Search PubMed⌕ Search

Biomedical subjects

J Pantel

Publications and source records attributed to J Pantel.

At least 37 records · Page 2Linked to original sources
PubMed2000

Syntactic comprehension deficits in Alzheimer's disease.

Syntactic comprehension of German patients with dementia of the Alzheimer type was investigated and compared to healthy controls matched with respect to age, sex, and education. Special attention was directed at syntactic structures, which, in contrast to a language like English, are feasible in a grammatically rich language like German. In a sentence picture matching paradigm, only semantically reversible sentences were used. Syntactic complexity ranged from simple active voice sentences to more complex sentences like center-embedded object relative sentences. In comparison to their controls, patients showed a deficit in nearly all categories. Their performance was not influenced by age, but was heavily influenced by the degree of cognitive impairment. Patients with mild cognitive impairment, as defined by a MMSE score of 20 or higher, showed only slight difficulties in syntactic processing, whereas patients with moderate to severe impairment (MMSE < 20) did not perform above chance limits in most syntactic categories. It appears as though syntactic comprehension is only mildly affected in the early stages of Alzheimer's disease and is rather severely impaired in more advanced stages. In the present report, results are discussed in terms of working memory demands for syntactic processing.

Aged↗
PubMed2000

NF1 gene analysis focused on CpG-rich exons in a cohort of 93 patients with neurofibromatosis type 1.

We studied the NF1 gene in 93 unrelated patients with neurofibromatosis type1, focusing the analysis on four exons that contain the highest number of possible mutations occurring at CpG sites. We used denaturing gradient gel electrophoresis to analyse exons 16, 28, 29 and 49, which contain 45 (25%) of the 183 possible mutations that could occur at the 120 CpG dinucleotides of the coding sequence. Six different mutations were identified, five of which are novel: two truncating mutations, W1810X and 5448insG, located in exon29; two splice defects leading to exon29 skipping, 5206-2A>G and 5546G>A; and one missense mutation, L844F, located in exon16. The already described R1748X mutation located in exon29 was found in two unrelated patients. The 5546G>A and R1748X mutations are located at CpG sites, whereas the W1810X involves a CpNpG site. Four novel polymorphisms, which may be helpful for family studies, were also identified. Overall, all but one mutations were found in exon29, a result which suggests that all the CpG sites of the NF1 coding sequence do not have the same mutability, and that exon29, the most CpG-rich exon, contains mutational hotspots associated with NF1.

Adolescent↗
PubMed2000

A new method for the in vivo volumetric measurement of the human hippocampus with high neuroanatomical accuracy.

Accurate and reproducible in vivo measurement of hippocampal volumes using magnetic resonance (MR) imaging is complicated by the morphological complexity of the structure. Additionally, separation of certain parts of the hippocampus from the adjacent brain structures on MR images is sometimes very difficult. These difficulties have led most investigators to either use arbitrary landmarks or to exclude certain parts of the structure from their measurements. Based on three-dimensional MR data, we have developed a reliable in vivo volumetric measurement of the human hippocampus. In contrast to most of the previously described volumetric MR-based methods, we aimed to sample the entire hippocampal formation using its true anatomical definition. This was accomplished by relying on the capacity of the BRAINS software to simultaneously visualize in multiple planes, to "telegraph" tracings or cursor position from one plane to another, and to simultaneously rely on multispectral data from three different image sets (T1, T2, and tissue classified). The methods for identifying boundaries and measuring the hippocampal volume are described. The method has excellent reliability, sensitivity, and specificity. The method may be of use in studies of structure-function relationships in neuropsychiatric disorders such as schizophrenia, temporal lobe epilepsy, and Alzheimer's disease. Future work will use these measurements as training data for a neural net-based technique to identify the anatomical boundaries automatically.

Adolescent↗
PubMed2000

[Cerebrospinal fluid protein tau levels in the differential diagnosis of Alzheimer's disease].

Tau protein concentration in cerebrospinal fluid was determined in 55 patients with Alzheimer's disease (AD), 18 patients with vascular dementia (VD), 19 patients with dementia caused by other disorders and 14 patients with major depression. Significantly (p < 0.05) elevated protein tau concentrations were found in AD patients (564.5 +/- 275.5 pg/ml) compared to all other patient groups (VD: 406.5 +/- 263.9 pg/ml; other dementia: 275.0 +/- 135.4 pg/ml; depression: 212.9 +/- 115.6 pg/ml). However, tau levels in AD patients covered a broad range (163.2 pg/ml-1200 pg/ml). AD patients with tau levels below the 25%-percentile of the distribution (among them a high percentage of patients with presenile onset) showed tau levels similar to those of the patients with late life depression. No significant correlations between tau levels and clinical variables such as severity of dementia, age, age of onset, duration of illness, and cerebral changes as assessed by volumetric magnetic resonance imaging could be demonstrated. Similarly, we could not find an influence of either APO-E genotype or psychotropic medication on the tau levels in AD patients. In accordance with other studies our results confirm elevated tau levels in AD compared to elderly not demented control subjects. Comparing groups, this finding applies as well with respect to VD and other dementing disorders. However, elevated tau levels cannot be detected in a subgroup of AD patients. This finding needs to be further investigated in future studies.

