Biomedical subjects

E Iseki

Publications and source records attributed to E Iseki.

At least 55 records · Page 3Linked to original sources

PubMed1997

Glial tau-positive structures lack the sequence encoded by exon 3 of the tau protein gene.

Tau protein comprises six distinct isoforms defined by the presence or absence of sequences encoded by alternatively spliced exon 2, 3 and 10. We have investigated immunohistochemically the expression of exon 3-derived fragment (E-3) of tau protein in brains of patients with Alzheimer's disease (AD) and other neurodegenerative diseases in which the abnormal accumulation of tau protein takes place. In AD, a subset of neurofibrillary tangles, neuropil threads and dystrophic neurites in senile plaques were stained positively with an anti-E-3 antibody. In sharp contrast, glial tau-positive structures, such as astrocytic plaques and oligodendroglial coiled bodies, were negative for E-3 in all cases examined in this study. This is the first report to discriminate tau-positive inclusions in glial cells from those in neurons at the molecular level.

Aged↗

PubMed1997

Close relationship between spongiform change and ubiquitin-positive granular structures in diffuse Lewy body disease.

The origin of spongiform change seen in diffuse Lewy body disease (DLBD) cases was elucidated, as compared with Alzheimer-type dementia (ATD) cases. Spongiform change was composed of numerous vacuoles in the neuropil, predominantly in layers II-IIIab of the transentorhinal cortex and in the intermediate area of the accessory basal amygdaloid nucleus. The distribution of spongiform change was identical to that of ubiquitin-positive granular structures (UPG) in non-demented cases. The degree of spongiform change was correlated with loss of the large pyramidal neurons in layers IIIc and V of the transentorhinal cortex and with the disappearance of their ubiquitin-positive granular processes. With electron microscopy, the early vacuoles of spongiform change appeared to arise in the presynaptic terminals as well as in the postsynaptic terminals and dendritic processes. These findings indicate that the vacuoles derive from degeneration of terminal axons of the large pyramidal neurons. The occurrence of spongiform change characteristic to DLBD suggests that the large pyramidal neurons degenerate more rapidly in DLBD than in ATD.

Aged↗

PubMed1997

Hippocampal pathology in diffuse Lewy body disease using ubiquitin immunohistochemistry.

Various ubiquitin-positive structures in the hippocampus in diffuse Lewy body disease (n=12) and non-demented aged subjects (n=3) were investigated immunohistochemically. These structures were composed of ubiquitin-positive granular structures (UPG), ubiquitin-positive neuritic structures (UPN), spheroidal structures, neuritic plaques, neurofibrillary tangles (NFT), Lewy bodies (LB) and ubiquitin-positive neurons. UPG, UPN, spheroidal structures and neuritic plaques were distributed with special reference to the hippocampal pathway assumed in this study. This pathway was thought to run along the stratum oriens, mostly perforating the stratum pyramidale at many sites of the subiculum and CA1-3, and to end partly in the CA2-3 and the subiculum of the uncus (UPG or UPN). After perforating the stratum pyramidale and giving off terminal branches (ubiquitin-positive neurons or neuritic plaques with degenerative neurites), it was thought to run along the stratum radiatum and continue along the stratum moleculare of the dentate gyrus, forming synapses with the apical dendrites from the stratum pyramidale and the stratum granulosum (spheroidal structures or neuritic plaques). These findings suggest that many of the ubiquitin-positive structures may be caused by degeneration of terminal or distal axons of this pathway. NFT and LB also had a somewhat orderly distribution with reference to this pathway.

Aged↗

PubMed1997

[Parkinsonism in Alzheimer's disease].

Parkinsonism occurs frequently in the patients with Alzheimer type dementia (ATD). The frequency ranges from 9% to 100% of ATD patients, depending on samples, clinical instruments and stages of illness. Several studies have described that rigidity and hypokinesia are the most prevalently observed signs of parkinsonism, and that resting tremor is less. The clinical progress of patients with parkinsonism is more rapid than those of patients without parkinsonism. Patients with parkinsonism are frequently associated with psychiatric symptoms such as depression and delusion. The pathogenesis of parkinsonism in ATD remains to be elucidated, but it should be noted that some cases with parkinsonism correlates with Parkinson's disease pathologic condition, and some have diffuse Lewy body disease.

Alzheimer Disease↗

PubMed1996

Immunohistochemical investigation of human leukocyte antigen (HLA)-DR-positive astrocytes in adrenoleukodystrophy brain.

