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C Duyckaerts

Publications and source records attributed to C Duyckaerts.

At least 19 recordsLinked to original sources
PubMed1992

The prevalence of ulcerated plaques in the aortic arch in patients with stroke.

BACKGROUND AND METHODS: The cause of cerebral infarction is obscure in up to 40 percent of patients with this disorder who are studied prospectively. In this investigation, we determined the frequency of ulcerated plaques in the aortic arch and explored the part they may play in the formation of cerebral emboli. Using an autopsy data bank, we studied the prevalence of ulcerated plaques in the aortic arch in 500 consecutive patients with cerebrovascular and other neurologic diseases who were studied at autopsy. RESULTS: Ulcerated plaques were present in 26 percent of the 239 patients with cerebrovascular disease but in only 5 percent of the 261 patients with other neurologic diseases (P less than 0.001). After we controlled for age and heart weight, the adjusted rates were 16.9 percent and 5.1 percent, respectively (adjusted odds ratio, 4.0; 95 percent confidence interval, 2.1 to 7.8; P less than 0.001). Among the patients with cerebrovascular disease, the prevalence of ulcerated plaques in the aortic arch was 28 percent in the 183 patients with cerebral infarcts and 20 percent in the 56 patients with brain hemorrhage. The prevalence of ulcerated plaques was 61 percent among the 28 patients with no known cause of cerebral infarction, as compared with 22 percent among the 155 patients with a known cause of cerebral infarction (P less than 0.001). After adjustment for covariates, the prevalence was 57.8 percent among patients with no known cause of cerebral infarction and 20.2 percent among those with a known cause (adjusted odds ratio, 5.7; 95 percent confidence interval, 2.4 to 13.6; P less than 0.001). The presence of ulcerated plaques in the aortic arch was not correlated with the presence of extracranial internal-carotid artery stenosis, suggesting that these were two independent risk factors for stroke. CONCLUSIONS: Ulcerated plaques in the aortic arch may play a part in causing cerebral infarction, especially in patients in whom cerebral infarction has no known cause.

Adult↗
PubMed1992

Biochemical, genetic and molecular characterization of new respiratory-deficient mutants in Chlamydomonas reinhardtii.

Eight respiratory-deficient mutants of Chlamydomonas reinhardtii have been isolated after mutagenic treatment with acriflavine or ethidium bromide. They are characterized by their inability to grow or their very reduced growth under heterotrophic conditions. One mutation (Class III) is of nuclear origin whereas the seven remaining mutants (Classes I and II) display a predominantly paternal mt- inheritance, typical of mutations residing in the mitochondrial DNA. Biochemical analysis has shown that all mutants are deficient in the cyanide-sensitive cytochrome pathway of the respiration whereas the alternative pathway is still functional. Measurements of complexes II + III (antimycin-sensitive succinate-cytochrome c oxido-reductase) and complex IV (cytochrome c oxidase) activities allowed to conclude that six mutations have to be localized in the mitochondrial apocytochrome b (COB) gene, one in the mitochondrial cytochrome oxidase subunit I (COI) gene and one in a nuclear gene encoding a component of the cytochrome oxidase complex. By using specific probes, we have moreover demonstrated that five mutants (Class II mutants) contain mitochondrial DNA molecules deleted in the terminal end containing the COB gene and the telomeric region; they also possess dimeric molecules resulting from end-to-end junctions of deleted monomers. The two other mitochondrial mutants (Class I) have no detectable gross alteration. Class I and Class II mutants can also be distinguished by the pattern of transmission of the mutation in crosses. An in vivo staining test has been developed to identify rapidly the mutants impaired in cyanide-sensitive respiration.

