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Biomedical subjects

C Duyckaerts

Publications and source records attributed to C Duyckaerts.

At least 163 records · Page 9Linked to original sources
PubMed1989

Subpopulations of somatostatin 28-immunoreactive neurons display different vulnerability in senile dementia of the Alzheimer type.

We tested whether the vulnerability of somatostatin (SST) neurons in senile dementia of the Alzheimer type (SDAT) depended upon their co-localization with neuropeptide Y (NPY). Density estimates of SST28- and NPY-immunoreactive neurons and percentage of double-labeled SST-NPY neurons were obtained in the cortex (areas 9 and 25) and the bed nucleus of stria terminalis (BST), in 6 SDAT and 5 control cases. Counts of senile plaques (SP) and neurofibrillary tangles (NFT) were done on thioflavin S stains. In both cortical areas, a decrease in the density of SST28-IR neurons was found in SDAT cases (-60% in area 25 and -80% in area 9), whereas density of NPY-IR neurons was unchanged. Accordingly, the proportion of single-labeled SST neurons decreased; this decrease was significantly correlated with SP (r = -0.89, P less than 0.001). We conclude that single SST-IR neurons, in cortical layers II-III, and V, are preferentially lost relative to co-localized SST-NPY neurons. In the BST, no significant reduction of SST-IR, NPY-IR neurons nor of the percentage of single labeled SST neurons was found, despite the presence of SP. Thus one subpopulation of SST neurons, defined by associated neurochemical characters (not co-localized with NPY nor with NADPH diaphorase) and by topography (cortical layers III and V) appears to be particularly vulnerable in SDAT. The potential importance of their position in neural circuitry is emphasized.

Aged↗
PubMed1989

[Alzheimer's disease: from morphology to pathogenic hypotheses].

Main changes of Alzheimer's disease (neuronal degeneration and death, neurofibrillary tangles, senile plaques, granulo-vacuolar degenerations) are described. Recent hypotheses concerning their causes, origin and development and their relationship with the mental changes are given.

Alzheimer Disease↗
PubMed1989

Striosomes and extrastriosomal matrix contain different amounts of immunoreactive choline acetyltransferase in the human striatum.

Cholinergic neuropil and cell bodies were identified in the human striatum by immunohistochemistry carried out with a polyclonal antibody raised against choline acetyltransferase (ChAT). The cholinergic neuropil was not uniformly distributed in the striatum, and especially in the caudate nucleus ChAT-poor zones corresponding to acetylcholinesterase (AChE)-poor striosomes were identified. Striosomal organization of ChAT-positive neuropil was also detected in striatal tissue from patients who had suffered parkinsonian and choreic disorders.

Aged↗
PubMed1989

Tau, paired helical filaments and amyloid in the neocortex: a morphometric study of 15 cases with graded intellectual status in aging and senile dementia of Alzheimer type.

Tau immunoreactivity was studied in temporal neocortex, area 22, in 15 cases with graded intellectual status and compared with the immunoreactivity observed with an antiserum against paired helical filaments (PHF) and with the density of amyloid revealed by thioflavin S. Samples came from women over 75 years either intellectually normal or affected by senile dementia of the Alzheimer type at various degrees of severity. Mental status had been prospectively assessed by the Blessed's test score. Anti-tau labelled a neuropil meshwork, the density of which increased with the severity of the disease. This meshwork was denser in layers II, III and V in the most affected cases. The number and the size of the tau-positive fibers within the senile plaques increased with the intellectual deficit. Senile plaques were more numerous in layers II and III and neurofibrillary tangles in layers III and V whatever the staining technique: tau or PHF immunocytochemistry, and thioflavin S. The densities of senile plaques and of neurofibrillary tangles (NFT) were correlated with the severity of the disease whatever the staining method. The three methods revealed a systematically different number of changes. This systematic difference could greatly influence the neuropathological diagnosis. It could be the consequence of various factors: different sensitivities of the staining methods or changes in the antigenic and amyloid composition of the lesion according to the stage of the disease. In line with the last hypothesis, a higher proportion of amyloid-rich plaques was noted in the less affected cases, suggesting that tau and PHF epitopes appeared secondarily.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Choline acetyltransferase-like immunoreactivity in the hippocampal formation of control subjects and patients with Alzheimer's disease.