Aged↗
PubMed2000

Measurement of plasma free luteinizing hormone beta-subunit in women.

Little is known about the physiological secretion of the free beta-subunit of LH (LHbeta). The aim of this study was to compare in women the secretion of LHbeta, using sensitive and specific two-site immunoassays, with dimeric LH and the free common alpha-subunit (FAS). The LHbeta assay does not recognize the dimeric LH and cross-reacts only with free hCG beta-subunit (CGbeta). Thus, all of the plasma samples were also tested with a highly specific immunoradiometric assay for free CGbeta. Molar concentrations (i.e. picomoles per L) were used to compare the plasma levels of LH and its free subunits. Plasma LH, LHbeta, FAS, and CGbeta levels were measured in five normally cycling women during the early follicular phase and the ovulatory peak of LH. The pulsatile profiles of LH, LHbeta, FAS, and CGbeta were studied in five postmenopausal women before and 21 days after injection of a depot preparation of the GnRH agonist D-Trp6 (3.75 mg, im) and in five women with functional hypothalamic amenorrhea (FHA), i.e. low plasma LH levels, during pulsatile GnRH administration (20 microg/pulse, 90 min, sc). Afterward, one of the patients with FHA received a single sc injection of 1350 U recombinant human LH, and plasma LH, LHbeta, FAS, and CGbeta levels were measured and compared with the high plasma levels of one postmenopausal woman. In cycling women, basal plasma LHbeta and CGbeta levels were below the detection limit of the assays (1.34 and 0.65 pmol/L, respectively), and plasma FAS levels were 13.60 +/- 0.13 pmol/L. During the LH surge, there was a parallel increase in LH, LHbeta, and FAS. Plasma CGbeta levels remained undetectable. In normal postmenopausal women, basal plasma dimeric LH, LHbeta, and FAS levels were increased in parallel, and their pulsatile profiles were similar, without measurable plasma CGbeta levels. After D-Trp6 administration, plasma LH and LHbeta levels were completely suppressed, whereas plasma FAS levels increased, and plasma CGbeta remained below 0.65 pmol/L. In FHA women, basal plasma levels of LH and FAS were low, without detectable LHbeta and CGbeta levels. During pulsatile GnRH administration, LHbeta became detectable, and pulses were synchronous with those of LH and FAS. The secretion of LH and LHbeta was almost equimolar. Plasma CGbeta levels remained undetectable. In the patient with FHA, administration of recombinant human LH increased only plasma LH levels, whereas plasma LHbeta and FAS levels remained very low. In conclusion, when the production of dimeric LH increases, a concomitant, parallel, and almost equimolar hypersecretion of uncombined and biologically inactive LHbeta occurs. Like the alpha-subunit, LHbeta may be secreted in the dissociated free form. This can lead to pitfalls during clinical investigations if assays of free CGbeta display some cross-reaction with free LHbeta.

Adult↗
PubMed1999

Topography of callosal atrophy reflects distribution of regional cerebral volume reduction in Alzheimer's disease.

It has been suggested that regional corpus callosum atrophy in Alzheimer's disease (AD) may serve as an in vivo index of neuronal loss in the neocortex. In this study total and regional size of the corpus callosum was evaluated with respect to the volumes of the frontal, temporal, and parietal lobes in 38 patients with AD (NINCDS-ADRDA criteria) using quantitative magnetic resonance imaging. Twenty healthy subjects matched for age and gender served as a control group. All quantitative measurements were performed by manual tracing using personal computer-based software. Both total size and the five measured regional subsections were significantly smaller in AD when compared to the control subjects. The severity of dementia was significantly correlated with the size of the middle sections of the corpus callosum (rostral body and midbody). Within the AD group, the rostral body of the corpus callosum was significantly correlated with the frontal lobe volumes, the midbody was correlated with the temporal lobe volumes, and size of the splenium was correlated with the parietal lobe volumes. We conclude that callosal atrophy in AD reflects the severity and pattern of cortical neuronal damage. Correlations between regional callosal atrophy and severity of dementia indicate that interhemispheric cortico-cortical disconnection may contribute to the dementia syndrome.

