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Biomedical subjects

K Kosaka

Publications and source records attributed to K Kosaka.

At least 37 records · Page 2Linked to original sources

Glial involvement in the degeneration process of Lewy body-bearing neurons and the degradation process of Lewy bodies in brains of dementia with Lewy bodies.

Glial involvement in the degeneration process of Lewy body (LB)-bearing neurons and the degradation process of LBs in the cerebral cortex and amygdala in brains of dementia with Lewy bodies was investigated immunohistochemically. HLA-DR-positive microglia frequently extended their processes to degenerated neurons with alpha-synuclein-positive LBs, while some GFAP-positive astroglial processes attached to weakly alpha-synuclein-positive extracellular LBs. Some intracellular LBs were immunoreactive to anti-C4d antibody, and these LB-bearing neurons were involved by activated microglia. About half of the intracellular LBs were immunoreactive to anti-chromogranin-A (CGA) antibody, and most of CGA-positive LB-bearing neurons were surrounded by microglia. Although we could find no evident participation of TNF-alpha, a candidate cytokine that is up-regulated by microglia following CGA stimulation, in the degeneration process of LB-bearing neurons, some intracellular LBs were immunoreactive to the antibody to NF-kappaB, a transcriptional factor activated by cytokines. These findings suggest that microglia participate in the degeneration process of LB-bearing neurons via varying immunogenic elements including complement proteins, CGA and probably some cytokines, and that astroglia participate in the degradation process of LBs.

Brain↗

Immunohistochemical localization of plasminogen activator inhibitor-1 in rat and human brain tissues.

We investigated immunohistochemically the localization of type 1 plasminogen activator inhibitor (PAI-1) in rat and human brain tissues. In rat, neurons and astrocytes were stained positively for PAI-1 after colchicine treatment. In post-mortem human brain, neurons were stained for PAI-1 but the number of positive neurons varied greatly from case to case. PAI-1 positive astrocytes occurred in the white matter lesions of some patients. In Alzheimer's disease, weak PAI-1 labeling was seen in association with senile plaques and ghost tangles. The present results support a notion that PAI-1 and its target proteases such as plasminogen activators and thrombin are involved in a variety of physiological and pathological processes in brain.

Aged↗

Familial frontotemporal dementia and parkinsonism with a novel N296H mutation in exon 10 of the tau gene and a widespread tau accumulation in the glial cells.

We report a 62-year-old Japanese man with familial frontotemporal dementia and a novel missense mutation (N296H) in exon 10 of the tau gene. The patient presented with frontal signs followed by temporal signs and parkinsonism. The brain showed localized frontotemporal lobe atrophy including the precentral gyrus and discoloration of the substantia nigra, and revealed severe neuronal loss with proliferation of tau-positive protoplasmic astroglia in the affected cerebral cortex, tau-positive coiled bodies and threads in the subcortical white matter, and tau-positive pretangle neurons in the subcortical and brain stem nuclei. There were no tau-positive neurofibrillary tangles, Pick bodies, tuft-shaped astrocytes or astrocytic plaques in the cerebral cortex. Immunoelectron microscopically, phosphorylated tau accumulated in both neurons and glial cells in different modalities, such as glial filaments in protoplasmic astroglia, straight tubules in coiled bodies, and free ribosomes in pretangle neurons. These findings suggest that tau proteins are not always assembled in abnormal filaments such as twisted ribbons, paired helical filaments and straight tubules in neurons and glial cells, which have been shown in previous cases with frontotemporal dementia and parkinsonism linked to chromosome 17. Immunoblotting of sarkosyl-insoluble tau exhibited accumulation of four-repeat tau isoforms in the brain. The N296H mutation may interfere with the ability of mutated tau to bind with microtubules and lead to tau aggregation. Further study is necessary to determine whether this mutation can account for the characteristic tau pathology of this case.

Dementia↗

Evaluation of the treatment performance of a multistage ozone/hydrogen peroxide process by decomposition by-products.

The performance of a multistage ozone/hydrogen peroxide (O3/H2O2) process was evaluated with respect to total organic carbon (TOC) removal of waste waters. An aqueous humic acid solution (5.2 mgC l(-1) as TOC) and a sand filtered secondary sewerage effluent (5.6mgC l(-1) as TOC) were used as model waste waters. Appropriate range of hydrogen peroxide (H2O2) dose at each stage depended upon the components of the tested solutions that changed as the process proceeded. Higher hydrogen peroxide dose was required at later stages in which low reactivity compounds with hydroxyl radical (HO*), low molecular fatty acids, were predominant. And, oxalic acid concentration related to H2O2 demand at later stages. This was assumed that the slow decomposition of oxalic acid was rate-determining step for TOC removal after its accumulation. Also, it is important to maintain dissolved ozone at low concentration for efficient TOC removal because rapid ozone consumption is required for the rapid formation of hydroxyl radical (HO*).