Animals↗
PubMed1992

c-fos protein-like immunoreactivity: distribution in the human brain and over-expression in the hippocampus of patients with Alzheimer's disease.

c-fos protein-like immunoreactivity was investigated in the human brain post mortem, using a polyclonal antiserum raised against the N-terminal conserved peptide of c-fos protein. Immunostaining was found in the cerebral cortex, hippocampus, striatum, thalamus and cerebellum but not in the upper brainstem and the adrenal gland. c-fos-like immunoreactivity predominated in neuronal elements, but was also observed in neuropil and glial cells. In addition to a nuclear localization, the staining could be seen in neuronal dendrites (i.e. in the pyramidal cells of hippocampus or in some cortical areas). In order to analyse the effect of brain injury on c-fos expression, the characteristics of the immunostaining were analysed in the hippocampus of patients deceased with Alzheimer's disease known to be associated with a preferential vulnerability of the pyramidal neurons. No staining was observed in the senile plaques or in neurofibrillary tangles, the histopathological stigmata of the disease. Densitometric measurement of the intensity of c-fos-like staining revealed a significant increase in the hilus, the fimbria and the CA1 field of the pyramidal layer in brains of patients with Alzheimer's disease compared to controls. These modifications may result from a suffering stage of hippocampal cells or from a compensatory mechanism in the still surviving neurons not yet affected by the pathological process.

Aged↗
PubMed1992

[Oligodendroglial inclusions, a marker of multisystemic atrophies].

Nine cases of multiple system atrophy and 1 case of autosomal dominant olivopontocerebellar atrophy (neuropathological diagnosis) were retrospectively examined for the presence of oligodendroglial inclusions. Clinical diagnosis in the first 9 cases had been: olivopontocerebellar atrophy (3 cases), atypical Parkinson's disease (2 cases), Shy-Drager syndrome (2 cases) and multiple system atrophy (1 case); one of the patients could not be included in any of the above mentioned groups. The oligodendroglial inclusions were argyrophilic and located in the cytoplasm around the nucleus. They were revealed by Bodian's method in all cases of multiple system atrophy. They were not found in the case of autosomal dominant olivopontocerebellar atrophy. They were labelled by anti-ubiquitin antibodies, and were negative with anti-tau antibodies. At electron microscopy, they consisted of rectilinear profiles coated with a fuzzy material (diameter: 20-33 nm); this aspect was compatible with microtubules. Oligodendroglial inclusions were prominent in regions selectively vulnerable in multiple system atrophy (tegmentum pontis, putamen, inferior olives, substantia nigra and cerebellar white matter), even in those areas where neuronal loss or fascicular atrophy were minimal or absent. They were also observed in regions considered to be spared in multiple system atrophy, such as the motor cortex and the corpus callosum. Argyrophilic oligodendroglial inclusions are an early and specific marker of multiple system atrophy. It is suggested that autosomal dominant olivopontocerebellar atrophy lacking oligodendroglial inclusions does not belong to multiple system atrophy.

Adult↗
PubMed1992

[Gerstmann-Sträussler-Scheinker disease. Pathologal and genetic study].

Gerstmann-Sträussler-Scheinker's disease is a familial spongiform encephalopathy whose pathological hallmark is the existence--especially in the cerebellum--of numerous amyloid plaques. We report here the third clinicopathological case in a French family. Brain tissue from one of its members--initially described as familial Creutzfeldt-Jakob's disease--has been reported as successfully inoculated to monkeys. We present the currently accumulating data favouring the hypothesis of a common etiology for familial Creutzfeldt-Jakob's disease and Gerstmann-Sträussler-Scheinker's disease. The familial characteristics, resulting in different durations of incubation and evolution, could lead to different clinical and histological expressions.

Amyloidosis↗
PubMed1991

Kinetic study of the aspartate/glutamate carrier in intact rat heart mitochondria and comparison with a reconstituted system.

The homologous exchange of external [14C] aspartate/internal aspartate catalyzed by the aspartate/glutamate carrier of rat heart mitochondria was investigated using aspartate-loaded, glutamate-depleted mitochondria. An inhibitor-stop technique was developed for kinetic studies by applying pyridoxal phosphate. Direct initial rate determinations from the linear phase of [14C] aspartate uptake were insufficiently accurate at high external and/or low internal substrate concentrations. Therefore, the full time-course of [14C] aspartate uptake until reaching isotope equilibrium was fitted by a single exponential function and was used to calculate reliable initial steady-state rates. This method was applied in bisubstrate analyses of the antiport reaction for different external and internal aspartate concentrations. The kinetic patterns obtained in double reciprocal plots showed straight lines converging on the abscissa. This result is consistent with a sequential antiport mechanism. It implies the existence of a catalytic ternary complex that is formed by the translocator and substrate molecules bound from both sides of the membrane. The Km values for aspartate were clearly different for the external and the internal sides of the membrane, 216 +/- 23 microM and 2.4 +/- 0.5 mM, respectively. These values indicated a definite transmembrane asymmetry of the carrier. The same asymmetry became evident when investigating the isolated protein from bovine heart mitochondria after reconstitution into liposomes. In this case the Km values for external and internal aspartate were determined to be 123 +/- 11 microM and 2.8 +/- 0.6 mM, respectively. This comparison demonstrates a right-side out orientation of the carrier after insertion into liposomal membranes. The sequential transport mechanism of the aspartate/glutamate carrier, elucidated both in proteoliposomes and in mitochondria, also seems to be a common characteristic of other mitochondrial antiport carriers.

