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Biomedical subjects

E Otomo

Publications and source records attributed to E Otomo.

At least 37 records · Page 2Linked to original sources
PubMed1998

Butyrylcholinesterase K variant and cerebral amyloid angiopathy.

BACKGROUND AND PURPOSE: Cholinesterases are found histochemically in the vessels affected with cerebral amyloid angiopathy (CAA). A gene for the K variant of butyrylcholinesterase (BCHE-K) may be associated with late-onset Alzheimer's disease (AD). In search of genetic risk factors for CAA, we investigated the association of BCHE-K with CAA. METHODS: The association between the severity of CAA and BCHE-K was investigated in 155 autopsy cases of the elderly, including 48 patients with AD. RESULTS: There was no significant association of BCHE-K with the severity of CAA in the total, AD, or non-AD cases. Status of the epsilon4 allele of apolipoprotein E gene did not influence the results. CONCLUSIONS: Our results may suggest that BCHE-K is not a definitive risk factor for CAA in the elderly, although further study with larger samples is necessary to confirm this.

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PubMed1997

Panencephalopathic type of Creutzfeldt-Jakob disease associated with cadaveric dura mater graft.

A 52 year old man with Creutzfeldt-Jakob disease who received a cadaveric dura mater graft 99 months before the onset is reported. The prion protein gene was homozygous for methionine at the polymorphic codon 129. Neuropathological examination disclosed a panencephalopathic type of Creutzfeldt-Jakob disease which was characterised by severe involvement of the cerebral white matter and cerebellum, as well as of the cerebral cortical and deep grey matter. Thus the panencephalopathic type of Creutzfeldt-Jakob disease may occur in association with cadaveric dura mater grafts.

Cadaver↗
PubMed1997

Association of presenilin-1 polymorphism with cerebral amyloid angiopathy in the elderly.

BACKGROUND AND PURPOSE: An intronic polymorphism of presenilin-1 (PS-1), a gene responsible for early-onset familial Alzheimer's disease, has been reported to be associated with late-onset sporadic Alzheimer's disease. In a search for a genetic risk factor of sporadic cerebral amyloid angiopathy (CAA), we investigated the association of the polymorphism of PS-1 with CAA. METHODS: The association between the severity of CAA and genotypes of a polymorphism in intron 8 of PS-1 was investigated in 137 autopsy cases of the elderly. RESULTS: A significant decrease of PS-1 2/2 genotype frequency was associated with severe or moderate CAA. CONCLUSIONS: Our results suggest that PS-1 intronic polymorphism may be associated with the severity of CAA in the elderly.

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PubMed1996

Apolipoprotein E genotype in elderly nondemented subjects without senile changes in the brain.

Only a small minority of elderly subjects can survive with a brain free of senile changes (senile plaques, neurofibrillary tangles, and amyloid angiopathy) beyond the age of 80 years. We demonstrated that an increase of epsilon 2 allele frequency and a decrease of epsilon 4 allele frequency of the apolipoprotein E gene are associated with such brain aging without senile changes.

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PubMed1996

Dementia characterized by abundant neurofibrillary tangles and scarce senile plaques: a quantitative pathological study.

We report an elderly case who had demonstrated progressive memory disturbance and disorientation for 4 years. The clinical features were indistinguishable from late-onset dementia of the Alzheimer type (DAT). Neuropathologically, however, senile plaques (SPs) were almost absent throughout the brain. In contrast, numerous neurofibrillary tangles (NFTs) were observed in the hippocampus and neighboring regions, with much higher density than age-matched normal controls. The immunohistochemical and ultrastructural properties of the NFTs were identical to those of typical DAT. The present case is histologically different from DAT because of the scarce SPs and indicates that numerous NFTs in the hippocampal region can be formed independently of the existence of SPs.

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PubMed1996

Influence of apolipoprotein E genotype on cerebral amyloid angiopathy in the elderly.

BACKGROUND AND PURPOSE: The inheritance of the epsilon 4 allele of the apolipoprotein E gene (APOE) is associated with increased risk of developing dementia of the Alzheimer type (DAT). We have investigated whether the APOE genotype influences the severity of cerebral amyloid angiopathy (CAA) in elderly individuals with or without DAT. METHODS: From a consecutive autopsy series, we studied 88 patients (85.2 +/- 8.1 years) without degenerative disorders other than DAT. The percentages of amyloid-laden vessels in the occipital lobes were calculated and compared between APOE genotypes. RESULTS: For epsilon 3/3 and epsilon 3/4 genotypes, there was a trend toward increased CAA in epsilon 3/4 individuals for non-DAT and conversely in epsilon 3/3 individuals for DAT patients, but these did not achieve significance. CONCLUSIONS: The present study suggests that the epsilon 4 allele is not a strong risk factor for CAA in elderly people.

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PubMed1996

Immune reactions associated with cerebral amyloid angiopathy.

