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Biomedical subjects

C Bouras

Publications and source records attributed to C Bouras.

At least 127 records · Page 7Linked to original sources
PubMed1984

The basal nucleus of Meynert in idiopathic Parkinson's disease.

The basal nucleus of Meynert (bnM) was examined in 6 patients with idiopathic Parkinson's disease and in 5 age-matched controls. The histopathological study was followed by a quantitative analysis of the magnocellular population of the nucleus, with the determination of the number of neurons and their nucleolar volume. In Parkinson's disease, there was a neuronal loss ranging from 29.9% to 68.3% (mean 45.8%) and numerous surviving cells containing Lewy inclusion bodies. The percentage loss of cells did not display a significant correlation with the age of the patients, the duration of the illness, the mental state or the drug regime. On the other hand, no significant differences in nucleolar volume of bnM neurons were detected between patients and controls. The damage of the basal nucleus of Meynert in Parkinson's disease is less severe than that generally observed in Alzheimer's disease, and is slightly more pronounced than that reported for progressive supranuclear palsy.

Aged↗
PubMed1983

Cerebral glucose utilization: local changes after microinoculation of scrapie agent in hamster.

The effects of scrapie agent on local cerebral energy metabolism were studied by the [14C]2-deoxyglucose (2-DG) autoradiographic method of Sokoloff et al. after stereomicroinoculation (0.5 microliter, 10(-2) of scrapie suspension) in hamster left striatum. From a group of 20 hamsters inoculated, 2 animals were killed every 10 days from the 30th day after inoculation to the terminal stage of the disease. Experiments were carried out according to the qualitative 2-DG procedure and cerebral autoradiographs of inoculated animals were compared to those of 3 controls. The results show changes of local cerebral glucose utilization in some discrete brain regions, ipsilateral to the side of inoculation, and their sequential spreading to other cerebral structures with a definite order: left anterior thalamus, left posterior thalamus, then medial geniculate body (ipsilateral, then controlateral), and finally some brainstem nuclei (inferior colliculus, superior olivary nucleus); the inoculated striatum is affected very late, after clinical signs. Metabolic changes which first occur ipsilaterally to the side of inoculation precede the clinical symptoms, while their contralateral spreading is concomitant with the clinical signs. The data demonstrate a rostral--caudal sequence of the cerebral metabolic changes, ipsilateral to the side of inoculation, which may reflect in part the slow spread of agent in the central nervous system from the inoculation site.

Animals↗
PubMed1983

Delta sleep-inducing peptide in the rat brain: an immunohistological microscopic study.

The authors have developed a method which makes it possible, for the first time, to visualize the delta sleep-inducing peptide in histological preparations and study it under the light and fluorescence microscope. Their research builds on Monnier 's discovery, in 1963, of a humoral hypnogenic factor in rabbits which was subsequently isolated and identified as a nonapeptide. Dubbed delta sleep-inducing peptide (DSIP), this factor was later detected in rat brain by radioimmunoassay but has eluded histological visualization until recently. In their work, the authors used an anti-DSIP antiserum suitable for immunohistological purposes. Two indirect immunohistological methods (PAP and immunofluorescence) allowed them to visualize, for the first time, structures containing specific DSIP-like immunoreactivity in some areas of the rat brain: indusium griseum, nucleus septi lateralis, hippocampus, striae longitudinales of Lancisi , bandeletta diagnalis of Broca, pallidum, hypothalamus, hypophysis and neocortex. Some DSIP pathways seem likely: (1) indusium griseum - striae longitudinales - hippocampus; (2) nucleus septi lateralis - striae longitudinales , bandeletta diagonalis - hippocampus; (3) neurons of the pyramidal layer of the hippocampus - gyrus dentatus; (4) pallidum - commissura of Ganser - hypothalamus. The possible correlations between DSIP neurons and neurons with other neurotransmitters are discussed. In preliminary clinical trials, DSIP has shown promise for the treatment of insomnia and the opiate and alcohol withdrawal syndromes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Putative peptide neurotransmitters in human neuropathology: a review of topography and clinical implications.

