Publications by authors named "Ursula Ptok"

Objectives: The aim of this study was to review psychodynamic formulation with respect to the language used and the evidence it provides about variations of clinical purpose.

Method: The purpose of the psychodynamic formulation is considered in training and clinical contexts. Three formulations are presented: two written from alternative theoretical perspectives and one designed to be spoken to the patient.

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Objective: The familial aggregation of late-onset Alzheimer's disease (AD) might be caused by the clustering of genetic risk factors in families. This study investigates the influence of variants of candidate genes on the familial aggregation of AD.

Methods: The occurrence of AD was examined in 1,420 first-degree relatives of 70 AD patients and 144 nondemented controls classified by the presence of AD and relevant candidate genes in index subjects.

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The endosomal lysosomal system might play a role in Alzheimer's disease, but its impact in major depression is unknown. The expression of the cation-dependent mannose 6-phosphate receptor (CD-MPR) is increased in Alzheimer's disease and the CD-MPR gene is located next to a region on chromosome 12 possibly linked to Alzheimer's disease. We investigated a C/T polymorphism in the CD-MPR gene in 188 Alzheimer's disease patients, in a control sample of 193 patients with major depression, as hospitalized controls, and in 259 healthy controls.

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The low-density lipoprotein receptor-related protein (LRP) is one of the most important cholesterol receptors in the brain. Gene variation of its ligand, apolipoprotein E, is a major genetic risk-factor for Alzheimer's disease (AD). The C-allele of the silent C766T polymorphism in exon 3 of the LRP gene might be associated with AD, however, results are conflicting and thus discussed controversially.

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Background: First-degree relatives of patients with Alzheimer's disease (AD) and major depression (MD) carry an increased genetic risk for the same disorders. Subjective memory complaints of the family members of patients might be an early sign or an indicator of an increased risk of either dementia or depression. Alternatively, they might be the consequence of the increased subjective awareness of relatives and spouses of patients of their own age-associated memory failures.

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Introduction: Depression is common in Alzheimer's disease (AD). The symptomatology of depression in dementia may differ from depression alone. Consequently, the reports on lifetime depressive symptoms were compared in AD patients and age-matched non-demented participants.

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Background: Several risk factors of depression, i. e., female gender and life-stress, have been identified.

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Inflammation is thought to promote neuronal cell death in Alzheimer's disease (AD). The proinflammatory interleukin-1 is a main component in inflammatory pathways and is overexpressed in the brain of AD patients. Investigation of different polymorphisms in the interleukin-1 genes (IL-1alpha -889, IL-1beta -511, IL-1beta +3953) revealed associations between specific alleles and AD in that they increased the risk or modified the age at onset of AD.

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The dysfunction of the cholinergic system in Alzheimer's disease (AD) supports the hypothesis that a decline in choline acetyltransferase (ChAT) activity in memory as well as in cognitive functions in AD might be functionally linked. To assess the physiological relevance of an allelic variation in the ChAT gene we investigated the presence of a possible polymorphism in AD patients and in elderly non-demented subjects as controls. By using polymerase chain reaction, single stranded conformation polymorphism or the LightCycler analysis we detected a single nucleotide polymorphism in the first common coding exon of the ChAT gene.

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Alzheimer's disease (AD) patients often present with concurrent major depression (MD). To investigate the reasons for this comorbidity, e.g.

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The intracellular aspartyl protease cathepsin D (catD) is involved in such Alzheimer's disease (AD)-related processes as the activation of the endosomal/lysosomal system and the cleavage of the amyloid precursor protein into amyloidogenic components, which may initiate neurodegeneration. A non-synonymous polymorphism (exon 2, C to T exchange leading to ala-->val substitution) of the gene encoding catD (CTSD) was previously associated with AD, in that the T allele increased the risk for AD. To investigate whether the T allele is associated with disease-related traits, we measured the concentration of the amyloid beta-peptide 1-42 (Abeta(42)) and 1-40 (Abeta(40)) in patients and control subjects.

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Introduction: The clustering of two or more disorders in the same family might indicate the presence of common genetic risk factors. The prevalence of various psychiatric disorders in relatives of Alzheimer's disease (AD) patients has rarely been investigated. Consequently, family study data were reinvestigated to assess, if there are indications for an overlap of genetic risk factors of AD and other psychiatric disorders.

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