Carbon↗

Frequency and distribution of TUNEL-positive neurons in brains of dementia with Lewy bodies: comparison with those in brains of Alzheimer's disease.

The present study investigated the frequency and distribution of TUNEL-positive neurons in brains of dementia with Lewy bodies (DLB) in comparison with those in brains of Alzheimer's disease (AD), Down syndrome (DS) and non-demented elderly persons. In DLB brains, TUNEL-positive neurons were increased in frequency compared with those in non-demented elderly brains, and showed a distribution similar to those in AD and DS brains. DLB cases with TUNEL-positive neurons showing severe Lewy pathology were all neocortical type, while DLB cases of the limbic type showing mild Lewy pathology did not demonstrate TUNEL-positive neurons. In addition, we investigated the relationships between TUNEL-positive neurons and pathological hallmarks of DLB or AD brains. TUNEL-positive neurons had no Lewy bodies or neurofibrillary tangles, and were not located within amyloid deposits. These findings suggest that neuronal damage showing DNA fragmentations occurs in DLB brains as well as in AD and DS brains, and that it is accelerated by progression of Lewy pathology as well as Alzheimer pathology, although it is not directly related to their pathological hallmarks.

Aged↗

No evidence of an association between CYP2D6 polymorphisms among Japanese and dementia with Lewy bodies.

Dementia with Lewy bodies (DLB) is the second most frequent degenerative dementia among the elderly, following Alzheimer-type dementia (ATD). An association of DLB with CYP2D6*4, one of the cytochrome P450IID6 (debrisoquine 4-hydroxylase; CYP2D6) gene polymorphisms, was reported previously, but this is controversial. Moreover, these reports have been restricted to Caucasian populations. Therefore, we compared frequencies of CYP2D6*3, *4, and *10 mutant alleles in 17 Japanese DLB patients to those among Alzheimer-type dementia (ATD) patients and healthy controls. Polymerase chain reaction amplification and restriction fragment length polymorphism analyses were used for genotyping. No significant difference of genotype or mutant allele frequencies was detected between DLB, ATD, and healthy controls. The present results do not support the suggestion that the CYP2D6 gene is related to DLB susceptibility, at least in the Japanese population.

Aged↗

Comparison of noradrenergic and serotonergic antidepressants in reducing immobility time in the tail suspension test.

We examined the effects of two noradrenergic tricyclic antidepressants and two selective serotonin re-uptake inhibitors in the tail suspension test, with a suspension period of 30 min instead of the usual 10 min. Within the first 10 min, desipramine, nortriptyline and fluvoxamine significantly reduced the duration of immobility. Whereas desipramine and nortriptyline were also efficacious in the rest of the test period, fluvoxamine was not. Fluoxetine showed no significant effect throughout the study period. These results suggest that a prolonged tail suspension test results in functional changes in the noradrenergic and serotonergic systems and alters the sensitivity to antidepressants.

Adrenergic Uptake Inhibitors↗

[An autopsied case of presenile dementia with tangles].

We report an autopsied case of presenile dementia showing neuropathologically abundant neurofibrillary tangles(NFT) without senile plaques(tangle only dementia). A Japanese woman developed memory disturbance when she was 60 years old. At age of 65, her ability to understand deteriorated and euphoria and wandering manifested but neither psychotic symptoms, including hallucination and delusion nor a change in character were observed. The patient was hospitalized at age 66 and a cranial CT scan revealed bilateral moderate atrophy of the cortex and moderate enlargement of the lateral ventricle, especially in the inferior horn. No lobar atrophy was detected. She exhibited an oral tendency and became appallic at her final stage and died at the age of 75. Autopsy showed that her brain weighed 850 g and neuropathological study showed numerous NFT mainly in the entorhinal (trans-entorhinal) region, subiculum, CA1-CA4, dentate gyrus, amygdara, subthalamic nucleus, basal nucleus of Meynert, substantia nigra and locus coeruleus. Severe neuronal loss with gliosis was noted in the temporal lobes including the hippocampal region. No senile plaque was detected in any of the brain regions. There have been some recent reports of patients with abundant NFT with the predominant involvement of the allocortex but no or very little senile plaque. All the patients in the reported cases were very elderly at onset(over 80 years of age). In our case, the onset was presenile and we could exclude any other diseases, that usually present with NFT, and to our knowledge, this is the first report of a presenile dementia with tangles.