We investigated immunohistochemically the expression of human leukocyte antigen (HLA)-DR in postmortem brain tissue of two adult patients with adrenoleukodystrophy (ALD). In addition to microglia and macrophages, a significant number of star-like cells were stained positively for HLA-DR in demyelinating lesions of both patients. Such cells congregated in the peripheral zone of the lesions. A mirror image analysis as well as double immunostaining for HLA-DR and glial fibrillary acidic protein established that these cells were a subset of reactive astrocytes. Together with other reports demonstrating that astrocytes express HLA-DR only under very limited conditions, the results of this study suggest the involvement of immune and inflammatory responses in the pathological processes of ALD.

Adrenoleukodystrophy↗

PubMed1996

Neuropathological evaluation and apolipoprotein E gene polymorphism analysis in diffuse Lewy body disease.

We performed a quantitative neuropathological investigation of senile plaques and neurofibrillary tangles in the brains of 14 Japanese patients with diffuse Lewy body disease (DLBD), and examined apolipoprotein E (APOE) gene polymorphism in these patients. Most DLBD brains had as many senile plaques as those with Alzheimer-type dementia (ATD), but fewer neurofibrillary tangles. The APOE epsilon 4 allele frequency in DLBD was 39.3%, similar to that previously reported in pathologically diagnosed ATD. DLBD and ATD are clinically and pathologically distinct, but may have common mechanisms with regard to the formation of amyloid deposition based on these findings. Future investigation of the pure form of DLBD may clarify the association between Lewy body dementia and APOE.

Aged↗

PubMed1996

Age-related ubiquitin-positive granular structures in non-demented subjects and neurodegenerative disorders.

The distribution and nature of age-related ubiquitin-positive granular structures (UPG) were examined in non-demented brains. In addition, their appearance pattern in some neurodegenerative disorders was investigated. In the transentorhinal cortex, they were distributed among cell islands of layer pre-alpha and in layers II and IIIab. In the amygdala, they were preferentially located in the accessory basal and basal nuclei. UPG were first observed in the transentorhinal cortex of non-demented middle-aged brains and increased in frequency and extended to other regions with increasing age. In Alzheimer-type dementia (ATD), they decreased with advance of the clinical stage. In diffuse Lewy body disease (DLBD), they decreased, accompanying linear neuritic structures. With the double-immuno-staining, UPG were frequently overlapped with neurofilament-positive granules. The multipolar cells of layer pre-alpha and pyramidal cells of layers IIIc and V were also immunostained with anti-neurofilament antibody, and the obliquely ascending fibers of these cells were found frequently to continue to these neurofilament-positive granules. Using ubiquitin immunoelectron microscopy, UPG appeared to derive from degenerating terminal axons. These findings suggest that UPG originate mainly from the recurrent collateral ascending axons in layers II-IIIab and from projecting axons in the amygdala. The occurrence of UPG in the limbic system is an important morphological hallmark of aging. In addition, further studies on the appearance pattern of UPG in ATD and DLBD may clarify whether a difference in the degenerative process of both disorders exists.

Adolescent↗

PubMed1996

Dementia with Lewy bodies.

Dementia with Lewy bodies is a generic term which was proposed at the first International Workshop on Lewy Body Dementia (Newcastle upon Tyne, 1995). It is an all encompassing term that includes various types of disorder such as diffuse Lewy body disease, senile dementia of Lewy body type, and Lewy body variant of Alzheimer's disease. Epidemiological, clinical, neuropathological, biochemical, molecular biological, and therapeutic contributions to the understanding of dementia with Lewy bodies are reviewed.

Alzheimer Disease↗

PubMed1995

Immunohistochemical investigation of tau-positive structures in the cerebral cortex of patients with progressive supranuclear palsy.

We have investigated tau-positive structures immunohistochemically in the cerebral cortex of patients with progressive supranuclear palsy (PSP). In addition to neurofibrillary tangles, a variety of tau-positive structures occur. They are particularly abundant in the precentral gyrus and other frontal cortices. Double immunostaining has demonstrated that coil-like structures (coiled bodies) are located in the oligodendroglial cell bodies. Three forms of tau-positive astrocytic inclusions are discerned: those with tuft-like profiles, thorn-like structures, and concentric clusters of short stubby fibers. The concentric clusters of tau-positive fibers are present in some, but not all, PSP brains. They appear to be identical to 'astrocytic plaques' previously reported in patients with corticobasal degeneration (CBD). PSP and CBD might share a common pathological background which causes abnormal accumulation of tau protein in neurons and glial cells of neuroectodermal origin.