In Huntington's disease, there is a decrease of the neuropeptides, substance P, enkephalins, and cholecystokinin in the striatonigral system, whereas in Parkinson's disease an increase of substance P is found in the substantia nigra. Several neuropeptides should be involved in Alzheimer's disease: substance P, endorphins, vasopressin, ACTH, somatostatin, vasoactive intestinal peptide, cholecystokinin, neurotensin, delta sleep-inducing peptide. Alterations of substance P, vasoactive intestinal peptide, cholecystokinin, somatostatin, and endorphins may be related to the pathophysiology of schizophrenia. Delta sleep-inducing peptide may interfere in addiction pathology.

Alzheimer Disease↗
PubMed1978

[Differences between human and rat blood towards 3,4-dihydroxy-L-phenylalanine and 5-hydroxy-L-tryptophan in vitro. Biochemical and histochemical data (author's transl)].

When incubated with whole human blood at ordinary temperature, 3,4-dihydroxy-L-phenylalanine remains unchanged for at least 30 min. Under the same experimental conditions, 5-hydroxy-L-tryptophan shows a tendency to decrease. When incubated with blood from pentobarbital anaesthetized rats, these aminoacids decrease to about 50% of the added quantity in less than 5 min; thereafter, their level remains stable (3,4-dihydroxy-L-phenyl-alanine) or slowly decreases (5-hydroxy-L-tryptophan).

5-Hydroxytryptophan↗
PubMed1977

Paradoxical sleep and brain catecholamines in the rat after single and repeated administration of alpha-methyl-paratyrosine.

This study is concerned with the role of catecholamines (CA) in the regulation of paradoxical sleep (PS) in the rat. Alpha-methyl-paratyrosine (alphaMPT), an inhibitor of tyrosine hydroxylase, was used in a multiple administration schedule in order to avoid toxic effects. From 2 to 10 doses of 75 mg/kg of alphaMPT, a progressive reduction of green fluorescence occurred in CA cell bodies as well as in terminals. The green fluorescence reduction was faster in dopaminergic than in noradrenergic neurons, and faster in cell bodies than in terminals. Sleep recordings showed a slight increase of PS after one or two doses of 75 mg/kg of alphaMPT, and a dose-related decrease after 3-7 injections. After two doses of 75 mg/kg, the number of PS phases was significantly increased. This can be due to the release of a non-CA PS primer mechanism. These experiments support the view that an intact synaptic transmission in CA neurons is necessary for the realization of PS.

Adrenergic Fibers↗
PubMedDate not supplied

Age-dependent accumulation of advanced glycosylation end products in human neurons.

Glucose can react nonenzymatically with free amino groups on proteins and form advanced glycosylation end-products (AGEPs), that have been previously isolated and characterised in aging human connective tissues. In this study, we used immunocytochemistry to examine the distribution of AGEPs in the aging human brain. Our findings show that the pyramidal neurons selectively accumulate AGEP-containing vesicles in an age-dependent manner. In addition, our results demonstrate that AGEPs accumulate in the same type of neuron that degenerates in Alzheimer's disease.

Adolescent↗
PubMedDate not supplied

Production and immunohistochemical application of monoclonal antibodies against delta sleep-inducing peptide.

Monoclonal antibodies were produced following immunization of rats with delta sleep-including peptide (DSIP). The spleen cells of the rats were fused with the myeloma cell line SP2/0. The supernatants of hybridomas were screened on a solid-phase immunoassay using dot-immunobinding of DSIP and some DSIP fragments. The supernatants of six stable producer clones were found to react with DSIP. From this procedure it was also deduced that all these monoclonal antibodies recognized epitope(s) of the penta carboxy-terminal region of DSIP (DSIP5-9). Application of these monoclonal antibodies to rat median eminence sections gave a strong immunolabelling of a large population of fibres and terminal-like structures, mainly localized through the lateral areas. Elution-restaining experiments using a monoclonal antibody to DSIP and a polyclonal antiserum to luteinizing hormone-releasing hormone (LHRH) showed that the patterns of immunoreactivity respectively visualized overlap almost completely. Although numerous LHRH-immunoreactive neuronal elements were also easily demonstrated in the median eminence of the mouse, the hamster and the gerbil species, incubation of sections with monoclonal antibodies to DSIP failed to give any immunoreaction. Taken together these data argue for the independence of the DSIP/LHRH immunolabelling systems. Furthermore, it was demonstrated that DSIP5-9-related epitopes detected in the rat median eminence have no counterpart in the three other rodent species investigated. These species differences may reflect the fact that the carboxy-terminal sequence of the nonapeptide DSIP originally discovered in the rabbit is not conserved in all rodent species.