Amino Acid Transport Systems, Acidic↗
PubMed1991

[Anatomy and memory].

Bilateral lesions involving the medial aspect of the hemisphere may induce pure amnestic syndromes. Which neural elements have to be destroyed remains open to question: hippocampus, mamillary body, dorso-medial nucleus of the thalamus play probably a role at one point or another of the memory process. Lesions of the dorso-lateral part of the frontal lobe disturb the chronological order of memories. Il has been suggested that 2 systems were involved: the first one is hippocampo-mamillo-thalamic (Papez circuit), the second one is amygdalo-thalamo-frontal. The respective role of each of these circuits remain controversial.

Brain↗
PubMed1991

Alterations of dopaminergic and noradrenergic innervations in motor cortex in Parkinson's disease.

The motor areas of the cerebral cortex contain dense dopaminergic and noradrenergic innervation in humans. We looked for changes of these innervations in cases with Parkinson's disease (PD). The density of fibers immunolabeled with tyrosine hydroxylase or dopamine-beta-hydroxylase was evaluated in the primary motor, premotor, and prefrontal cortical regions in 6 cases with PD and 7 control cases. Reductions of both noradrenergic and dopaminergic cortical innervations were observed, with similar magnitudes of reduction found in the motor and prefrontal regions of the cortex. Depletion of noradrenergic innervation was diffuse, involving all cortical laminae. Depletion of dopaminergic innervation was laminar specific, with the most significant reductions in layers I and II; reductions in layers V and VI were either less marked (prefrontal cortex) or not detectable (primary motor). The results suggest the existence of two separate mesocortical dopaminergic systems in humans, with the one distributing to upper cortical layers being preferentially involved in PD.

Aged↗
PubMed1991

Subtypes and differential laminar distributions of beta A4 deposits in Alzheimer's disease: relationship with the intellectual status of 26 cases.

beta A4 immunoreactivity was studied in temporal neocortex, area 22, of 26 cases with graded intellectual status. Sampling was performed in psychometrically assessed women over 75 years, either intellectually normal or affected by senile dementia of Alzheimer type of various degrees of severity. beta A4 antibodies labelled various types of beta A4 deposits in 22/26 cases: (1) small, stellate deposits; (2) diffuse deposits, (3) primitive, (4) classic and (5) compact, or burn-out, plaques. The densities of the stellate deposits, primitive and classic plaques were always positively linked with the severity of the intellectual status, whereas those of the diffuse deposits were not. This was due to a single case with normal mental status and numerous beta A4 deposits. Densities of stellate and diffuse deposits were higher in layers I, III and IV, whereas densities of primitive, classic, and neuritic plaques observed with Bodian's technique were higher in layers II and III. Topographical distribution of each subtype did not vary as a function of the severity of the intellectual status. These data suggest that deposits of beta A4 protein appear a necessary but not a sufficient condition for inducing neuritic plaque formation, in the neocortex as in other brain areas. beta A4 proteins could accumulate either as diffuse deposits, which do not cause an intellectual deficit, or as dense deposits, associated with argyrophilic neurites, i.e., classic neuritic plaques, highly correlated to the intellectual impairment. This evolution could depend on factors which are laminarily distributed in the neocortex.

Aged↗
PubMed1991

Differential vulnerability of cholinergic projections to the mediodorsal nucleus of the thalamus in senile dementia of Alzheimer type and progressive supranuclear palsy.