BACKGROUND AND PURPOSE: Cerebral amyloid angiopathy (CAA) occasionally coexists with cerebral vasculitis. An immune system may influence deposition or degradation of the amyloid in cerebral blood vessels. The purpose of this study was to elucidate immune reactions associated with CAA. METHODS: In 11 elderly patients with sporadic CAA, 2 patients with Icelandic familial CAA, and 2 patients with CAA and granulomatous angiitis, the cerebrovascular amyloid proteins and infiltrating inflammatory cells were analyzed immunohistochemically. RESULTS: In both sporadic CAA (beta-protein amyloid angiopathy) and Icelandic familial CAA (cystatin C amyloid angiopathy), leptomeningeal and cortical vessels were associated with an increase or activation of monocyte/macrophage lineage cells. In the cases of CAA with granulomatous angiitis, the vascular amyloid was of beta-protein and associated with infiltration of many monocyte/macrophage lineage cells, which included multinucleated giant cells containing the amyloid in the cytoplasm as well as T cells composed of CD4+ and CD8+ subsets. Amyloid P component, which was reported to be a common component of amyloid deposits and to prevent phagocytic proteolysis of amyloid fibrils of beta-protein, was negative for the vascular amyloid in a case of CAA with granulomatous angiitis but positive in the others. CONCLUSIONS: In both the beta-protein and cystatin C amyloid angiopathies, cerebrovascular amyloid deposition was associated with an increase or activation of monocyte/macrophage lineage cells. Prominent reactions of monocyte/macrophage lineage cells admixed with CD4+ and CD8+ T cells (granulomatous angiitis) were occasionally associated with beta-protein angiopathy. In some of these cases, the absence of amyloid P component might be related to pathogenesis of the granulomatous reaction.

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PubMed1995

[The survival rate of impaired glucose tolerance groups in the elderly].

We analyzed a total of 468 cases, all inmates of the Yokufukai Home for the Aged who had undergone a 50-gram oral glucose tolerance test (OGTT) from January 1980 to December 1981 and who were followed up to the end of March 1994. All cases were divided into different normal, borderline and diabetic categories according to glucose tolerance. 1) Normal cases accounted for 39.6% of males and 39.2% of females, 50% and 52.5% were borderline cases in males and female and these were 10.4% and 8.3% diabetic cases, respectively. 2) The overall survival rate of females was significantly higher than that of males groups (p < 0.05). 3) There was no significant difference in survival rate of males and females in the normal and impaired glucose tolerance groups (border and diabetic). CONCLUSION. Mildly impaired glucose tolerance could be considered as part of the normal aging process.

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PubMed1994

A variant of Gerstmann-Sträussler-Scheinker disease carrying codon 105 mutation with codon 129 polymorphism of the prion protein gene: a clinicopathological study.

A case was reported of variant Gerstmann-Sträussler-Scheinker disease (GSS) carrying codon 105 mutation (Pro to Leu) with codon 129 polymorphism (Met/Val) of the prion protein (PrP) gene. The male patient had developed clumsiness of the right hand at age 42, and subsequently exhibited slowly progressive spastic paraparesis, ataxia, dysarthria, memory disturbance and apraxia. Myoclonus or periodic synchronous discharge was not observed. He died at age 53. The cerebral cortex and white matter showed atrophy, which was prominent in the frontal regions. There were numerous amyloid plaques throughout the cerebral cortex, which were reactive with the antibody to PrP, but not to beta/A 4 peptide. PrP immunostaining also revealed many amorphous deposits in the deep cortical layers, where neuronal loss and glial proliferation was evident. The cerebellum was almost intact, except a few amyloid plaques in the white matter. This variant GSS with codon 105 mutation has been found in four pedigrees, only in Japan up to the present, and the clinicopathological phenotype is summarized as follows: (1) onset at age 38-48, with a duration of 7-11 years, (2) prominent spastic paraparesis, associated with dementia and ataxia, (3) numerous amyloid plaques in the cerebral cortex, (4) amorphous PrP deposits with neuronal loss in the deep cortical layers, and (5) minor change of cerebellum.

Adult↗
PubMed1994

[A clinicopathological study of senile dementia of Alzheimer's type (SDAT) and white matter lesions of Binswanger's type].

A clinicopathological study of senile dementia of Alzheimer's type (SDAT) accompanied by the white matter lesions of Binswanger's type was carried out. Fifty-seven patients, who were diagnosed as suffering from SDAT based on clinical and pathological criteria, were classified into two groups based on the white matter lesions of Binswanger's type. Namely, group 1 consisted of the SDAT patients without any subcortical or white matter lesions (30 cases); group 2 consisted of those with white matter lesions of Binswanger's type (11 cases). The other 9 cases included those with vascular lesions and 4 with some of the same pathological changes found in Parkinson's disease. Clinically, group 2 patients showed subcortical symptoms such as urinary incontinence, Parkinsonian gait, being accompanied by hypertension and arrhythmias. Periventricular lucency (CT) were common in group 2. Macroscopically, both groups showed moderately to severe atrophy, and the width of the corpus callosum of group 2 was narrower than that of group 1. There was no difference in cerebral arteriosclerosis between the groups. In microscopic findings, patients in group 2 showed diffuse distribution of cortical changes such as senile plaques as well as Alzheimer's senile plaques as well as Alzheimer's neurofibrillary tangles while those in group 1 showed various types of diffuse or local distribution. Arteriolosclerosis of the white matter were found in both groups. There was no difference in aortic atherosclerosis and/or heart disease. The complication of white matter lesions of Binswanger's type was not a rare finding in SDAT.