Aged↗

PubMed1995

Fas antigen expression in brains of patients with Alzheimer-type dementia.

Fas antigen (CD95) is a cell surface protein that mediates apoptosis. We have investigated the immunohistochemical localization of Fas antigen in postmortem brain tissue from control subjects, patients with Alzheimer-type dementia (ATD), and from a few patients with diffuse Lewy body disease, progressive supranuclear palsy and adrenoleukodystrophy. In all brains, including controls, vascular endothelial cells and residual blood plasma were weakly stained. In ATD brains, senile plaques and a small number of star-like cells were brains of patients with neurological diseases other than ATD. In double immunostaining for Fas and glial fibrillary acidic protein (GFAP), a small number of cells were positive for both antigens. The majority of Fas-positive astrocytes were, however, negative for GFAP. This implies the downregulation of GFAP production in these cells. Doubly labeled astrocytes were also found around senile plaques, suggesting that the Fas immunoreactivity in senile plaques was derived from astrocytic membranes. The results of this study indicate that Fas antigen is expressed by a subset of reactive astrocytes in degenerative neurological diseases. Such astrocytes may undergo the Fas-mediated apoptotic process.

Aged↗

PubMed1995

Investigation of tau-2 positive microglia-like cells in the subcortical nuclei of human neurodegenerative disorders.

An anti-tau monoclonal antibody tau-2 was demonstrated to react with the cells which characteristically appeared in the subcortical nuclei of certain neurodegenerative disorders. These cells had rod-like cell bodies and elongated processes, whose morphology was consistent with that of reactive microglia (tau-2 positive microglia-like cells; TPMC). TPMC were diffusely scattered in the subcortical nuclei, especially the putamen, irrelevant to focal tissue injury such as infarcts and amyloid deposits. TPMC were positively immunostained with anti-ferritin antibody, but negatively with LN3, anti-GFAP, other kinds of anti-tau and anti-neurofilament antibodies. TPMC were found in some cases of Alzheimer type dementia and diffuse Lewy body disease, but not in the cases of Parkinson's disease, Pick's disease and control without neurological disorder. Similar microglia-like cells were found around infarctic foci and amyloid cores of senile plaques, regardless of the disorder. They were, however, different from TPMC in that they were positively immunostained with LN3.

Aged↗

PubMed1990

Morphological characteristics of senile plaques in familial Alzheimer's disease.

The distribution and morphology of senile plaques (SPs) in the cerebral cortices and subcortical nuclei of six cases of familial Alzheimer's disease (AD) were examined using the Methenamine-Bodian method and compared with those of sporadic AD cases. SPs were grouped into three types according to their morphology. SP types were generally constant at each anatomical site in all of the cases. The SPs of familial cases, however, had a greater tendency to fuse together than those of sporadic cases, especially in the cingulate cortex, presubiculum and striatum. This tendency was more evident in cases with severe amyloid angiopathy. Here it appeared that a SP type corresponding to "diffuse plaques", at least in part, might be formed by transformation from another type. In the globus pallidus, all the familial cases had many compact-like plaques which appeared to be derived from "drusige Entartung" of the capillaries. Furthermore, the regional proportion of two types of SPs occurring in this nucleus varied along its anteroposterior axis. These findings may be the histological hallmarks of atypical AD rather than familial AD.

Alzheimer Disease↗

PubMed1989

Distribution and morphology of brain stem plaques in Alzheimer's disease.

The morphology, incidence and distribution of senile plaques in the brain stem were examined in 15 cases of Alzheimer's disease, using mainly the Methenamine-Bodian method. The plaques were found in all cases and were grouped into three types according to their morphology. They were not randomly scattered in the brain stem, but had a distribution common to all cases. There were numerous plaques in the periaqueductal gray, superior colliculus, fourth-ventricle floor and superior central nucleus. The plaques were also found less abundantly in the reticular formation, substantia nigra, pontine nucleus and inferior olivary nucleus. There was a tendency for certain plaque types to be associated with specific regions. In the familial cases, the plaques tended to occur even in the regions where they were rare in other cases. The capillaries with plaque-like degeneration were observed not infrequently in the brain stem. The distribution of plaques did not always coincide with that of neurofibrillary tangles.

Aged↗

PubMed1988

Two necropsy cases of chronic encephalomyelitis: variants of Neuro-Behçet's syndrome?

