Biomedical subjects

Peter Schönknecht

Publications and source records attributed to Peter Schönknecht.

10 recordsLinked to original sources

PubMed2006

International quality control survey of neurochemical dementia diagnostics.

UNLABELLED: Currently, neurochemical dementia diagnostics (NDD) are increasingly entering routine clinical neurochemistry, offering improved early and differential diagnosis of dementias. However, there is an obvious lack of standardization in pre-analytical sample handling and systematic quality surveys. Therefore, in this study, 14 laboratories in Germany, Austria, and Switzerland were given aliquots of a human cerebrospinal fluid (CSF) sample, and were asked to measure Alzheimer's disease (AD) biomarkers (amyloid beta (Abeta) peptides, total Tau protein, and phosphorylated Tau protein (P-tau(181P))) according to their routine protocols. RESULTS: The inter-laboratory coefficients of variation of the results obtained by the laboratories participating in this study were in the range of 20-30%. Although the results of this quality control survey are promising, the quality of measurements has to be further optimized.

Alzheimer Disease↗

PubMed2006

Dissociation between CSF total tau and tau protein phosphorylated at threonine 231 in Creutzfeldt-Jakob disease.

To study the potential diagnostic value of abnormally phosphorylated tau protein in Creutzfeldt-Jakob disease (CJD) compared to Alzheimer's disease (AD), we determined levels of tau phosphorylated at threonine 231 (p-tau231) and of total tau (t-tau) in cerebrospinal fluid (CSF) of CJD patients, AD patients, and healthy controls (HC). CJD patients showed excessively high t-tau levels but relatively low p-tau(231) concentrations compared to the AD group. t-tau alone yielded the best diagnostic accuracy to differentiate between CJD and AD patients, when compared to p-tau231 and the p-tau231/t-tau ratio (97, 78, and 95% correctly allocated cases, respectively). Our findings indicate a dissociation in the direction of change in CSF levels of t-tau and p-tau231 in CJD when compared to AD.

Age Distribution↗

PubMed2005

Prevalence and natural course of aging-associated cognitive decline in a population-based sample of young-old subjects.

OBJECTIVE: "Mild cognitive impairment" refers to cognitive deficits in older age that exceed age-related cognitive decline but do not fulfill criteria for dementia. Affected subjects are assumed to be at higher risk for the development of dementia, such as Alzheimer's disease. However, little is known about the group of young-old subjects with respect to the prevalence and natural course of cognitive decline. METHOD: Within the population-based Interdisciplinary Longitudinal Study on Adult Development and Aging, neuropsychological functioning was assessed in 500 community-dwelling young-old subjects of two German urban regions who were born during 1930-1932. The participants were carefully screened for physical and mental health and reexamined 4 years later. The concept of "aging-associated cognitive decline" was applied. RESULTS: At baseline, 13.4% of the subjects fulfilled criteria for aging-associated cognitive decline. Four years later, the prevalence rates for rose to 23.6%; 52.3% of the subjects initially classified as having aging-associated cognitive decline retained the diagnosis at follow-up. Although subjects with aging-associated cognitive decline showed a reduced performance in all neuropsychological domains addressed, a significant decline was confined to delayed verbal memory test performance during the 4-year follow-up period in relation to comparison subjects. Aging-associated cognitive decline did not predict conversion to dementia during the follow-up interval. CONCLUSIONS: In young-old community-dwelling individuals, aging-associated cognitive decline is a frequent condition with a high temporal stability. During a 4-year follow-up, subjects with aging-associated cognitive decline deteriorated specifically in measures of episodic memory, underscoring the value of the respective deficits in characterizing "mild cognitive impairment."

Adult↗

PubMed2004

Distribution of cerebral atrophy assessed by magnetic resonance imaging reflects patterns of neuropsychological deficits in Alzheimer's dementia.

Neuropsychological deficits were investigated with respect to regional distribution of cerebral atrophy as assessed by volumetric magnetic resonance imaging (MRI) in 50 patients with Alzheimer's dementia (AD; NINCDS-ADRDA criteria) and 20 healthy volunteers. When compared between groups, test performance of all investigated neuropsychological domains including declarative memory, language, praxia, psychomotor speed, as well as attention and concentration was significantly impaired. These deficits were differentially correlated with regional atrophic changes. In particular, volumes of the right amygdala-hippocampus complex correlated with declarative memory performance, whereas volumes of the left temporo-parietal regions correlated with performance in naming and praxia. Furthermore, left frontal lobe atrophy was associated with verbal fluency. Our data confirm the central role that medial temporal atrophy plays for declarative memory deficits in AD and indicate that additional changes in the parietal, temporal and frontal lobes are responsible for further neuropsychological deficits characteristic of this disorder.

Aged↗

PubMed2003

Hippocampal glucose metabolism is associated with cerebrospinal fluid estrogen levels in postmenopausal women with Alzheimer's disease.

Animal studies indicate that estrogens, such as 17beta-estradiol (E(2)), may enhance hippocampal metabolism and function. In postmenopausal Alzheimer's disease (AD) patients, cerebrospinal fluid (CSF) E(2) levels were significantly lower than in non-demented controls. This finding was inversely correlated with CSF beta-amyloid levels. To address the potential impact of this finding, E(2) levels in CSF were correlated with regional cerebral [18F]2-fluoro-2-deoxy-D-glucose (FDG) uptake as measured using positron emission tomography (PET) in six postmenopausal AD patients. CSF E(2) levels were determined using an electro-chemiluminescence-immunoassay on the Roche Elecsys 2010 immunoassay analyzer. Basic image processing was done by MEDx, using SPM routines for spatial normalization and statistics. CSF E(2) levels were significantly correlated with cerebral glucose metabolism in the left hippocampus. This is the first clinical study indicating an association between CSF E(2) concentration and hippocampal glucose metabolism in postmenopausal women with AD.