Amino Acid Sequence↗
PubMedDate not supplied

Regional distribution of neurofibrillary tangles and senile plaques in the cerebral cortex of elderly patients: a quantitative evaluation of a one-year autopsy population from a geriatric hospital.

Detailed analyses of the neuropathologic changes in the cerebral cortex of elderly individuals and Alzheimer's disease patients have demonstrated that certain components of the neocortical and hippocampal circuits are likely to be selectively vulnerable. Based on the distribution of neurofibrillary tangles (NFTs) and senile plaques, it has been proposed that a global corticocortical disconnection leads to the loss of integrated functions observed in Alzheimer's disease. In order to investigate the distribution of lesions associated with aging as well as with the earliest symptoms of senile dementia, we performed a quantitative neuropathologic evaluation of a large series of elderly patients representing the entire autopsy population for the year 1989 from a geriatric hospital. Among the 145 cases quantitatively assessed, there were 102 nondemented patients, 33 patients presenting clinically with globally intact intellectual function but early signs of impairment of specific cognitive functions, and 10 cases with senile dementia of the Alzheimer type. All of the cases had NFTs in layer II of the entorhinal cortex, regardless of their clinical diagnosis, and most cases had some NFTs in the CA1 field of the hippocampus. Severe pathologic changes within the inferior temporal neocortex were observed only in the demented cases. The extent of amyloid deposition was not correlated with the clinical diagnosis and seemed to be present in the neocortical areas earlier than in the hippocampal formation. Also, several cases contained NFTs without amyloid deposition, but amyloid never occurred without NFTs. These results suggest that involvement of certain structures within the hippocampal formation is a consistent feature of aging. Thus, involvement of the hippocampal formation may be a necessary, but not sufficient, condition for the clinical expression of dementia, which is likely to be more closely related to the progressive degeneration of select neuronal populations in the neocortex.

Aged↗
PubMedDate not supplied

No detected mutations in the genes for the amyloid precursor protein and presenilins 1 and 2 in a swiss early-onset Alzheimer's disease family with a dominant mode of inheritance.

Mutations have been found in more than a hundred early-onset families with Alzheimer's disease (AD) in the genes for the amyloid precursor protein, presenilin 1 and presenilin 2. The object of our investigation was to identify if these mutations or novel ones were operating in a Swiss early-onset AD family (mean age of onset: 53.3 years) with 7 members available, all neuropathologically confirmed. No known or new mutations were detected. Thus, our data support the existence of a yet unknown mutation, or other genes, contributing to familial early-onset AD. CopyrightCopyright 1999S.KargerAG,Basel

Adult↗
PubMedDate not supplied

Impaired processing of famous faces in Alzheimer's disease is related to neurofibrillary tangle densities in the prefrontal and anterior cingulate cortex.

To examine the neuroanatomical correlates of impaired processing of famous faces in Alzheimer's disease (AD), we performed an anterograde clinicopathological study of 25 patients with clinically and neuropathologically confirmed AD. Famous face recognition, identification and naming was assessed using the Famous Face Test. The assessment of neurofibrillary tangle (NFT) and senile plaque (SP) densities was performed in ten cortical areas in both hemispheres, and statistical analysis was made using forward stepwise logistic regression models. A statistically significant relationship was found between NFT densities in Brodmann's areas 9 and 24 in both hemispheres and impaired famous face naming and identification. SP counts did not correlate with any of the neuropsychological parameters. These data suggest that NFT formation in prefrontal and anterior cingulate cortex, two areas involved in semantic memory processes, is a key event in famous face naming and identification deficits. In agreement with previous studies, they also indicate that SP densities are not a good pathological correlate of neuropsychological deficits in AD.

