Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors measured the middle ear muscle activity during REM sleep of normal subjects (N = 13) and patients with schizophrenia (N = 11), schizoaffective disorder (N = 8), or major depressive disorder (N = 10). The rates of middle ear muscle activity for 5 schizophrenic patients were higher than the highest rates of the other groups. The patients with major depressive disorder had normal rates, and the rates of those with schizoaffective disorder were below normal. Within the schizophrenic patients, high middle ear muscle activity could not be directly attributed to background sleep disturbances, age, anxiety, depression, or diagnostic subtype.
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PMID:Middle ear muscle activity during REM sleep in schizophrenic, schizoaffective and depressed patients. 713 99

The rates of middle ear disease in 70 patients with schizophrenia from a defined catchment population were compared with the rates in 359 nonpsychiatric controls who were matched for age, sex and general practice. A relative risk (odds ratio) of middle ear disease in schizophrenia of 1.92 was found. This was raised to 2.29 when ear disease occurring after the onset of schizophrenia was excluded. Excluding aetiological factors such as brain damage or family history raised the odds ratio further to 2.50 and 2.71 respectively. The implications of these results are discussed, and it is suggested that middle ear disease may be an aetiological factor in some cases of schizophrenia.
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PMID:Ear disease and schizophrenia: a case-control study. 883 68

22q11.2 Deletion Syndrome (22q11DS) arises from an interstitial chromosomal microdeletion encompassing at least 30 genes. This disorder is one of the most significant known cytogenetic risk factors for schizophrenia, and can also cause heart abnormalities, cognitive deficits, hearing difficulties, and a variety of other medical problems. The Df1/+ hemizygous knockout mouse, a model for human 22q11DS, recapitulates many of the deficits observed in the human syndrome including heart defects, impaired memory, and abnormal auditory sensorimotor gating. Here we show that Df1/+ mice, like human 22q11DS patients, have substantial rates of hearing loss arising from chronic middle ear infection. Auditory brainstem response (ABR) measurements revealed significant elevation of click-response thresholds in 48% of Df1/+ mice, often in only one ear. Anatomical and histological analysis of the middle ear demonstrated no gross structural abnormalities, but frequent signs of otitis media (OM, chronic inflammation of the middle ear), including excessive effusion and thickened mucosa. In mice for which both in vivo ABR thresholds and post mortem middle-ear histology were obtained, the severity of signs of OM correlated directly with the level of hearing impairment. These results suggest that abnormal auditory sensorimotor gating previously reported in mouse models of 22q11DS could arise from abnormalities in auditory processing. Furthermore, the findings indicate that Df1/+ mice are an excellent model for increased risk of OM in human 22q11DS patients. Given the frequently monaural nature of OM in Df1/+ mice, these animals could also be a powerful tool for investigating the interplay between genetic and environmental causes of OM.
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PMID:Hearing loss in a mouse model of 22q11.2 Deletion Syndrome. 2424 19