Aged↗

Expression of CD40 in the brain of Alzheimer's disease and other neurological diseases.

We have investigated immunohistochemically the expression of CD40 in post-mortem human brain tissues. In control brain, the blood vessels were stained weakly for CD40. Vascular expression of CD40 was enhanced in the lesions of Alzheimer's disease and some other neurological diseases. In such diseases, reactive microglia were also positive for CD40. The results of this study suggest that CD40 expression by microglia is up-regulated upon a variety of brain insults and is not limited to lesions with amyloid beta-protein deposits.

Alzheimer Disease↗

Accumulation of human alpha-synuclein in different cytoskeletons in Lewy bodies in brains of dementia with Lewy bodies.

We investigated the origin of alpha-synuclein-immunoreactive components in Lewy bodies (LB) in brains of dementia with Lewy bodies (DLB) using immunohistochemistry and immunoelectron microscopy with anti-alpha-synuclein antibodies and anti-cytoskeleton antibodies. alpha-Synuclein-positive LB light microscopically consisted of phosphorylated neurofilament (PN)-positive LB, tubulin-positive LB and LB that were negative for both stains. Immunoelectron microscopically, PN-positive LB were composed of PN-positive and alpha-synuclein-positive filamentous components, suggesting that these filamentous components originate from neurofilaments with partially reduced immunoreactivity and alpha-synuclein accumulation. However, tubulin-positive LB were composed of tubulin-positive and alpha-synuclein-positive tubular components, suggesting that these tubular components originate from microtubules with diffusely reduced immunoreactivity and alpha-synuclein accumulation. The results of the present study suggest that alpha-synuclein accumulates in different cytoskeletons in the LB in DLB brains presumably due to a blockage of axonal transport.

Aged↗

Degeneration process of Lewy bodies in the brains of patients with dementia with Lewy bodies using alpha-synuclein-immunohistochemistry.

We investigated the degeneration process of Lewy bodies (LB) in the brains of dementia with Lewy bodies, using alpha-synuclein-immunohistochemistry. Intracellular LB, LB-related neurites and some extracellular LB were positively immunostained with anti-alpha-synuclein antibodies. Concentric LB-bearing neurons had no microglial involvement, while degenerated neurons with ill-defined LB displayed intense microglial involvement. The late stage of extracellular LB were immunoelectron-microscopically composed of loose aggregates of filamentous components with lost alpha-synuclein-immunoreactivity and penetrated astroglial processes. These findings suggest that microglias are involved during the stages from degenerated LB-bearing neurons to extracellular LB, while astroglias are involved during the stage of extracellular LB. Some intracellular LB were positive for anti-C3d and -C4d antibodies, suggesting that the classical complement pathway is activated in degenerated LB-bearing neurons, inducing microglial activation and neuronal death.

Aged↗

Cyclin-dependent kinase 5 (Cdk5) associated with Lewy bodies in diffuse Lewy body disease.

We investigated the cyclin-dependent kinase (Cdk) 5 distribution pattern in diffuse Lewy body disease brains using immunohistochemistry. Cdk5 immunoreactivity was detected in both brainstem-type Lewy bodies (LBs) and cortical LBs. The number of Cdk5-positive LBs was less than that of ubiquitin- or alpha-synuclein-positive LBs, and more than that of phosphorylated neurofilament-positive LBs. Immunoelectron microscopy revealed Cdk5-immunolabeled granulo-filamentous components in LBs and LB-related neurites. These data suggest that Cdk5 may be associated with LB formation.

Aged↗

Occurrence of human alpha-synuclein immunoreactive neurons with neurofibrillary tangle formation in the limbic areas of patients with Alzheimer's disease.

We examined alpha-synuclein immunoreactivity in the brains from 23 patients with Alzheimer's disease (AD) and two patients with Down's syndrome. In ten of the 23 AD cases and both the two Down's syndrome cases, alpha-synuclein immunoreactivities were observed in the neurons of the limbic areas, predominantly of the amygdala. Nearly all alpha-synuclein-positive neurons had tau-positive neurofibrillary tangles (NFT) in the same neurons, and these consisted of intermingled-type and superimposed-type. By immunoelectron microscopy, the intermingled-type revealed aggregations of alpha-synuclein-positive filamentous components, which were in continuity with paired helical filaments (PHF), while the superimposed-type revealed accumulations of alpha-synuclein-positive non-filamentous components in PHF bundles. These findings suggest that alpha-synuclein can accumulate in PHF and form filamentous aggregations in neurons of the limbic areas in AD cases.

