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Biomedical subjects

E Marinescu

Publications and source records attributed to E Marinescu.

At least 19 recordsLinked to original sources
PubMed2001

Different familial transmission patterns in bipolar I disorder with onset before and after age 25.

Gene identification in common disorders such as Alzheimer disease and breast cancer has greatly profited from the use of age of onset as criterion to delineate subgroups of disease characterized by different inheritance patterns. In bipolar affective disorder, where the majority of linkage studies have produced conflicting results, studies reporting clinical characteristics and familial occurrence of disease have suggested that age of onset might serve as an indicator for identifying more homogeneous subgroups of disease. Our study was the first to examine this hypothesis by the means of segregation analysis. We investigated a sample of 177 bipolar I probands recruited from consecutive admissions and their first- and second-degree relatives (2,407 subjects). Probands were subdivided into an early-onset (n = 107) and a late-onset group (n = 70) using an age of onset of 25 as a cut-off point. This age was chosen because the observed age of onset distribution was bimodal with a cut-off of 25 years. Morbid risks for affective disorder were found significantly higher (P = 0.01) in relatives of probands with an early onset than in probands with late onset of disease. The segregation analysis showed that the disease is transmitted differently in early- and late-onset groups. In the early-onset group, a non-Mendelian major gene with a polygenic component was favored while the data in the late-onset group were compatible with a multifactorial model. This result may have important implications for future molecular studies aiming at the identification of disease-associated genes.

Adult↗
PubMed1998

Patterns of parental transmission and familial aggregation models in bipolar affective disorder.

Two recent studies [McMahon et al., 1995: Am J Hum Genet 56:1277-1286; Gershon et al., 1996: Am J Med Genet (Neuropsychiatr Genet) 67:202-207] reported an excess of maternal transmission in bipolar affective disorder in multiply affected families. In a sample of 130 families ascertained through a bipolar proband without regard to psychiatric family history we analysed the frequency of maternal (MAT) and paternal (PAT) transmissions, the morbid risk (MR) in relatives of transmitting mothers and fathers and the inheritance patterns in families with MAT vs. PAT transmission of the disease. In the total sample of 130 families we identified 39 families where the disease was transmitted from the paternal side (PAT families) and 35 families where the disease was transmitted from the maternal side (MAT families). Counting PAT and MAT transmissions in these unilineal families we found nearly equal numbers for both transmission types under a narrow (BP: bipolar disorder, schizoaffective-bipolar type disorder) and a broad definition (AFF: BP, recurrent unipolar depression) of the phenotype. The MRs for narrow and broad phenotypes were not significantly different in any type of PAT relative in PAT families vs. MAT relatives in MAT families. However, in PAT families there were two times more affected females than males with both disease models, while in MAT families there was no MR difference by relatives' sex. The transmission of BP was compatible with the Mendelian major gene model in PAT families and with the multifactorial model in MAT families. Extension of the relatives' phenotype led to borderline non-Mendelian major effects in PAT families and reproduced the multifactorial model in MAT families.

Bipolar Disorder↗
PubMed1995

Clinical evidence for genomic imprinting in bipolar I disorder.

The phenotypic indicators of the genomic imprinting model were applied to clinical psychopathology data on 100 bipolar (BP) I probands and their families. The paternal transmission was associated with a significantly younger age of onset of the BP illness in probands and a higher rate of affective disorders in first- and second-degree relatives. The effect of the sex of the transmitting parent on age of onset in probands decreased but remained significant when controlling for the effect of the probands' age at investigation. Probands' sex had no significant influence on their age of onset. The severity of the BP illness in probands in terms of number of illness episodes and annual frequency was not influenced by the sex of the transmitting parent.

Adolescent↗
PubMed1991

Adolescent offspring of endogenous unipolar depressive parents and of normal parents.

Ninety-six children aged 10-17 of unipolar endogenous depressive proband parents and 96 matched control children of well parents were investigated using DSM-IIIR diagnostic criteria. Both sets of parents were also studied. Although the rate of psychopathology was significantly higher in proband than in control children, adaptive functioning as a measure of the severity of the psychopathology did not differentiate the two groups of children. Among factors related to the mental status of the children were: severity and onset under 30 years of age of the parental depression and lifelong association of parental anxiety with depression. Personality measurements performed in children showed different personality structures in proband offspring. Data on adolescent psychopathology and personality showed little evidence of a homotypic relationship with the adult affective disorders.

Adolescent↗
PubMedDate not supplied

Psychopathology in children aged 10-17 of bipolar parents: psychopathology rate and correlates of the severity of the psychopathology.

Seventy-two proband children aged 10-17 of bipolar parents, matched with 72 control children of normal parents, were investigated using DSM-III diagnostic criteria and multiple sources of information. The psychopathology rate in children (61% in probands versus 25% in controls) was related to the impact of psychic disorders on the children's adaptive functioning. The effect of several variables describing the psychiatric status of both parents and familial environment on the severity of psychopathology in children was analysed. Disordered and non-disordered probands were compared with respect to illness characteristics of their parents, familial environment, personality traits, and IQ by means of canonical discriminant analysis.

Adolescent↗
PubMedDate not supplied

Children aged 10-17 of endogenous unipolar depressive parents and of normal parents. I. Psychopathology rate and relationship of the severity of the psychopathology to familial and environmental variables.

Seventy two children aged 10-17 of 42 endogenous unipolar depressive parents (proband children) and 72 children aged 10-17 of 66 normal parental couples (control children) were studied. Overall rate of psychopathology (disorders present at the time of investigation and one year before) reached 51% in proband children and 29% in control children. Depressive disorder rate reached 10% in proband children and 4% in control children. The sex of the depressive parent did not influence the psychopathology rate in offspring, while the early age of onset of the illness (under 30 years) in parent increased the psychopathology risk in children. The severity of the psychopathology in children defined as functional impairment was significantly dependent on the severity of the depressive illness in proband parent, the presence of psychopathology in the spouse of the depressive parent, the presence of psychopathology in the relatives of both parents, the socio-cultural level of the family and the violence expressed in the familial atmosphere.

Adolescent↗