A qualitative and quantitative immunohistochemical study of cholinergic systems in the human hippocampal formation was performed with an antibody against choline acetyltransferase. Four control subjects and six patients with Alzheimer's disease, matched for age and post-mortem delay, were examined. Immunoreactive nerve fibres and terminals were visualized, but no cholinergic cell bodies were seen. The distribution of the fibres and terminals suggests that a major afferent cholinergic pathway enters the hippocampus dorsally via the fimbria-fornix, a minor input entering from the temporal lobe along the alvear path. The cholinergic innervation suffers some degenerative change in normal aged subjects, but decreases considerably in density in patients with Alzheimer's disease. The extent of the decrease differs somewhat among the subregions of the hippocampus, but is homogeneously distributed within each subregion, and throughout the rostrocaudal extent of the structure. Compensatory sprouting in reaction to denervation was not detected.

Aged↗
PubMed1989

Alzheimer's disease: neuropathological and etiological data.

The important pathological changes in Alzheimer's disease are described with their morphology, biochemistry and selective topography. The most significant hypotheses concerning the origin of these changes, their interrelationship and link with mental deterioration are reviewed. Some of the characteristic findings, such as neurofibrillary tangles, senile plaques, granulo-vacuolar degeneration, amyloid angiopathy, death and regeneration of neurons, are analyzed. The main neurotransmitter defects are mentioned in brief and similarities and differences between normal aging and Alzheimer's disease emphasized.

Aged↗
PubMed1989

Induction and characterization of mitochondrial DNA mutants in Chlamydomonas reinhardtii.

In addition to lethal minute colony mutations which correspond to loss of mitochondrial DNA, acriflavin induces in Chlamydomonas reinhardtii a low percentage of cells that grow in the light but do not divide under heterotrophic conditions. Two such obligate photoautotrophic mutants were shown to lack the cyanide-sensitive cytochrome pathway of the respiration and to have a reduced cytochrome c oxidase activity. In crosses to wild type, the mutations are transmitted almost exclusively from the mating type minus parent. A same pattern of inheritance is seen for the mitochondrial DNA in crosses between the two interfertile species C. reinhardtii and Chlamydomonas smithii. Both mutants have a deletion in the region of the mitochondrial DNA containing the apocytochrome b gene and possibly the unidentified URFx gene.

Acriflavine↗
PubMed1989

Effects of vigabatrin and of GABA on myelinated rat cerebellar cultures: preliminary data.

1. The aim of this study was to evaluate the effect of high concentrations of vigabatrin (gamma-vinyl GABA) and of GABA on myelin of the central nervous system cultures. 2. Explants of rat cerebellum were cultured for 14-19 days in vitro on collagen-coated coverslips in Leighton tubes. They were exposed for up to 14 days to 500 nmol ml-1 vigabatrin or to 1000 nmol ml-1 GABA. 3. Qualitative and quantitative blind examination of living cultures and of Sudan black B-stained slides showed mild toxicity of both drugs for myelinated fibres. No clear-cut differences could be demonstrated between the two compounds, although vigabatrin seemed slightly more toxic than GABA at these doses. 4. In electron microscopy, no patent intramyelinic oedema nor primary demyelination were seen. On the contrary, some degenerating myelinated fibres and astrocytic gliosis were seen in both experimental conditions. The changes involved axons as well as myelin sheaths. 5. The toxicity of GABA and vigabatrin was surprisingly mild in this very sensitive model.

Aminocaproates↗
PubMed1989

[Cerebellar infarction in the area of the posterior cerebellar artery. Clinicopathology of 28 cases].

We report a neuropathological study of cerebellar infarctions involving the territory of the posterior inferior cerebellar artery (PICA) in 28 cases. Fifteen cases involved the PICA territory only. In 13 cases infarctions in the anterior inferior cerebellar artery (AICA) territory and/or in the superior cerebellar artery (SCA) territory were also present. A thorough post-mortem study of the arterial supply of the brain from the heart up to the cerebellar arteries, including the cervical spine segment of the vertebral arteries was performed in 27 cases. The territory of the cerebellar infarcts has been ascertained. In 15/28 cases (54 percent), infarction involved the PICA territory only (17 infarcts). All of these cases had a benign outcome and death was due to another cause. Six of these were recent infarctions. None had evidence of swelling and tonsillar herniation. Infarcts were generally of small size and involved the entire PICA territory in only 2 cases. Most of these cases were unexpected discovered at autopsy. Cerebellar infarction in the territory of the medial branch of the PICA (9/17 infarcts) drew grossly a set square with a dorsal base and a ventral top headed for the IVth ventricle. Five out of these cases were associated with infarction in the dorsal and lateral medullary territories. Retrospective clinical study showed that they had been unnoticed or overshadowed by other neurological disorders (4 cases), or presented as Wallenberg's syndromes (4 cases), or as a pure vestibular syndrome (due to an infarction involving only the cerebellum) mimicking an acute labyrinthine disorder (1 case). Infarctions in the territory of the lateral branch of the PICA (5/17 infarcts) always occurred without medullary involvement. All of them were unexpectedly discovered at autopsy, and were unnoticed during the life (3 infarcts) or were overshadowed by other neurological disorders (2 infarcts). That was also the case in 2 cases of infarction in the whole PICA territory (3/17 infarcts). Thus infarctions strictly localized to the entire PICA territory only were rare. Thirteen/28 cases (46 p. 100) of infarction in the whole PICA territory were associated with infarction in the AICA and/or the SCA territories. This resulted from an association with other infarctions and not from an abnormally large territory of the PICA. Cerebellar swelling with brain stem compression and tonsillar herniation occurred 8/13 cases (62 p. 100). There were other massive median and paramedian brain stem infarctions involving midbrain, pons or medulla in 55 p. 100 of 13 cases.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1989

