[Genetic aspects of Alzheimer's disease].
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Alzheimer Disease↗
Biomedical subjects
J Tateishi
Publications and source records attributed to J Tateishi.
[Clinical significance of precordial ST segment depression during acute inferior myocardial infarction].
To investigate the mechanisms and clinical significance of precordial (V1-V4) ST segment depression during acute inferior myocardial infarction, stress thallium-201 scintigrams and coronary angiograms were obtained within four to eight weeks after the onset of myocardial infarction in 37 patients experiencing their first acute inferior myocardial infarction. Among 18 patients with precordial ST depression (group 1), 11 with concomitant disease of the left anterior descending artery (LAD) had positive results on exercise test, whereas in seven patients without LAD lesion, only two had positive exercise test (p less than 0.01). In 19 patients without precordial ST depression (group 2), 11 had severe stenosis in the LAD. However, among these 11 patients, only two had positive exercise tests. Patients with precordial ST depression demonstrated a higher frequency of positive exercise tests than those without it (p less than 0.01). On stress thallium-201 scintigraphy, a perfusion defect involving the inferior wall was present in all patients, but additional anterior wall ischemia was present in only five of the 18 patients in group 1. These five patients had chest pain on exercise tests and a severe stenosis greater than 90% in the LAD. There was no significant difference in the frequency of additional posterolateral wall infarction between groups 1 and 2. In 18 patients in group 1, sigma ST (total degrees of ST segment depression in leads V1, V2, V3, and V4 in the acute stage) was significantly greater in 11 patients with LAD lesion than in seven without (p less than 0.05), and sigma ST greater than five mm was observed in 12 of 13 patients who had additional anterior wall ischemia and posterolateral wall infarction on stress thallium-201 scintigraphy (p less than 0.05). Myocardial revascularization, such as aortocoronary bypass surgery or percutaneous transluminal coronary angioplasty (PTCA), was performed in six of the 18 patients in group 1 in the chronic stage, but in only one of the 19 patients in group 2. Thus, in patients with initial acute inferior myocardial infarction, those with precordial ST depression seemed to be a high-risk group. It was suggested that, during the early stage of myocardial infarction, this abnormality on electrocardiograms is related to the summation of effects of anterior wall ischemia and posterolateral wall infarction. Furthermore, the sigma ST evaluation is useful in differentiating a mirror image of inferior wall infarction from anterior wall ischemia and posterolateral wall infarction as the mechanism of precordial ST depression.
Angiography↗
[Recent topics on Alzheimer's disease. The possibility of Alzheimer's disease as a delayed-type infection--study on prions of proteinaceous infective particles].
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Aged↗
[An autopsy case of Gerstmann-Sträussler-Scheinker's disease with family history].
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Aged↗
Immunohistochemical confirmation of Creutzfeldt-Jakob disease with a long clinical course with amyloid plaque core antibodies.
Amyloid plaques have been found in the brains of some patients with Creutzfeldt-Jakob disease (CJD) and all patients with Gerstmann-Sträussler syndrome (GSS). We examined paraffin sections from 45 patients with CJD or GSS and from 51 patients with other neurologic diseases, using an antiserum against GSS amyloid plaque cores. The GSS amyloid plaque core antiserum revealed not only birefringent amyloid plaques but also small plaques that cannot be detected by the staining with Congo red dye. Positive immunolabeling was demonstrated in 59% of 34 Japanese patients with CJD, in 100% of 11 patients with GSS, and in none with other neurologic diseases. All cases of CJD of short duration (less than 11 months) were evaluated as being negative, and 95% of 21 long survivors (over 12 months) were positive. This immunohistochemical approach revealed that amyloid plaque is a hallmark of CJD with a long clinical course.
Amyloid↗
Unique distributions of natriuretic hormones in dog brain.
We examined the regional distributions of atrial natriuretic polypeptide (ANP) and digoxin-like immunoreactivity (DLI) in dog brain, using specific radioimmunoassay. The molecular form of the dog brain ANP was similar to that of alpha-hANP, in gel filtration and reversed-phase HPLC. Distribution of ANP in dog brain differed from rat brain. A significant amount of ANP-like immunoreactivity (ANPLI) was observed in the periaqueductal grey, ventral thalamus and spinal cord, however, only a trace amount was seen in the hypothalamus. The DLI was widely distributed in the dog brain, especially with over 2 ng/g wet wt. of the immunoreactivity content in mammillary body, septum, striatal body, hypothalamus and periaqueductal grey. Different from the localizations of natriuretic hormones in rat brain, the periaqueductal grey matter in dog brain may be an important source of both natriuretic hormones.
