Age at Onset in Schizophrenia

Kendler, Kenneth S.; Tsuang, Ming T.; Hays, Peter L.

doi:10.1001/archpsyc.1987.01800220047008

Cited by 124 publications

(53 citation statements)

References 56 publications

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“…However, our results are consistent with those in the Roscommon Family Study (58). These low age at onset correlations do provide, indirectly, evidence about ascertainment bias (56). Given the substantial correlation in ages of siblings in a heterogeneous sample (r=0.91 in the Irish Study of High-Density Schizophrenia Families for pairs concordant for schizophrenia), if the ascertainment procedure had a "short memory" (e.g., could find only pairs whose onset of illness occurred within a few years of one another), this would induce a substantial correlation in age at onset.…”

Section: Resemblance For Gender and Age At Onsetsupporting

confidence: 89%

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Resemblance of psychotic symptoms and syndromes in affected sibling pairs from the Irish Study of High-Density Schizophrenia Families: evidence for possible etiologic heterogeneity

1997

AJP

112

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Section: Resemblance For Gender and Age At Onsetsupporting

confidence: 89%

“…The observed correlations were toward the lower end of the range (usually 0.15 to 0.30) previously found in sibling pairs concordant for schizophrenia (55)(56)(57). However, our results are consistent with those in the Roscommon Family Study (58).…”

Section: Resemblance For Gender and Age At Onsetsupporting

confidence: 89%

Resemblance of psychotic symptoms and syndromes in affected sibling pairs from the Irish Study of High-Density Schizophrenia Families: evidence for possible etiologic heterogeneity

1997

AJP

112

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“…Some studies have reported an association between early onset schizophrenia and an increased risk of schizophrenia in relatives [1,2,20,26,32,33,35], suggesting that the early form of illness may have a higher familial liability to schizophrenia than later onset forms. However, other studies have reported either no association between early onset and familial risk in schizophrenia [19,21], or have observed the association in males only [29,39]. Similarly, several studies have reported an association between early onset and morbidity risk in relatives in both bipolar disorder and major depression [15,17,27,31,34,40].…”

Section: Introductionmentioning

confidence: 99%

“…In other words, is heritability stronger in younger onset cases of each of these disorders? Relative to past studies, in particular those related to schizophrenia, the Penrose sample is large and representative and, thus, has the potential to resolve the observed inconsistent findings, if indeed they result from low statistical power and selective sampling, as suggested by others [19,21].…”

Section: Introductionmentioning

confidence: 99%

Heritability of schizophrenia and major affective disorder as a function of age, in the presence of strong cohort effects

Husted

Greenwood

Bassett

2005

Eur Arch Psychiatry Clin Neurosci

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It remains unclear whether age at onset for major psychiatric disorders is a useful marker of etiologic and genetic heterogeneity. The authors examined how heritability of schizophrenia and major affective disorders varied with age at onset. The sample was drawn from a large archival data set collected by Lionel Penrose, comprising 3,109 families with two or more members first hospitalized in Ontario between 1874 and 1944. The authors studied 1,295 sibships with schizophrenia (n = 487), major affective disorder (n = 378), both (n = 234) or neither (n = 196) of these disorders. Proportional hazards models were used to estimate how the hazard of hospitalization for each disorder (schizophrenia or major affective disorder) varied with proband age at onset, adjusted for changes in age at onset distribution between 1874 and 1944. A sibling's risk of hospitalization for the same illness significantly increased for each 10-year decrease in age at onset of the proband both for schizophrenia (hazard ratio = 1.21, 95 % confidence interval: 1.06, 1.39), and for affective disorder (hazard ratio = 1.29, 95 % CI: 1.14,1.45). Gender of proband was unrelated to sibling risk of the same illness, and tests of interaction effects between proband age at onset and gender on sibling risk were nonsignificant.

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“…For example, preclinically SNAP-25 expression is under hormonal influence (Lustig et al 1993). This observation may be useful when identifying markers to study the biology associated with the increased incidence of schizophrenia in adolescence (Remschmidt 1993;Kendler et al 1999). A second preclinical observation is that developmental SNAP-25 expression changes with in utero virus exposure (Fatemi et al 1998).…”

Section: Resultsmentioning

confidence: 96%

CSF SNAP-25 in Schizophrenia and Bipolar Illness A Pilot Study

Thompson

1999

Neuropsychopharmacology

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Research efforts to identify and understand the In the past 20 years, scientists have conducted extensive research to identify the pathology and etiology of schizophrenia and bipolar illness. In schizophrenic subjects, neuroimaging and functional analysis has identified abnormalities in various brain structures (Nasrallah 1990). Neuropathological studies of schizophrenics have revealed brain changes ranging from loss of gray matter to disorganization of the normal neuronal architecture (Bloom 1993). More recently, changes in vesicular-and growth-associated proteins have been identified in post-mortem brains of schizophrenics (Barbeau et al. 1995;Browning et al. 1993;Eastwood et al. 1995;Perrone-Bizzozero et al. 1996). Based on the accumulated clinical and laboratory information, investigators have developed two models to explain the pathophysiology of schizophrenia.The neurodegeneration hypothesis proposes that schizophrenia is the result of degeneration or loss of neurons, similar to Alzheimer's disease. This hypothesis dates to 1919, when schizophrenia was referred to as "dementia praecox" (Kraepelin 1919). However, postmortem studies have not consistently identified evidence of abnormal neurodegeneration in schizophrenic brains (Arnold et al. 1991).An alternative hypothesis states that the pathology Received November 24, 1998; revised April 8, 1999; accepted June 7, 1999. 718 P.M. Thompson et al. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 21 , NO . 6 of schizophrenia arises during embryonic and fetal developmental (Bloom 1993;Saugstad 1989). In this hypothesis, Weinberger (Weinberger 1987) proposes that a static brain lesion is established early in development and that neurodegeneration is not a major factor in the adult pathology. As the brain matures, it compensates for the lesion until the adaptations are overwhelmed. When the brain adaptions are insufficient to compensate, the final groups of behavioral symptoms are collectively described as schizophrenia. As in the neurodegenerative hypothesis, supporting data are circumstantial (Raedler et al. 1998).In bipolar illness, less is known about brain pathology than with schizophrenia. Consistent findings include mood state-dependent changes in erythrocyte Na-K-ATPase activity (Looney and el-Mallakh 1997) and an increased risk for structural brain abnormalities (Altshuler et al. 1995). Both types of studies may indicate subtle neuronal damage. A question raised by both schizophrenia and bipolar studies is whether there is ongoing neuronal damage or degeneration.The direct approach to test the hypothesis that schizophrenia and bipolar illness are not associated with ongoing neurodegeneration is to study neuronal tissue from living patients. However, moral and ethical restrictions eliminate this type of study. One way to bypass this limitation is to study a protein that has been demonstrated to be involved with the adult post-mortem pathology and can be measured in living subjects. Synaptosomal-associated protein 25kDa (SNAP-25) is a candidate protein for th...

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Age at Onset in Schizophrenia

Cited by 124 publications

References 56 publications

Resemblance of psychotic symptoms and syndromes in affected sibling pairs from the Irish Study of High-Density Schizophrenia Families: evidence for possible etiologic heterogeneity

Resemblance of psychotic symptoms and syndromes in affected sibling pairs from the Irish Study of High-Density Schizophrenia Families: evidence for possible etiologic heterogeneity

Heritability of schizophrenia and major affective disorder as a function of age, in the presence of strong cohort effects

CSF SNAP-25 in Schizophrenia and Bipolar Illness A Pilot Study

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