Aged↗
PubMedDate not supplied

Mild amyloid pathology in the primary visual system of nonagenarians and centenarians.

In order to study the patterns of Alzheimer disease (AD)-related pathology in the primary visual system of the oldest old, we performed a quantitative analysis of senile plaques (SP), diffuse beta amyloid (A beta) deposit and neurofibrillary tangle (NFT) distribution in primary area 17, and a semi-quantitative analysis in the dorsal lateral geniculate nucleus (LGN), lateral inferior pulvinar (LIP) and superior colliculus (SC) of 21 individuals aged between 93 and 102 years. Among them, 10 cases were considered as non-demented (ND), while 9 presented very mild cognitive impairment (VMCI), and 2 cases had a clinical diagnosis of AD. Silver methenamine and Gallyas staining, A beta and tau immunostaining revealed the distribution of AD lesions. In primary area 17, most cases, either ND or with VMCI displayed a low to medium number of SP. There was no significant difference in SP and A beta deposit densities between ND and VMCI groups. On the whole, 0.4--2.4% of the cross-sectional cortical area was covered with A beta deposits. Only 6 cases, either ND or with VMCI, were totally devoid of SP and diffuse A beta deposits. Among the subcortical structures, the LIP and SC exhibited low densities of SP and A beta deposits in about half of the ND and VMCI cases, while the LGN was totally spared. NFT were almost absent in area 17 and subcortical nuclei of ND and VMCI cases. These data imply that the ageing of the primary visual system in ND and VMCI nonagenarians and centenarians is characterised by the frequent development of mild amyloid pathology in area 17 in the absence of NFT. In agreement with previous studies in very old cohorts, they also suggest that amyloid deposition is not related to the early stages of the dementia process in the oldest old.

Aged↗
PubMedDate not supplied

Dementia in the oldest-old: quantitative analysis of 12 cases from a psychiatric hospital.

To examine the neuropathological characteristics of senile dementia of the Alzheimer type (SDAT) in very old people, we performed a quantitative analysis of the distribution of neurofibrillary tangles and senile plaques in the brains of 12 demented patients aged from 96 of 104 years. The hippocampal formation and the inferior temporal cortex displayed numerous neurofibrillary tangles in most cases, whereas the superior frontal cortex was relatively spared. The only statistically significant difference between demented and control cases was in the density of neurofibrillary tangles in the CA1 field of the hippocampus. High senile plaque densities were observed in the cerebral cortex and were correlated with the duration of SDAT. These results confirm the crucial role of the hippocampus in the neuropathological diagnosis of SDAT in oldest-old patients. Furthermore, they suggest that senile plaque formation may be a pathological hallmark of severe SDAT in this particular age group.

Aged↗
PubMedDate not supplied

Motor cortex involvement in presenile dementia: report of a case.

Alzheimer's disease (AD) is characterized neuropathologically by high densities of neurofibrillary tangles (NFT) and neuritic plaques (NP) in the cerebral cortex, in particular in neocortical association areas and in the hippocampal formation. We report here the case of an AD patient who developed signs of motor dysfunction early in the clinical evolution. A quantitative neuropathologic analysis revealed much higher densities of NFT and NP in the primary motor cortex than is usually observed in AD. This case, together with other reports, points to the existence of neurologically defined subgroups of AD with unusual clinical deficits that are correlated with the regional and laminar distribution of NP and NFT, and further supports the hypothesis that the symptomatology presented by AD patients results from the loss of specific neuronal populations leading to a syndrome of global cortical disconnection.

Aged↗
PubMedDate not supplied

The morphologic and neurochemical basis of dementia: aging, hierarchical patterns of lesion distribution and vulnerable neuronal phenotype.