Aged↗
PubMed1999

Cerebrospinal fluid A beta42 is increased early in sporadic Alzheimer's disease and declines with disease progression.

All mutations known to cause familial Alzheimer's disease (AD) act by increasing the levels of soluble beta-amyloid peptide (A beta), especially the longer form, A beta42. However, in vivo elevation of soluble A beta in sporadic AD has so far not been shown. In the present study, we used enzyme-linked immunosorbent assays specific for A beta42 and A beta40 to investigate cerebrospinal fluid from sporadic AD at different stages of disease severity, to clarify the roles of A beta42 and A beta40 during disease progression. We also evaluated three other groups--one group of patients with mild cognitive impairment who were at risk of developing dementia, a cognitively intact, nondemented reference group diagnosed with depression, and a perfectly healthy control group. We found that A beta42 is strongly elevated in early and mid stages of AD, and thereafter it declines with disease progression. On the contrary, A beta40 levels were decreased in early and mid stages of AD. The group of cognitively impaired patients and the depression reference group had significantly higher levels of A beta42 than the healthy control group, implying that A beta42 is increased not only in AD, but in other central nervous system conditions as well. Our data also point out the importance of having thoroughly examined control material. The initial increase and subsequent decrease of A beta42 adds a new biochemical tool to follow the progression of AD and might be important in the monitoring of therapeutics.

Aged↗
PubMed1999

[The evaluation of research performance in psychiatry. Potential and pitfalls of bibliometric analysis].

Recent scientific and economic developments have emphasized the need for objective and operationalized criteria for the evaluation of collective and individual research performance. In this context the present article discusses the possibilities and limitations of bibliometric analysis in the evaluation of psychiatric research. Taking into account recent scientometric knowledge, the potentials and pitfalls of the so called impact factor are critically discussed with respect to its usefulness in the evaluation of psychiatric research performance in Germany. A major criticism arises from the observation that the unreflecting use of the impact factor may overemphasize quantitative aspects to the disadvantage of qualitative aspects of research. This may however lead to unwanted distortions and misjudgements. The critical analysis of the current use of scientometric indices in the evaluation process emphasizes the need for alternative criteria, which should take into account disciplinary as well as national idiosyncrasis. Accordingly, the authors aim to induce and contribute to a discussion process within the scientific community, which may lead to a more appropriate evaluation of psychiatric research performance.

Bibliometrics↗
PubMed1998

Corpus callosum in Alzheimer's disease and vascular dementia--a quantitative magnetic resonance study.

We investigated atrophic alterations in different regions of the corpus callosum in Alzheimer's disease (AD) and vascular dementia (VD) with respect to clinical changes. 32 patients with AD (NINCDS-ADRDA criteria), 17 patients with VD (NINDS-AIREN criteria) and 13 healthy control subjects were included. 3-D MRI sequences were acquired using a 1.5T MRI scanner. The size of the corpus callosum and its subdivisions was sampled on 5 mid-saggital slices using a personal computer-based software. Total callosal size was significantly reduced in AD but not in VD. Furthermore, the most rostral parts of the corpus callosum were significantly smaller in AD when compared to controls. Again, these changes were not found in patients with VD. Severity of dementia was significantly correlated with the size of the midbody of the corpus callosum in AD. Callosal atrophy in AD may reflect the severity and pattern of cortical neuronal damage occurring mostly in the inferior frontal, anterior parietal and midtemporal regions. Correlations between regional callosal atrophy and severity of dementia indicate that interhemispheric cortico-cortical disconnections may contribute to the dementia syndrome.

Aged↗
PubMed1998

Prevalence of mild cognitive impairment in an elderly community sample.

The term "mild cognitive impairment" refers to cognitive deficits which exceed normal physiological aging processes, but do not fulfill the criteria for dementia. While recent studies indicate that the respective deficits can be reliably assessed, different diagnostic criteria have prevented a wide application of this diagnosis in clinical practice. The aims of the present study were (1) to assess the prevalence rates of four current diagnostic concepts and (2) to investigate mild cognitive impairment with respect to psychological and sociodemographic variables. Data from 202 probands recruited from the interdisciplinary longitudinal study on adult development were analyzed. On the time of examination, probands were between 60 to 64 years old and in a good health. The following prevalence rates were determined: 13.5% for age-associated memory impairment (AAMI), 6.5% for age-consistent memory impairment (ACMI), 1.5% for late-life forgetfulness (LLF), and 23.5% for aging-associated cognitive decline (AACD). Complaints of cognitive deficits were significantly correlated with higher scores on depression and neuroticism scales but with none of the neuropsychological measures. Reduced performance in neuropsychological tests was associated with a lower educational level and socioeconomic status. We conclude that the prevalence rates of mild cognitive impairment are highly dependent on the diagnostic criteria applied. In this respect the self-report of cognitive decline might be a less useful criteria. Longitudinal studies are warranted to further elucidate the predictive value of these diagnostic criteria.

