis. A fourth, but much more infrequently unstable CAG/CTG repeat has been identified within the 5' untranslated region of the gene, MAB21L1, on 13q13. A fifth CAG/CTG repeat locus has been identified within the coding region of an ion transporter, KCNN3 (hSKCa3), on 1q21. Although neither large alleles nor instability have been observed at KCNN3, this repeat locus has been extensively analyzed in association and family studies of major psychosis, with conflicting findings. Studies of polyglutamine containing genes in major psychosis have also shown some intriguing results. These findings, reviewed here, suggest that, although a major role for unstable trinucleotides in psychosis is unlikely, involvement at a more modest level in a minority of cases cannot be excluded, and warrants further investigation.
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PMID:The unstable trinucleotide repeat story of major psychosis. 1081 8


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