Actin Cytoskeleton↗

Cdk5 and munc-18/p67 co-localization in early stage neurofibrillary tangles-bearing neurons in Alzheimer type dementia brains.

Hyperphosphorylation of tau protein occurs during the formation of paired helical filament (PHF) in the brain with Alzheimer's disease. As previously reported, cyclin-dependent kinase (cdk) 5 can phosphorylate tau at the site of abnormally phosphorylated in PHF. To characterize the relationship between cdk5 and PHF-tau, we investigated the localization of cdk5 and its regulator, p67 (munc 18), in the hippocampus and temporal lobes from 12 Alzheimer type dementia (ATD) patients and 5 controls using immunohistochemical procedures. The specificity of antibodies was confirmed with Western blot analysis. Anti-cdk5 antibody diffusely stained the perikarya of some tau2-positive or neurofibrillary tangle (NFT)-bearing neurons in ATD brains, while cdk5-positive staining was scarcely found in control brains. Anti-p67 antibody also showed stronger immunoreactivity of pyramidal neurons in ATD brains than in control brains. Double immunostaining with anti-cdk5 and anti-p67 antibodies revealed co-localization of both molecules in some pyramidal neurons. These findings suggest that cdk5 is activated by p67 at the early stage of NFT formation and accelerates NFT formation. In cdk5-positive and p67-negative neurons, cdk5 may be activated by other regulator molecules such as p35. In addition, cdk5-positive reactive astrocytes were found close to cdk5-positive NFT-bearing neurons m ATD brains but not in control brains, suggesting a correlation between NFT and reactive astrocytes.

Aged↗

A manic episode associated with bereavement in a patient with lung cancer. A case report.

We describe a manic episode associated with bereavement in a lung cancer patient. The patient became manic 4 days after the death of a close friend also suffering from lung cancer, though the deceased was not a member of his immediate family. Manic episodes in cancer patients are rare, and our report of a manic episode associated with bereavement may also serve to highlight possible precipitating factors, which have not been adequately emphasized in the literature to date.

Aged↗

Molecular modelling and conformational analysis of novel glycoprotein (Gp) IIb/IIIa antagonists. Molecular orbital calculation and the condensed heterocyclic derivatives.

A naphthalene compound was chosen as lead compound to develop a new series of fibrinogen receptor antagonists. Eight new compounds with different condensed heterocyclic parts were prepared and their in vitro activities were evaluated. 5-Amidinobenzofuran compound 2, 6-amidinobenzothiophene 7, and 5-amidinofuro[2,3-b]pyridine 8 were more active than lead compound 1. Molecular orbital calculation studies suggested the presence of a preferred spatial orientation between the amidine and the carboxylic acid.

Acetates↗

Chemically defined neuron groups and their subpopulations in the glomerular layer of the rat main olfactory bulb--IV. Intraglomerular synapses of tyrosine hydroxylase-immunoreactive neurons.

Synapses of intraglomerular processes of tyrosine hydroxylase-immunoreactive neurons in the rat main olfactory bulb were examined by electron microscopic immunocytochemistry. Prominent characteristics of intraglomerular synapses of tyrosine hydroxylase-immunoreactive elements were that the vast majority (about 80%) of their synaptic inputs were asymmetrical synapses from olfactory nerve terminals and, though far smaller in proportion, one half of the remaining were asymmetrical synapses from mitral/tufted cell dendrites and the other half were symmetrical synapses from gamma-aminobutyric acid-like immunoreactive elements. So far, we have observed no typical reciprocal synapses between tyrosine hydroxylase-immunoreactive processes and mitral/tufted dendrites; however, we have often identified serial synapses; that is, asymmetrical synapses from olfactory nerve terminals or mitral/tufted cell dendrites to tyrosine hydroxylase-immunoreactive processes, and then symmetrical synapses from the latter to different mitral/tufted cell dendrites. These synaptic connections of tyrosine hydroxylase-immunoreactive neurons were very different from those of Calbindin-D(28k)-immunoreactive neurons, which received no synaptic contact directly from olfactory nerve terminals but formed reciprocal synapses with mitral/tufted cells as we analysed previously.Thus, our present and previous electron microscopic studies combined with confocal laser scanning light microscopy clearly indicated for the first time the heterogeneity of periglomerular neurons, not only in their chemical and morphological features, but also in their synaptic organization in the olfactory glomerulus.

Animals↗