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PubMed1993

Subpial beta/A4 peptide deposits are closely associated with amyloid angiopathy in the elderly.

In order to clarify the significance of subpial beta/A4 peptide deposits (SP beta PD), we examined the brains of 160 consecutive autopsied cases (average age 84.4 +/- 7.7 years) with or without dementia of the Alzheimer type (DAT) pathologically and immunohistochemically. SP beta PD and amyloid angiopathy (AA) showed a significant positive correlation in their severities, both in the DAT and non-DAT groups. AA was present in most cases with SP beta PD, but was absent in all cases without SP beta PD. Our results suggest that SP beta PD and AA would be the related lesions, and that SP beta PD would be formed previous to AA.

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PubMed1993

Cerebral amyloid angiopathy: a significant cause of cerebellar as well as lobar cerebral hemorrhage in the elderly.

We investigated consecutive 1000 autopsied cases (average age 82.9 years) clinicopathologically in order to reveal the significance of cerebral amyloid angiopathy (CAA) as a cause of senile intracranial hemorrhages. We found 101 cases with intracerebral hemorrhages, and CAA accounted for 10.9% of them (31.0% of lobar cerebral hemorrhages, and 14.3% of cerebellar ones). In contrast to hypertensive hemorrhages, CAA-related ones (1) ruptured into the subarachnoid space without exception, (2) often coexisted with dementia of Alzheimer's type, and (3) frequently occurred in the night without elevated blood pressure at onset. The cerebrovascular amyloid was strongly immunoreactive with antibody to beta-protein in all of the cases with CAA-related hemorrhages, and less intensively with antibody to cystatin C in 91% of them. Our data indicate that CAA is an important etiological factor of cerebellar hemorrhages, as well as lobar cerebral hemorrhages, in normotensive, aged patients.

Aged↗
PubMed1993

Subarachnoid haemorrhage in the elderly: a necropsy study of the association with cerebral amyloid angiopathy.

To clarify the contribution of cerebral amyloid angiopathy (CAA) to subarachnoid haemorrhage (SAH) in the elderly, relationships between SAH and CAA were investigated in 997 necropsy cases aged 60 years or older. Primary SAH (bleeding from subarachnoid vessels) was found in 15 cases (1.5%). There was no case in which primary SAH was clearly attributed to CAA. Secondary SAH [secondary rupture of intracerebral haemorrhage (ICH) through the cortex to the subarachnoid space] was found in 23 patients (2.3%). In 11 (48%) of them, ICH with secondary SAH was associated with CAA. The results indicated that primary SAH is rarely related to CAA, however, CAA is the most frequent cause of ICH accompanying secondary SAH in the elderly.

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PubMed1993

Computer-assisted three-dimensional image analysis of cerebral amyloid angiopathy.

BACKGROUND AND PURPOSE: Microaneurysms and fibrinoid necrosis of cerebral cortical arteries have been reported to be related to the pathogenesis of intracerebral hemorrhage associated with cerebral amyloid angiopathy. To elucidate the pathogenesis of such vascular lesions, we conducted the present study. METHODS: Five hundred serial sections from brain tissue of a patient with severe amyloid angiopathy and intracerebral hemorrhage were analyzed histologically and immunohistochemically. Three-dimensional reconstructions of the vascular lesions were performed using a computer-assisted image analysis system. RESULTS: The microaneurysms were found to develop in small cortical arteries with diameters of about 40 to 50 microns. They were spindle-shaped dilatations, with a maximum diameter of about 200 microns, and appeared within vascular segments bearing severe amyloid deposition. In the walls of the aneurysms, the intima was thickened, and the media and adventitia showed thinning and disruption. Fibrinoid necrosis was found in the vascular walls of the most dilated, middle portions of the aneurysm. The vascular walls undergoing fibrinoid necrosis did not show any beta/A4 or cystatin C but presented with fibrinogen-like immunoreactivities, indicating invasion of plasma components. CONCLUSIONS: These results suggested the following sequential events for the pathogenesis of the cerebral amyloid angiopathy-associated vascular lesions leading to hemorrhage: (1) damage of the media and adventitia due to severe amyloid deposition results in dilatation of the cortical arteries, (2) the vascular dilatation progresses and is accompanied by thickening of the intima and disruption of the media and adventitia (microaneurysm formation), (3) plasma components invade to the vascular wall (fibrinoid necrosis), and (4) finally, hemorrhage develops.

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