Two necropsy cases of chronic encephalomyelitis of unknown aetiology are presented. Skin hyperreactivity occurred in both cases although there were no mucocutaneo-ocular symptoms. There was confluent perivenous necrosis with marked glio-mesenchymal reactions and persistent inflammatory changes, predominantly in the diencephalon and brain stem. These cases are clinico-pathologically analogous to Neuro-Behcet's syndrome.

Adult↗

PubMed1987

A case of adult neuronal ceroid-lipofuscinosis with the appearance of membranous cytoplasmic bodies localized in the spinal anterior horn.

An autopsy case of adult neuronal ceroid-lipofuscinosis was examined. The clinical picture was characterized by gait disturbance, bulbar palsy and dementia. Histopathologically, diffuse neuronal loss was found throughout the central nervous system. The remaining neurons, predominantly in the motor nuclei of the spinal cord and brain stem, were swollen with storage material. Observed under the electron microscope the storage material showed various ultrastructures, such as lipofuscin-like bodies, pleomorphic lipid bodies, curvilinear profiles and finger-print profiles, in different regions of the central nervous system. In the ballooned neurons of the spinal anterior horn, many membranous cytoplasmic bodies and curvilinear profiles were intermingled within the same cell and were continuous with each other. Biochemically, N-acetyl neuraminic acid content was significantly increased in the spinal anterior horn. These findings suggest the localized increase of ganglioside in that region.

Gangliosides↗

PubMed1987

Nasu-Hakola's disease (membranous lipodystrophy).

An autopsy case of Nasu-Hakola's disease (membranous lipodystrophy) is reported. A 43-year-old Japanese man, whose parents were not consanguineous, had been suffering from frequent long bone fractures since the age of 10. Neuropsychiatric symptoms, which were characterized by euphoria, disturbance of attention and dementia, appeared at his thirties and generalized and/or localized seizures and apallial syndrome at the later stage. The neuropathology revealed diffuse leukoencephalopathy of the cerebrum. The peculiar aspects in this case were membranocystic changes in the lungs [Yagishita et al. Virchows Arch [A] 408:211-217 (1985)], diffuse degeneration of the cerebral cortex, chiefly in frontal and temporal lobes, and many axonal spheroids throughout the cerebral cortex. The ultrastructure of spheroids in the cerebral cortex demonstrated aggregations of mitochondria, dense bodies and minute concentric bodies and a small amount of neurofilaments.

Adult↗

PubMed1987

Tardive dyskinesia with inflated neurons of the cerebellar dentate nucleus. Case reports and morphometric study.

Four autopsied cases of tardive dyskinesia manifesting oral hyperkinesia revealed markedly inflated neurons in the cerebellar dentate nucleus (DN), which had not been described previously. The inflation of the neurons was proved to be statistically significant (P less than 0.01) by morphometric study. The nuclei were usually situated in the central portion of the cytoplasm. This inflated change was different from both central chromatolysis and grumose degeneration of the DN, typically observed in progressive supranuclear palsy and dentatorubropallidolysian atrophy, and seemed to be easy to miss without careful observation, since neuronal loss and gliosis were very mild in the DN. Among a few autopsied cases of tardive dyskinesia reported previously, degeneration of the DN was described in only two. It is believed, however, that the inflated neurons of the DN may not be so rare and may be related to the occurrence of some involuntary hyperkinesia, especially oral hyperkinesia following some neurotoxic disorders and/or neuroleptic medications.

Aged↗

PubMed1986

Virus-like particles in cultured C3H/St mouse cells treated with a carcinogenic polycyclic hydrocarbon.

Virus-like particles with cylindrical form were found in cultured alveolar macrophages and lung fibroblasts of C3H/St mice, after treating these cells with a carcinogenic polycyclic hydrocarbon, 1, 2, 5, 6,-Dibenzanthracene (DBA). Their morphology looked identical to those observed in vivo in the reactive cells which engulfed DBA crystals implanted into the brain and muscle of the same mouse strain. These particles were not found in either the untreated cells of C3 H/St mice or the treated cells of BALB/c mice. In the alveolar macrophages, these particles appeared first at 3 days after DBA treatment and reached the maximum number around the 30th day. They still kept their morphology in the degenerating cells which had lost the cytoplasmic organelles. These findings suggest the possibility that DBA induced the expression of the viral genome endogeneous to C3H/St cell.

Animals↗