Biomedical subjects

C Bouras

Publications and source records attributed to C Bouras.

133 records · Page 8Linked to original sources

PubMedDate not supplied

Asymmetrical cerebral atrophy in Alzheimer's disease.

In most Alzheimer patients brain atrophy seems to be symmetrical. Recent neuropsychological and brain imaging investigations suggest, however, that in some patients one hemisphere is more severely affected from the onset of symptoms. We have observed four Alzheimer patients with grossly asymmetrical cerebral atrophy at autopsy, in whom the topography of the most severe atrophy was consistent with the earliest clinical signs of focal brain damage. In the three patients who at onset had relevant language disorders, atrophy of the brain was more severe in the association areas surrounding the left sylvian fissure. In the fourth patient, who first complained of visuospatial troubles, the right, nondominant hemisphere was more affected. These clinical and pathological findings suggest that association areas of one hemisphere were involved quite early in the evolution of the disease, conceivably at the same time as the hippocampus and related limbic structures. In these patients, a morphometric analysis of cortical changes in homologous areas of the cortex (area 22) was carried out in order to investigate the effect of the evolution of the disease upon cortical changes. This analysis showed that the numerical densities of nerve cells and tangle-bearing neurons were lower on the more atrophied side and suggested that the severity of cortical atrophy might have affected the size, but not the density, of senile plaques.

Aged↗

PubMedDate not supplied

[Huntington chorea. Anatomoclinical and genetic study of 17 cases].

Seventeen cases of Huntington's chorea have been studied on a clinical and anatomopathological basis. Fourteen genealogical trees have been established. Clinically, involuntary movements of choreic type and an impairment of higher brain functions are constant symptoms. Gait disorders, dysarthria and a tendinous hyperreflexia are usual (present in 95, 95 and 80% of cases). Anorexia, muscular hypotony and dysphagia are also frequent (present in 75, 60 and 50% of cases). The neuropathological examination shows macroscopically a neostriatal atrophy in 90% of cases and a cerebral cortical atrophy in 75%. Microscopically, a neuronal loss--mainly in small cells (Golgi II)--is evident in the neostriatum of all the cases. The pallidum is also affected, but to a lesser degree. A cortical cell loss is present in 90% of the cases, mainly in layers III, IV, V and sometimes also in layer VI of frontal and parietal lobes. In 75% of the cases, a cortical gliosis is noticed, mostly at the level of the frontal pole.

Adult↗

PubMedDate not supplied

Distribution and colocalization of delta sleep-inducing peptide and luteinizing hormone-releasing hormone in the aged human brain: an immunohistochemical study.

The distributions of delta sleep-inducing peptide (DSIP)- and luteinizing hormone-releasing hormone (LHRH)-immunoreactive neurons were investigated in the human brain with special emphasis on the basal forebrain (from the septum to the hypothalamus), using indirect immunofluorescence. With a modified elution technique, sequential stainings on the same section showed that DSIP- and LHRH-immunoreactivities were often colocalized. Small numbers of LHRH/DSIP-immunoreactive cells were essentially detected in the diagonal band of Broca, the medial septum and the ventral hypothalamus. The richest areas displaying fibres and terminal-like structures were the preoptic area, the ventromedial and ventrolateral hypothalamic areas, the periventricular region and certain circumventricular organs (i.e. median eminence, vascular organ of the lamina terminalis). Few isolated fibres were observed in the subfornical organ. The topographical relationships between DSIP- and LHRH-immunoreactivities in the neurosecretory systems suggest that DSIP may play a role as important as that of LHRH.

Aged↗

PubMedDate not supplied

Immunohistochemical mapping of delta sleep-inducing peptide in the cat brain and hypophysis. Relationships with the LHRH system and corticotropes.