[A simple system for semi-automatic image analysis].

A device using a Macintosh microcomputer and a light microscope equipped with a drawing tube is described. The mirror of the drawing tube is turned to the screen of the microcomputer. An example of its use in morphometry of peripheral nerves is given. At a 1000X magnification, the resolution of the system is 10 pixels per 2.6-microns. The coefficient of variation between 20 measurements of diameter of thin (3 microns in diameter) and large (12 microns in diameter) myelinated fibers was 8% and 2% respectively. This precise and inexpensive system could be easily run in laboratories of morphology.

Humans↗
PubMed1988

Does amyloid precede paired helical filaments in the senile plaque? A study of 15 cases with graded intellectual status in aging and Alzheimer disease.

The density of senile plaques in 15 women over 75 years of age was higher when evaluated by thioflavine S than by immunocytochemistry with a polyclonal antibody against paired helical filaments. Mental status had been prospectively assessed in this cohort by the test score of Blessed et al. A difference between the two methods was found whatever the degree of mental impairment. Senile plaques were exceptionally immunolabeled in the least affected cases. This could not be explained only by differences in sensitivity of the stains and suggests that the amyloid is surrounded by anti-PHF positive neurites only in the latest stages of the senile plaque.

Aged↗
PubMed1988

Is senile dementia of the Alzheimer type associated with hippocampal plasticity?

The density of binding sites for excitatory amino acids in the hippocampus of SDAT (senile dementia of the Alzheimer type) patients has been investigated. This was compared to that found in younger and old non-dement cases. In the SDAT hippocampi there was a significant decrease in the glutamate and kainate binding. This reduction correlated positively with the degree of the severity of neurological and pathological disease. In spite of an extensive denervation of SDAT hippocampi, there was no sign of sprouting of mossy fibers; this observation indicates a loss of plasticity in the hippocampus of SDAT patients.

Adult↗
PubMed1988

[Thrombopenia and disseminated intravascular coagulation during treatment with heparin: 2 cases with neurological complications].

We report two cases of heparin-induced thrombocytopenia (H.T.) associated with a disseminated intravascular coagulopathy (DIC). Heparin was prescribed after a cerebral infarct in the first case and after an orthopedic surgical procedure in the second case. The DIC induced neurological complications and the death of both patients. Heparin-induced thrombocytopenia is common but is exceptionally associated with neurological symptoms. Heparin-induced DIC is quite uncommon, since only 20 cases have been reported but neurological complications (focal deficits or disturbances of consciousness) are noted in about one third of the cases and the outcome is fatal in 60 percent of the cases. The treatment of heparin-induced DIC and thrombocytopenia is disappointing. Monitoring of the platelets count is warranted during heparin treatment to prevent this severe complication.

Disseminated Intravascular Coagulation↗
PubMed1988

[Anoxic encephalopathy after cardiocirculatory insufficiency. Neuropathological study apropos of 16 cases].

Sixteen cases of anoxic encephalopathy in adult patients admitted to the intensive Care Department of Raymond Poincaré Hospital (Garches) have been selected on the following criteria: resuscitation by external cardiac massage for cardio-respiratory failure, without any previous history of anoxia and with detailed data on the subsequent evolution of neurological signs and symptoms. Main clinical features were compared to the results of the neuropathological examination. The pattern and the distribution of changes are detailed. The cerebral cortex was always involved by diffuse ischemic cell changes or by laminar necrosis. The Sommer's sector of Ammon's horn was affected in 15 cases, the basal ganglia in 14, the cerebellum in 11, the brain stem in 6. The very rarely mentionned necrotic brain stem changes, which involved inferior colliculi, periaqueductal gray matter and substantia nigra were sometimes associated with lesions of the floor of the IVth Ventricle and of the mamillary bodies. They were different from Wernicke's encephalopathy with could be dismissed on clinical and pathological grounds. No clinical signs or symptoms specific for this distribution of changes could be found by the retrospective study of the clinical files.

Adolescent↗