The cholinergic innervation of the mediodorsal nucleus of the thalamus, which is thought to originate primarily in the laterodorsal tegmental nucleus and the substantia innominata, was studied by acetylcholinesterase histochemistry and immunohistochemistry with a polyclonal antiserum against human choline acetyltransferase on autopsy tissue from eight control subjects, five patients with progressive supranuclear palsy and four patients with senile dementia of Alzheimer type. In controls, cholinergic innervation of the mediodorsal nucleus of the thalamus was distributed heterogeneously in densely labelled patches surrounded by less heavily stained matrix. In patients with progressive supranuclear palsy, the density of choline acetyltransferase-positive varicosities decreased by 75% in the matrix and 60% in the patches. The number of choline acetyltransferase-positive cell bodies decreased by 84% in the laterodorsal tegmental nucleus, but more moderately (-33%) in the substantia innominata. In patients with senile dementia of Alzheimer type, choline acetyltransferase-positive varicosities decreased by 34% in the matrix, but 46% in the patches. Choline acetyltransferase-labelled cell bodies were spared in the laterodorsal tegmental nucleus, whereas severe loss (-80%) was observed in the substantia innominata. These results suggest that cholinergic innervation of mediodorsal nucleus matrix derives mainly from the laterodorsal tegmental nucleus and mediodorsal nucleus patches from the substantia innominata. Differential loss of innervation to the matrix and patches in progressive supranuclear palsy and senile dementia of Alzheimer type may in turn differentially affect mediodorsal nucleus innervation of the frontal cortex, resulting in dissimilar symptomatologies.

Acetylcholinesterase↗
PubMed1991

Leuko-araiosis.

Leuko-araiosis is an unspecific radiologic sign, seen with CT scan or with MRI. It can be found as well in normal elderly persons as in pathological conditions. For the sake of clarity, CT scan and MRI images have to be distinguished. CT leuko-araiosis is linked with vascular risk factors and with age. The situation is more complex for MRI leuko-araiosis (likely on account of the higher sensitivity of MRI). Some images (caps and rims), frequently seen in normal, even young, individuals, are more frequent in aging. On the contrary, abnormal images at a distance from the ventricle are more difficult to interpret. Some of them are due to pathological well defined conditions (small infarcts, Binswanger's disease, cysts, plaques). Others may be secondary to remote pathologies (such as infarcts). Others are due to little specific conditions, such as perivascular dilatations ('état criblé' due to brain vasogenic edema, or to brain atrophy whatever its cause, and more frequently seen in the elderly). Other changes, such as incomplete infarction or myelin pallor with gliosis, have been described. At last, in some cases, no clearcut pathological lesion could be found. Leuko-araiosis may be present in primary degenerative dementia of the Alzheimer type, but it is neither necessary nor sufficient to establish the diagnosis of Alzheimer's disease, and it does not seem more frequent than in elderly controls. The mechanism of leuko-araiosis in Alzheimer's disease is likely multifactorial (for example, cerebral atrophy, amyloid angiopathy, associated hypertensive arteriolosclerosis could be involved). The relationship between leuko-araiosis, myelin pallor and white matter atrophy is poorly understood, and remains to be studied.

Adult↗
PubMed1991

Mesencephalic cholinergic nuclei in progressive supranuclear palsy.

Using an antibody against choline acetyltransferase (ChAT), mesencephalic cholinergic cell nuclei were studied in autopsy material from 3 cases of progressive supranuclear palsy (PSP) and 4 controls. ChAT-immunoreactive neurons were quantified in sections that spanned the rostrocaudal extent of each nucleus. In PSP, there was a significant decrease in the number of neurons with detectable immunoreactivity for ChAT in and adjacent to the central gray substance in the following nuclei: the nucleus of Edinger-Westphal (69%); the rostral interstitial nucleus of the medial longitudinal fasciculus (97%); the interstitial nucleus of Cajal (78%). A cell loss was also evident in a group of neurons found in the deep layers of the superior colliculus (93%). In contrast, the estimated number of ChAT-immunoreactive cell bodies in cranial nerves III and IV, in the mesencephalic reticular formation, and in the parabigeminal nucleus was not different from that of controls. The results are compatible with the notion that, in PSP, there is a regionally selective destruction of cholinergic neurons.

Aged↗
PubMed1991

Progressive supranuclear palsy: loss of choline-acetyltransferase-like immunoreactive neurons in the pontine reticular formation.