Using the indirect immunofluorescence method, the distribution of the delta sleep-inducing peptide was studied in the cat brain and hypophysis. Delta sleep-inducing peptide-like-immunoreactive cell bodies mostly visualized in colchicine-pretreated animals were mainly found scattered throughout the diagonal band of Broca, the ventral septum and the anterior hypothalamic areas. A few immunoreactive cell somata were also seen in the ventrolateral hypothalamic area and more occasionally in the triangular septal nucleus. The heaviest concentrations of delta sleep-inducing peptide-like-immunoreactive varicose fibres and terminal-like structures were observed in the septo-preoptic region, in the median eminence and pituitary stalk. Some other brain regions supplied with few delta sleep-inducing peptide-immunoreactive fibres included the fimbria-fornix, the dorsal part of the subfornical organ, the medial habenular nucleus and more caudally, the periaqueductal gray. Elution-restaining experiments revealed that delta sleep-inducing peptide-like immunoreactivity frequently occurred in luteinizing hormone-releasing hormone-immunoreactive neurons and vice versa. At the pituitary level, delta sleep-inducing peptide-like immunoreactivity was detected in most, if not all, melanocorticotropes of the pars intermedia and further in a large subpopulation of corticotropes mainly located in the zona tuberalis of the pars distalis. Taken together these anatomical findings support the view that delta sleep-inducing peptide (or a closely related molecular form) could play a modulatory role at various levels of the hypothalamo-pituitary system.

Animals↗

PubMedDate not supplied

[Neuromodulators and Alzheimer's disease].

Alzheimer's disease (AD) is one of more than 60 disorders that may produce dementia. It is characterized clinically by memory deficits and by the presence of aphaso-apracto-agnosic disorders. In the general population, AD has an incidence of 0.3 to 1% and is very common in the elderly (more than 50% of dementia cases). The pattern of pathological changes in the brain in AD is relatively specific. Neuritic plaques, neurofibrillary tangles and cell loss, occur primarily in the cerebral neocortex and hippocampus. On the other hand, neurochemical deficiencies related to the illness have now been identified. The vulnerability of the cholinergic system of the basal nucleus of Meynert was first documented. Following the discovery of the cholinergic reduction in AD and among a dozen of neurotransmitter systems involved in AD, somatostatin, substance P, neuropeptide Y, corticotropin releasing factor and amino acid glutamate were investigated and are the most affected in AD. Results of previous publications and our own investigations are presented here.

Acetylcholine↗

PubMedDate not supplied

[Molecular biology of beta A4 protein and Alzheimer disease].

Senile plaques, neurofibrillary tangles and neuronal loss are the major histopathologic hallmarks of Alzheimer's disease. A prominent component of the senile plaques is a polypeptide (beta A4) of about 40 amino acids derived via proteolytic cleavage from a set of larger protein isoforms collectively referred to as the amyloid precursor protein (APP). The protein APP is a widely distributed transmembrane glycoprotein structurally related to a cell surface receptor. APP is encoded by a single gene on chromosome 21 in which missense mutations have been demonstrated in several cases of familial Alzheimer's disease. It is thought that various factors fostering the APP-processing pathway by which the polypeptide beta A4 is generated might be pathogenic. Thus the mechanisms that govern the rate of transcription of the APP gene, the differential splicing of the precursor messenger and the proteolytic processing of APP are current subjects of intensive investigation. Theoretically, each of these events represents a potential target for a therapeutic intervention. However, the relationships between amyloidogenesis and the formation of the neurofibrillary tangles associated to the neuronal loss remain to be elucidated.

Alzheimer Disease↗

PubMedDate not supplied

Frontal arachnoid cyst. A case of bilateral frontal arachnoid cyst without clinical signs.

The purpose of this study is to report a case of a very large arachnoid cyst in a patient having spent a very active life and who had never presented any neurological or psychiatric symptomatology beside a dementia in the last years of her life. The gross examination of the brain revealed the presence of a voluminous frontal bilateral cyst, located in the midline and displacing laterally the frontal lobes, so they displayed a foliated aspect. Microscopically, the examination of the cyst walls confirmed its arachnoid origin and the cerebral cortex contained lesions typical for senile dementia. This case exemplifies the histological nature and the pathogeny of arachnoid cysts, in particular of congenital origin. This also shows that the very early occurrence of such a malformation does not prevent the development of functional neuronal pathways, owing to the important plasticity of the central nervous system.

Aged↗