Adult↗
PubMed1998

[Volumetric brain findings in late depression. A study with quantified magnetic resonance tomography].

A number of observations including clinical manifestation, course, outcome, and family history, support the view that patients presenting with a major depression occurring first in late life should be treated as a nosological subgroup. In this study quantitative magnetic resonance imaging (MRI) was used to investigate volumes of different brain structures in 19 patients with late onset major depression (age of onset > 50) and 13 age matched controls. 3-D MRI sequences were acquired using a Siemens 1.5T scanner. Whole brain volume, CSF volume, volume of the frontal and temporal lobes and the volume of the amygdala-hippocampus complex were assessed using the software NMRWin. Compared to the controls, depressed patients showed a significantly lower whole brain volume and a significantly higher CSF volume, whereas volumes of the frontal and temporal lobes as well as the amygdala-hippocampus complex volumes were not significantly decreased. In addition, depressed patients exhibited a higher ventricle-brain ratio suggesting a higher degree of central atrophy compared to healthy individuals. Our results indicate that cerebral changes involving subcortical structures are of relevance in the pathogenesis of late-onset depression. Defining the aetiology of these lesions may be important for the development of preventive treatment of depression in the elderly.

Aged↗
PubMed1998

[Mild cognitive deficit in the elderly. Results of a gerontologic study].

The term "mild cognitive impairment" refers to cognitive deficits which exceed normal physiological aging processes, but do not fulfill the criteria for dementia. The prevalence rates of four current concepts were compared in a sample of 202 healthy 60-64 year-old participants recruited from the interdisciplinary longitudinal study on adult development and aging (ILSE). Furthermore, the relationships between cognitive deficits and psychological and sociodemographic variables were examined. The following prevalence rates were determined: 13.5% for age-associated memory impairment, 6.5% for age-consistent memory impairment, 1.5% for late-life forgetfulness and 23.5% for aging-associated cognitive decline. Subjective cognitive complaints did not correlate with results obtained from neuropsychological tests. Significant correlations were however found between subjective cognitive complaints and higher scores on depression and neuroticism scales. Significant correlations were also found between a reduced test performance and a lower educational level and socioeconomic status. Longitudinal studies are warranted to further elucidate the predictive value of these diagnostic concepts.

Adult↗
PubMed1998

Severe akathisia during olanzapine treatment of acute schizophrenia.

Olanzapine is a newly developed atypical neuroleptic with a marked affinity to the 5-HT2, D2 and D4 dopamine receptors. Like other atypical neuroleptics olanzapine is considered to show a reduced prevalence of extrapyramidal side effects when compared to classical neuroleptic drugs. We report on three patients with acute schizophrenia, who developed severe akathisia during treatment with olanzapine (20-25 mg/d). In two of these cases akathisia resolved after withdrawal of olanzapine and substitution by a classical or an atypical neuroleptic agent, respectively. In one of these patients olanzapine was well tolerated when reintroduced in combination with lorazepam after complete remission of akathisia. In the third patient akathisia was sufficiently controlled by dose reduction. Akathisia is generally considered to result from D2 dopamine receptor antagonism. In the case of atypical neuroleptics such as olanzapine a low but still considerable D2 dopamine receptor occupancy may be compensated by the 5-HT2 antagonism. However, this mechanism may fail under certain circumstances, in particular if D2 dopamine antagonism exceeds a certain threshold. One should therefore be aware of possible extrapyramidal side effects with olanzapine that are reduced compared to classical neuroleptic drugs but not completely eliminated.

Adult↗
PubMed1998

Characterization of human lutropin carboxyl-terminus isoforms.