We performed a quantitative immunocytochemical study using a polyclonal antibody directed against choline acetyltransferase (ChAT) in the lower pontine reticular formation in four control subjects and three patients with progressive supranuclear palsy (PSP). In the normal brains, there was detectable ChAT-like immunoreactivity in the nucleus papillioformis, a precerebellar reticular nucleus, and in the nucleus pontis centralis caudalis. In PSP patients, the mean estimated total number of ChAT-like immunoreactive cells was 54% of controls in nucleus papillioformis and 40% of controls in nucleus pontis centralis caudalis. The demonstration of ChAT-like immunoreactivity in nucleus papillioformis is consistent with studies suggesting an extrinsic cholinergic innervation of the cerebellar cortex. Loss of cholinergic cells in nucleus pontis centralis caudalis that corresponds largely to the paramedian pontine reticular formation may be related to disturbances of horizontal saccades in PSP patients.

Aged↗
PubMed1991

[Central and peripheral neurologic lesions in primary Gougerot-Sjögren syndrome. Clinicopathological study of a case].

A 51 year old woman presented with cerebellar ataxia and paralysis of conjugate lateral movement of the eyes. She had xerophtalmia and xerostomia. Biopsy of minor salivary glands showed mononuclear infiltrates typical of Sjögren's syndrome. Peripheral neuropathy was of the axonal type, and nerve biopsy showed a vasculitis made of a mononuclear infiltrate with only a few polymorphonuclears. The patient deteriorated despite corticosteroid therapy, plasma exchange and cyclophosphamide. Ciclosporin seemed to be transitorily beneficial. Epileptic seizures (auditory hallucinations) occurred. MRI showed hypersignal in the right temporal lobe. At post-mortem examination, a small ischaemic lesion with a large lymphocytic infiltrate was present in the left putamen. Neuronal loss and gliosis with some rod cells and glial stars were found in the brainstem, dentate nucleus and internal part of the right temporal lobe. Inflammatory changes were limited. The posterior columns of the spinal cord were pale, and some residual nodules of Nageotte were present in the spinal ganglia. These lesions were similar to those seen in encephalomyelitic syndromes associated with carcinoma. Lesions of the peripheral nerves were associated with vasculitis but changes in the central nervous system were morphologically similar to those observed as remote effects of carcinoma.

Central Nervous System Diseases↗
PubMed1991

[Familial mitochondrial encephalopathy. A clinicopathologic study].

We report the cases of 2 siblings with progressive encephalopathy. The first symptoms were noted when they were 6 years old. The full clinical picture included myoclonus, seizures, cerebellar ataxia, blindness due to optic atrophy and retinal degeneration, deafness, swallowing difficulties with relatively spared intellectual functions. The course was progressive and led to death within 8 years. The pathological findings included bilateral and almost symmetrical lesions involving the thalami, the colliculi, and the pontine and medullar tegmentum, similar to the changes described in Leigh disease. Neuronal loss and gliosis were noted in the dentate nucleus and in the inferior olive, as in MERRF syndrome. Laminar necrosis of the cerebral cortex could have been due to episodes of severe hypotension before death. Cytochrome c oxidase deficiency was found in case 2. The enzyme deficiency was present in muscle and in fibroblasts in culture.

Brain↗
PubMed1991

[Effect of diabetes mellitus and blood glucose on the size of cerebral infarction and causes of death. Neuropathological study of 77 cases of infarction in the sylvian artery area].

The influence of diabetes mellitus and hyperglycemia on cerebral infarction has been studied on 77 patients who died of infarcts in the territory of the middle cerebral artery. The size of the infarcts was assessed by transferring the surface of the infarcted area onto 8 schematic drawings corresponding to 8 brain slices and measuring this surface by means of a planimeter. An infarction volume index (IVI) was calculated by measuring the ratio of the infarcted area to the theoretical area of the middle cerebral artery territory on the 8 slices. The causes of death were assessed by full post-mortem examination. There was no statistically significant difference in size of infarcts and causes of death between diabetics and non-diabetics. However, the stroke-to-death interval was shorter (p = 0.05) in non-diabetic patients. It appears from this study that diabetes mellitus has no deleterious effect on cerebral infarction. Equally, there were non statistically significant differences in size of infarcts, stroke-to-death interval and causes of death between patients with and without hyperglycemia.

Aged↗