Aged↗

PubMed2003

Cerebrospinal fluid tau levels in Alzheimer's disease are elevated when compared with vascular dementia but do not correlate with measures of cerebral atrophy.

Increased tau levels are a well-established finding in Alzheimer's disease (AD). In contrast, the potential value of tau levels in the differential diagnosis of AD, vascular dementia (VD) and major depression warrants further investigation. The potential impact of psychotropic medication also needs to be established. We investigated cerebrospinal fluid (CSF) tau protein concentrations in 88 patients with AD, 23 patients with VD, 25 patients with major depression and 17 age-paralleled controls without cognitive impairment with respect to important clinical variables, type and dosage of psychotropic medication and cerebral changes as assessed by magnetic resonance imaging (MRI). The AD patients showed significantly elevated tau levels compared with patients with VD or major depression and controls. Tau levels obtained in the VD group were intermediate, with significant differences from both AD patients and patients with major depression and controls. Within the AD group, no significant correlation between tau levels, severity of dementia, age, duration of disease, type and dosage of psychotropic medication or MRI volumetric changes arose. A subgroup of AD patients without increased tau levels was characterized by a significantly larger percentage of patients with presenile onset.

Aged↗

PubMed2003

Levels of total tau and tau protein phosphorylated at threonine 181 in patients with incipient and manifest Alzheimer's disease.

Cerebrospinal fluid tau protein levels are considered to be a promising marker for Alzheimer's disease (AD) and may facilitate early detection. Using the newly developed INNOTEST Phospho-Tau((181P)) kit examination of total tau and tau protein phosphorylated at threonine 181 (phospho-tau 181) revealed significantly (P<0.05) higher values in both patients with incipient and manifest AD than in controls. In patients with vascular dementia, phospho-tau 181 levels were not different from controls but were significantly lower than in patients with manifest AD. These findings suggest that total and phosphorylated tau protein may facilitate early detection and differential diagnosis of AD.

Aged↗

PubMed2003

Impairment in basal limbic function in schizophrenia during affect recognition.

Patients with schizophrenia routinely fail to perform affect recognition tasks as accurately as healthy controls. The investigation of performance-related changes in cerebral activation in healthy subjects may facilitate the understanding of adaptation processes to different levels of difficulty and help to interpret the activation changes found in schizophrenic patients. Nine first hospitalized partly remitted schizophrenic patients and 10 healthy controls participated in an fMRI study with a facial affect discrimination and labeling task. Seven of the 10 healthy subjects were reexamined with changed stimulus conditions adapted according to the mean accuracy scores detected in schizophrenic patients. Controls showed a significantly increased activation of the right gyrus frontalis medialis with rising task difficulty during both tasks. The schizophrenic patients demonstrated a significantly decreased activation of the anterior cingulate during facial affect discrimination and of the amygdala-hippocampal complex bilaterally during facial affect labeling. In addition, an increased activation of the gyrus frontalis medialis bilaterally became apparent in the schizophrenic patients. It is suggested that the latter may reflect a compensatory effort for deficits in more basal limbic functions.

Adult↗

PubMed2003

Cerebrospinal fluid tau protein levels in schizophrenia.

Increased cerebrospinal fluid (CSF) tau protein levels are generally considered to provide a sensitive marker of neurodegenerative processes such as Alzheimer's disease (AD). Since a more pronounced cognitive decline has been described in older schizophrenic patients, it has been hypothesized that these patients might be at a higher risk of developing AD. CSF levels of total tau protein and tau protein phosphorylated at threonine 181 (phospho-tau) were determined among 19 older and younger patients with schizophrenia compared to 20 age-matched healthy controls. No significant differences in CSF total tau and phospho-tau levels arose between patients with schizophrenia and controls. Although our results do not exclude a progressive neurodegenerative pathology, they provide evidence against major neuronal degeneration such as an AD-related pathology associated with increased tau levels in schizophrenia.

Adult↗

PubMed2002

Cerebrospinal fluid 24S-hydroxycholesterol is increased in patients with Alzheimer's disease compared to healthy controls.

Experiments in cell cultures indicate that accumulation of cholesterol in hippocampal neurons results in an accelerated cleavage of amyloid precursor protein into amyloidogenic components. To be eliminated from the brain, cholesterol is converted to 24S-hydroxycholesterol which may reflect cerebral cholesterol turnover. We investigated cerebrospinal fluid (CSF) concentrations of 24S-hydroxycholesterol in a group of 14 Alzheimer's disease (AD) patients and ten healthy controls without any cognitive deficits or psychiatric or neurological disorders. To exclude potential effects of circulating plasma cholesterol on CSF 24S-hydroxycholesterol levels, only patients and controls with cholesterol levels in the normal range of 150-230 mg/dl were included. We found significantly elevated 24S-hydroxycholesterol CSF but not plasma levels in AD patients compared with healthy controls. Our results demonstrate that CSF 24S-hydroxycholesterol is increased in AD. This effect does not seem to be triggered by plasma cholesterol levels since the latter did not significantly differ between groups.

Age Factors↗