Human lutropin (hLH) exhibits both carbohydrate and peptidic heterogeneities that affect its biological potency and the duration of its activity in vivo. Peptidic changes within the hLH beta-subunit are characterized as intrachain proteolytic nicking and carboxyl terminus heterogeneity. To date, the carboxyl terminus of hLHbeta appears to end at either position Gln114 or Gly117, as determined by sequencing of purified subunit. Furthermore, the complementary DNA for hLHbeta predicts a protein containing an additional peptidic stretch, which would make the beta-subunit 121 residues long. This extension may be responsible for the particular intracellular behavior of hLHbeta. To investigate the carboxyl terminus polymorphism of natural hLHbeta, monoclonal antipeptide antibodies were raised against a synthetic peptide mimicking the 104-119 portion of hLHbeta. One antibody, designated LHP09, was found to specifically react with the recombinant hLHbeta ending at position hLHbeta[Leu119] but not with other recombinant forms ending at [Ser116], [Phe120] or [Leu121]. Immunochemical analysis of hLH, either pituitary or urinary in origin, indicated that only pituitary hLH contains a Leu119-ending form of hLHbeta. Finally, immunohistochemical detection was performed using LHP09 and showed specific staining of a normal adult pituitary gland. These observations support the in vivo existence of intrapituitary molecular forms of hLHbeta ending at various positions between Gln114 and Leu121.

Amino Acid Sequence↗
PubMed1997

Quantitative magnetic resonance imaging in geriatric depression and primary degenerative dementia.

Quantitative magnetic resonance imaging (MRI) was used to investigate volumes of different brain structures in 19 patients with late-onset major depression (DSM-III-R), 27 patients with Alzheimer's disease (NINCDS-ADRDA criteria) and 13 age matched controls. 3-D MRI sequences were acquired using a Siemens 1.5 T scanner. Whole brain volume, CSF volume, volume of the frontal and temporal lobes and the volume of the amygdala-hippocampus complex were assessed using the software NMR Win. Compared to the controls, depressed patients showed a significantly lower whole brain volume and a significantly higher CSF volume, whereas volumes of the frontal and temporal lobes as well as the amygdala-hippocampus complex volumes were not significantly decreased. In addition, depressed patients exhibited a higher ventricle-brain ratio suggesting a higher degree of central atrophy compared to healthy individuals. In contrast, Alzheimer patients showed significantly lower volumes than depressed patients and controls with respect to all volumetric parameters. Although the findings indicate the presence of brain atrophy in patients with late-onset depression, the pattern of volumetric changes in these patients differs markedly from that observed in patients with primary degenerative dementia.

Aged↗
PubMed1997

Quantitative magnetic resonance imaging and neuropsychological functions in dementia of the Alzheimer type.

BACKGROUND: The aim of the present study was to investigate neuropsychological functions in dementia of the Alzheimer type (DAT) with respect to morphological changes that were revealed by quantitative magnetic resonance imaging (MRI). METHODS: Twenty patients with DAT (NINCDS-ADRDA criteria) and 10 healthy age and sex matched controls were included. The neuropsychological function was evaluated on a test battery covering the severity of dementia, verbal and visual memory, concentration and attention, language skills and general intelligence as well as activities of daily living. 3D MRI sequences were acquired using a 1.5 T Siemens MAGNETOM. Whole brain volume, total intracranial volume (TIV), volume of the frontal and temporal lobes and volumes of the amygdalahippocampus complex (AHC) were assessed using the newly developed software NMR Win. RESULTS: Apart from TIV all morphometric parameters differed significantly between the diagnostic groups. AHC volumes discriminated best between the groups, with only a small overlap. AHC atrophy exceeded generalized atrophy. These findings were confirmed when the data were reanalysed after dividing the DAT patients into a mildly and moderately affected group. The severity of dementia was significantly correlated with the volumes of the AHC and the volumes of the temporal lobes bilaterally, but not with the whole brain volume and the volumes of the frontal lobes. CONCLUSIONS: These results underline the important role of the temporal substructures for aetiology and progression of DAT. They indicate that the volume of the AHC can be monitored by MRI and may be used to follow up the disease process.

Aged↗
PubMed1997

Two cases of deep vein thrombosis associated with a combined paroxetine and zotepine therapy.

Thromboembolic events arising as a side-effect of neuroleptic and thymoleptic therapy, although rare, represent serious complications. We report on two patients suffering from an acute deep vein thrombosis after administration of a combined therapy with paroxetine and zotepine. The absence of common risk factors for the development of venous thrombosis in both patients led us to reconsider the potential impact that the drugs administered may have on thrombogenesis. Possible influences of the neuroleptic and thymoleptic therapy on the coagulation system are discussed. Although the clinical observations do not necessarily imply a strict causal relationship between drug administration and thrombosis, there are features of these two cases that should enhance our awareness of the possibility of thrombotic events occurring as a consequence of neuroleptic and thymoleptic therapy.

Aged↗