Animals↗
Effects of intracarotid hyperosmolar mannitol in triethyl tin (TET)-induced rat brain edema--preservation of blood-brain barrier (BBB) in TET edema.
The effect of intracarotid hyperosmolar mannitol on the blood-brain barrier (BBB) in triethyl tin (TET)-induced rat brain edema was examined by using intravenous Evans blue (EB, MW 68,000) and Adriamycin (ADM, MW 580) as tracers. Three ml of 1.4 M mannitol solution were administered through the right carotid artery during 45 s for BBB opening. The barrier was opened for 60-120 minutes and then re-established. The reversibility was preserved in TET-treated rats and controls. In fact, the intravenous injection of EB stained both TET-treated and non-treated cerebral hemispheres with mannitol-induced transient BBB disruption, but not without BBB disruption. BBB was resistant to both high and low molecular weight substances in TET-induced edema. The importance of this hyperosmotic studies provides the evidence for normal BBB function in TET-induced brain edema.
Animals↗
Neurotoxicity of adriamycin passed through the transiently disrupted blood-brain barrier by mannitol in the rat brain.
Neurotoxicity of adriamycin (ADM) was investigated following the transient disruption of the blood-brain barrier (BBB) in rats. The BBB disruption by the hyperosmotic agent (1.4 M mannitol) was confirmed by the leakage of ADM and Evans blue administered intravenously. Neuropathological changes due to the toxicity of ADM were found as early as day 4. The neurons in the cerebral cortex and nucleus caudatus-putamen showed focal clearing of the nuclear chromatin, increased dense bodies in the cytoplasm and dilatation of the cisternae of the rough endoplasmic reticulum (r-ER) and Golgi apparatus. By day 7, nucleolar segregation and irregular membranous structures appeared in the nuclei with the progression of cytoplasmic changes. By day 10, the cytoplasm of many neurons was vacuolated. Electron-microscopically, the cisternae of the r-ER and Golgi apparatus were prominently dilated in these neurons. Neuronal microtubules were increased in number, in particular in the perinuclear region. Numerous whorl-like membranous structures and separation of nuclear membrane were also observed. Some astrocytic processes surrounding the blood vessels revealed loss of organelles and a few pericytes showed an increased number of lysosomes on days 7 and 10. This experiment clearly demonstrates that ADM has strong neurotoxic effects in the central nervous system when the BBB is disrupted, and provides the warning for the possibilities of neurotoxic side effects when ADM is administered, in combination with a hyperosmotic agent, for the treatment of human malignant tumors, including brain tumors.
Animals↗
Immunoblotting of Creutzfeldt-Jakob disease prion proteins: host species-specific epitopes.
Creutzfeldt-Jakob disease (CJD) is a rare dementia that is generally found in older people and is caused by unusual infectious pathogens or prions. Using rabbit antisera raised against hamster scrapie prion proteins (HaPrPSc), we identified by immunoblotting human CJD prion proteins (HuPrPCJD) in the brains of 14 patients dying of CJD. Extracts from 6 of the patients were transmitted to mice after prolonged incubation. The rabbit antisera raised against HaPrPSc also reacted with the mouse CJD prion proteins (MoPrPCJD) found in the brains of these experimentally infected mice. When mice were immunized with HuPrPCJD, they produced antibodies that reacted with HuPrPCJD but not with MoPrPCJD. Mice immunized with MoPrPCJD produced antibodies to neither murine nor human prion proteins. Our results provide evidence for host species-specific epitopes on prion proteins. The existence of such epitopes is consistent with the apparent lack of an immune response during prion infections and the finding that prion protein molecules are encoded by host genes.
Brain↗
Cerebellar efferent fibers around the dentate nucleus. Pathological anatomy in olivo-ponto-cerebellar and dentato-pallido-luysian atrophy.
