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Your search keyword '"Tooyama I"' showing total 9 results
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9 results on '"Tooyama I"'

1. [Glutaminergic neurotransmission in Alzheimer's disease].

Author

Tooyama I and Yanagisawa D

Subjects
Amino Acid Transport System X-AG physiology, Hippocampus physiology, Humans, Neuronal Plasticity physiology, Receptors, Glutamate physiology, Alzheimer Disease physiopathology, Glutamates physiology, Synaptic Transmission physiology
Published
2011

2. [Dystonia update].

Author

Kaji R, Tamiya G, Makino S, Shimazu H, Murase N, Sakamoto T, Tooyama I, and Urushihara R

Subjects
Humans, Dystonia physiopathology
Published
2006

3. [Genetic risk factors for Alzheimer's disease].

Author

Tooyama I, Matsuo A, and Yasuhara O

Subjects
Aldehyde Dehydrogenase genetics, Aldehyde Dehydrogenase, Mitochondrial, Apolipoproteins C genetics, Chromosomes genetics, Humans, Low Density Lipoprotein Receptor-Related Protein-1 genetics, Receptors, LDL genetics, Risk Factors, Twin Studies as Topic, Alzheimer Disease genetics, Apolipoproteins E genetics, alpha-Macroglobulins genetics
Published
2004

4. [Chemical neuroanatomy of cholinergic neurons].

Author

Kimura H and Tooyama I

Subjects
Acetylcholine physiology, Animals, Choline O-Acetyltransferase analysis, Choline O-Acetyltransferase genetics, Immunohistochemistry methods, Rats, Recombinant Proteins, Acetylcholine analysis, Cholinergic Fibers chemistry, Neurons chemistry
Abstract

Acetylcholine (ACh), the first neurotransmitter to be discovered from the frog heart, is distributed widely in both the central and peripheral nervous systems. In the brain, for example, ACh plays important roles in several higher functions such as memory and learning. In peripheral organs, ACh has been shown to be a neurotransmitter in spinal motoneurons, all autonomic preganglionic neurons, all parasympathetic postganglionic neurons, and an exceptional sympathetic postganglionic neurons innervating the sweat gland. There has been, however, no good method to visualize ACh in tissues and organs. So far, immunohistochemistry for its synthetic enzyme choline acetyltransferase (ChAT: E. C. 2. 3. 1. 6) has been used as the most reliable marker for morphological studies of cholinergic neurons. Despite the fact that most antibodies against ChAT clearly stain central cholinergic systems, they have poor ability to detect peripheral cholinergic systems. We found that there are two types of ChAT expressed in the rat pterygopalatine ganglion. One is identical to the ChAT in the brain, and another (pChAT) lacks exons 6, 7, 8, and 9. The peripheral cholinergic system is now clearly demonstrated by immunohistochemistry using our antiserum raised against the recombinant pChAT.

Published
1998

5. [LRP (alpha 2-macroglobulin receptor) and Alzheimer lesions].

Author

Akiyama H and Tooyama I

Subjects
Alzheimer Disease immunology, Alzheimer Disease metabolism, Amyloid beta-Peptides metabolism, Brain metabolism, Humans, Inflammation, Ligands, Low Density Lipoprotein Receptor-Related Protein-1, Receptors, Lipoprotein, Alzheimer Disease etiology, Receptors, Immunologic metabolism, Receptors, Immunologic physiology
Published
1996

6. [Role of growth factors in regulation of food intake].

Author

Oomura Y, Tooyama I, and Kimura H

Subjects
Animals, Binding Sites, Fibroblast Growth Factors metabolism, Humans, Receptors, Fibroblast Growth Factor physiology, Eating physiology, Fibroblast Growth Factors physiology
Published
1995

8. [Fibroblast growth factors (FGFs) in neurodegenerative disorders].

Author

Tooyama I

Subjects
Alzheimer Disease metabolism, Animals, Brain metabolism, Humans, Huntington Disease metabolism, Parkinson Disease metabolism, Rats, Fibroblast Growth Factors metabolism, Nervous System Diseases metabolism
Abstract

Fibroblast growth factors (FGFs) are a family consisting of at least seven members, and the FGF family will continue to expand. The best studied members of this family are acidic and basic FGF (aFGF and bFGF). They are richly concentrated in brain, and have potent trophic effects for neurons and glia. I now report that expressions of aFGF and bFGF are altered in several neurodegenerative disorders such as Alzheimer disease (AD), Huntington disease (HD) and Parkinson disease (PD). In AD aFGF was upregulated in reactive astrocytes in severely affected areas. The bFGF-positive astrocytes were also increased. In addition, bFGF was detected in senile plaques, neurofibrillary tangles and neuropil threads. In AD, aFGF and bFGF showed a similar alteration pattern. A large number of aFGF- or bFGF-positive astrocytes were observed in the striatum. Some remaining neurons were strongly stained for aFGF or bFGF. In PD, marked loss of bFGF was observed on midbrain dopaminergic neurons, The depletion of bFGF preceded the loss of tyrosine hydroxylase. Since bFGF has a potent trophic effect on midbrain dopaminergic neurons, this depletion may be related to the disease process.

Published
1993

9. [A case of schwannomatosis--clinical, pathological and biochemical studies].

Author

Matsuo A, Tooyama I, Akiguchi I, Kimura J, and Kameyama M

Subjects
Adolescent, Biomarkers, Tumor analysis, Cranial Nerve Neoplasms pathology, Diagnosis, Differential, Electrophoresis, Humans, Magnetic Resonance Imaging, Male, Molecular Weight, Myelin Basic Protein analysis, Myelin Basic Protein chemistry, Neurilemmoma pathology, Neurofibroma diagnosis, Spinal Cord Neoplasms pathology, Cranial Nerve Neoplasms diagnosis, Neoplasms, Second Primary, Neurilemmoma diagnosis, Spinal Cord Neoplasms diagnosis
Abstract

A case of schwannomatosis is described, including clinical, pathological and biochemical features. A 16-year-old male patient was admitted because of multiple subcutaneous tumors without family history. No café au lait spots were found. Magnetic resonance images (MRI) revealed multiple tumors of cranial and spinal nerves. The tumors in the scalp, right forearm and left spinal nerve at the level of C5 were excised out surgically. The pathological study of all tumor specimens showed a typical appearance of schwannoma with Antoni A and B tissues but not that of neurofibroma. Electrophoretic study of the extract from the tumor detected a basic protein at a molecular weight of 18.5 KD, which has been reported to be a tumor marker protein of benign schwannoma. From these findings, this patient had the features of schwannomatosis, clearly distinguished from those of neurofibromatosis.

Published
1991

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