Alzheimer's disease is the most common form of dementia in elderly individuals. Approximately 11% of the population older than 65, and up to 50% of individuals over 85 qualify as having "probable Alzheimer's disease" on the basis of clinical evaluation. Since the early description of the clinical symptoms and neuropathologic features of Alzheimer's disease, there has been an extraordinary growth in the knowledge of the morphologic and molecular characteristics of Alzheimer's disease. Although the pathogenetic events that lead to dementia are not yet fully understood, several hypotheses regarding the formation of the hallmark pathologic structures of Alzheimer's disease have been proposed. In this context, the use of specific histochemical techniques in the primate brain has greatly expanded our understanding of neuron typology, connectivity and circuit distribution in relation to neurochemical identity. In this respect, very specific subsets of cortical neurons and cortical afferents can be identified by their particular content of certain neurotransmitters and structural proteins. In this article, we discuss the possible relationships between the distribution of pathologic changes in aging, Alzheimer's disease, and possibly related dementing conditions, in the context of the specific elements of the cortical circuitry that are affected by these alterations. Also, evidence for links between the neurochemical phenotype of a given neuron and its relative vulnerability or resistance to the degenerative process are presented in order to correlate the distribution of cellular pathologic changes, neurochemical characteristics related to vulnerability, and affected cortical circuits.

Age Distribution↗
PubMedDate not supplied

[Alzheimer's disease and Down's syndrome. Some recent etiopathogenic data].

The present status of research clearly demonstrates the occurrence of lesions characteristic of Alzheimer's disease in patients suffering from a Down's syndrome or trisomy 21. The senile plaques appear very early in trisomy 21 (from the age of 20) and are constant after 40 or 45 years. In these two illnesses, the beta-amyloid protein or A4 protein (4.2 kD) leads to deposits in preferential regions of the central nervous system within two compartments: 1) intracellular, contributing to the formation of neurofibrillary tangles and 2) extracellular, making up the amyloid center of senile plaques as well as around the wall of some blood vessels, then corresponding to the amyloid congophilic angiopathies. Unexpectedly, larger proteins including the A4 sequence have been shown to be normally present in several tissues of normal as well as sick individuals and represent possible precursors of the A4 protein. Alzheimer's disease may happen either sporadically or following a familial incidence associated with an autosomic dominant mode of transmission. Moreover, the risk of incidence of trisomy 21 seems to be enhanced for collaterals of Alzheimer's disease patients. Since 1987, the use of molecular biology tools has revealed particularly fruitful. A linkage analysis has been undertaken that showed an association of the putative gene for the familial form of Alzheimer's disease (FAD) with the gene coding for amyloid precursor proteins (APP).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Cardiovascular polymorbidity as a function of psycho-organic status. A series of 904 pathological and neuropathological comparisons].

In the past decades, the recognition of polymorbidity as an important characteristic of geriatric medicine lead to important improvements in the multidisciplinary approach of the elderly. Coexistence of somatic and psychiatric diseases with various forms of etiopathogenic relations has been described early in this century. Dementia may be caused, aggravated, revealed or randomly accompanied by somatic diseases and inversely. However, very few attempts have been made in order to analyze the significance of these associations. This study is meant to give a better epidemiological knowledge of the relation between cardiovascular diseases and cerebral aging. This could lead to a better diagnostic approach and to a more complete physiopathological conception of dementia. 904 autopsy reports (patients who died between 1972 and 1986 in the Hôpital de Gériatrie of Genova) have been reviewed and classified in three groups according to neuropathological findings: 335 subjects with vascular encephalopathy of various types, 382 patients with degenerative diseases of Alzheimer type and 187 patients with normal brain. The subjects of these three groups had not all been considered demented. For each patient, age, sex, cause of death and 14 cardiovascular items have been appointed. The patients of the Alzheimer group died older and were more often women than those of the two other groups. The subjects of the vascular group died older than those of the normal group and were more often men than those of the two other groups. Stoke was considered to be the cause of death in 3% of the vascular patients whereas, by definition, it was absent from the two other groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