In patients with olivo-ponto-cerebellar atrophy (OPCA), the deep cerebellar white matter showed evidence of severe degeneration and gliosis. However, the circumferential white matter enclosing the dentate nucleus was less involved. In addition, the Holzer stain verified the presence of mild gliosis inside the wrinkled band of the dentate gray matter. In contrast, dentato-rubro-pallido-luysian atrophy (DRPLA) affected the mantle layer covering the dentate nucleus. The fibers encircling the dentate nucleus, which degenerate in DRPLA and are spared in OPCA, are anatomically noticeable to be dentatofugal pathways. Moreover, the afferent fibers from the cerebellar cortex and other systems may reach the dentate nucleus partly from the medial aspect via the hilus, as was noted in cases of OPCA.
Cerebellar Ataxia↗
Formalin fixed brains are useful for magnetic resonance imaging (MRI) study.
We carried out magnetic resonance imaging (MRI) studies on human brains which had been fixed in formalin solution for over 2 years and had been proven neuropathologically to be cases of multiple sclerosis (MS), progressive multifocal leukoencephalopathy (PML), and Balo's concentric sclerosis (Balo). Using spin echo (SE) and inversion recovery (IR) pulse sequences to detect demyelinated lesions in a living person with MS, the demyelinated lesions of the fixed brains in cases of MS, PML and Balo definitely re-appeared, although T1 and T2 in the gray and white matter were reduced following fixation. High signal areas on the SE images corresponded not only to the characteristic distribution of demyelinated lesions in the white matter but also to sparse myelin, gliosis and mild perivascular cuffing in the white matter around the demyelinated foci in cases of the fixed MS, PML and Balo brains. On the IR images, only MS plaques were evident. This MRI study of fixed brains proved useful to elucidate clinicopathological correlations.
Adolescent↗
Effects of methylcobalamin on vitamin B1- and B-deficient encephalopathy in rats.
Vitamin B1- and B-deficient encephalopathy was produced in adult Wistar rats and the effect of methylcobalamin was studied. These experiments were performed in vitamin B1- or B-deficient rats with or without the administration of guanidine, a magnesium antagonist. These encephalopathic rats showed symmetrical lesions in the pontine tegmentum. No pathological changes in the brainstem were seen in guanidine-administered rats. This suggests that guanidine itself doesn't produce these brainstem lesions. Moderate to severe pathological changes occurred in vitamin B-deficient rats with guanidine administration, whereas these pathological changes were milder in vitamin B1-deficient rats with guanidine administration and in vitamin B1- and B-deficient rats with the combination of the guanidine and methylcobalamin administrations. These facts suggest that vitamin B12, methylcobalamin, plays an important preventive role in the development of the pontine lesions in this experiment.
Animals↗
Lack of effect of thymus and spleen on the incubation period of Creutzfeldt-Jakob disease in mice.
Genetically athymic and asplenic (Lasat), athymic (Nude), asplenic (Dh) or normal littermate (Hetero) mice with a BALB/c genetic background were injected either intracerebrally or intraperitoneally with a 1% or 10% homogenate of mouse brains infected with the Fukuoka 1 strain of the Creutzfeldt-Jakob disease (CJD) agent. As there were no significant differences in incubation periods among the five groups (Lasat, Nude, Dh, Hetero and BALB/c) inoculated with the same dilution, via the same route, it was concluded that cell-mediated immunity dependent on the thymus plays no significant role in host defence against the CJD agent, and the spleen, a critical site of agent replication, is apparently not an obligatory source from which infection spreads to the central nervous system.
Animals↗
Formic acid pretreatment enhances immunostaining of cerebral and systemic amyloids.
The purpose of this study was to design a method by which immunoperoxidase staining can be applied to formalin-fixed, paraffin-embedded tissue sections to demonstrate amyloid deposits in cerebral and systemic amyloidotic tissues. We used anti-prion protein, anti-beta-protein, anti-amyloid A, and anti-prealbumin antisera. The tissue sections were first treated with 100% formic acid for 5, 20, or 60 minutes and the unlabeled immunoperoxidase method (biotin-streptavidin system reagents) was used. This formic acid pretreatment enhanced immunoreactivity of the amyloid deposits which reacted positively with specific antiserum. The specificity of the immunostainings was well preserved. This method can also be used to demonstrate interspecies cross-reactivity, by using anti-human amyloid A and anti-scrapie hamster prion protein antisera, which stained negatively or faintly with amyloid deposits of heterogenous species. The technique is expected to reveal the buried epitopes of amyloid deposits in tissue sections.
Alzheimer Disease↗
[Right ventricular ejection and regional wall motion evaluated by cardiac blood pool emission computed tomography].
Calculating right ventricular (RV) ejection fraction (EF) is difficult because of geometrical problems such as irregular trabeculations, a separate infundibulum, and variations in the right ventricular shape. We performed 99mTc ECG-(dual)gated cardiac blood pool emission computed tomography (ECT) in 10 patients with ischemic heart disease, three patients with dilated cardiomyopathy (DCM), and eight normal subjects as controls, and RVEF and % shortening of the RV were calculated to evaluate right ventricular function. Methods were as follows: 1) RVEF: The region of interest (ROI) of the RV was determined on reconstructed short-axial images, and then the RV counts in the ROI were summed from the apical slice to the RA-RV boundary slice. (Formula: see text) 2) % shortening of the RV: At the RV mid-portion, the contour from the short-axial image was obtained using the threshold method; the end-diastolic contour was superimposed on the end-systolic contour, and then shortenings in the RV free wall and septum respectively, were calculated. To evaluate reliability of RVEF obtained by this method, left ventricular ejection fraction (LVEF) calculated using the same method was compared with results obtained by the previously validated method: There were significant correlations with contrast cineangiography (r = 0.69) and the conventional multigated method (r = 0.90), respectively. Cases with decreased RVEF showed a variety of right ventricular abnormal findings, including positive uptake on 99mTc-PYP scintigraphy, occlusion of the right coronary artery, RV dilatation on echocardiography. The mean RV free wall shortening in the decreased RVEF group was lower than that of the normal group (p less than 0.01), whereas there was no significant difference in the decreased LVEF group.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[Effects of dobutamine on hemodynamics, myocardial metabolism and mechanical efficiency in patients with old myocardial infarctions].
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Adult↗
Flow-dependence of vasodilatory response in renal vascular bed to hemorrhage in dogs.
The vasodilatory response in the renal vascular bed was studied after quick mild hemorrhage under different levels of renal blood flow. In neuraxis intact dogs, the renal vascular resistance increased or decreased within 5 s after hemorrhage and reached a stable level close to the control within 10 s. The responses under neuraxis intact conditions may involve both responses of the renal vascular resistance to changes in renal sympathetic nerve activity caused by the baroreceptor reflex and responses to decrease in renal perfusion pressure after hemorrhage. In order to exclude baroreflex neural regulation of renal blood flow, we sectioned the carotid sinus and vagus nerves. The renal vascular resistance decreased within 5 s after hemorrhage, and was maintained at around this level for about 2 min. The decrease in renal vascular resistance and control (prehemorrhage) renal blood flow revealed a significant hyperbolic relationship. Since the systemic arterial pressure was not restored after hemorrhage and reflexogenic changes in sympathetic nerve activity were excluded after barodenervation, the vasodilatory response in the renal vascular bed after hemorrhage should reflect only hemodynamic changes. We conclude that the vasodilatory response to pressure fall in the renal vascular bed increases with a decrease in the control renal blood flow.
Animals↗
Congophilia in cerebral amyloidosis is modified by inactivation procedures on slow transmissible pathogens.
Cerebral tissues with amyloid deposits were treated by various chemicals which inactivated the agent of subacute spongiform encephalopathy (SSE). We discovered Congophilia in the amyloid plaques in cases of Creutzfeldt-Jakob disease (CJD) and Gerstmann-Sträussler syndrome (GSS) correlated to the chemical inactivation profiles of SSE. After incubation with trichloroacetate, guanidine-SCN, guanidine-HCl, formic acid, phenol and autoclaving, amyloid plaques in unfixed frozen sections of human brains with CJD or GSS, lost the affinity of Congo red and green birefringence under polarized light. In formalin-fixed, paraffin-embedded tissue sections, amyloid plaques of CJD and GSS lost the affinity of Congo red after most of these treatments. On the other hand, senile plaques in the aged, patients with Alzheimer's disease and with senile dementia of the Alzheimer type did not lose the affinity of Congo red after most of these treatments. Therefore, the amyloid deposits in the amyloid plaques differ from those in senile plaques. The methods we used facilitate differentiation of amyloid and senile plaques in formalin-fixed, paraffin-embedded tissues.
Alzheimer Disease↗