Abstract
APPsw transgenic mice showing substantial features of brain Abeta amyloidosis such as senile plaques and behavioral abnormalities were examined by immunostaining to determine whether Abeta deposits could induce the subsequent disturbance of neurotransmitter systems including somatostatin, substance P and choline acetyltransferase (ChAT), which are prominent in the Alzheimer's disease brain. Somatostatin, substance P and ChAT disappeared in the areas of senile plaque and were accumulated in dystrophic neurites around the amyloid cores. These findings suggest a potential role of brain Abeta amyloidosis in disturbance of the neurotransmitter systems leading to memory disturbance of Alzheimer's disease.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amygdala / metabolism
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Amygdala / pathology
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Amyloid beta-Protein Precursor / biosynthesis*
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Amyloid beta-Protein Precursor / genetics
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Amyloidosis / genetics
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Amyloidosis / metabolism*
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Amyloidosis / pathology
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Animals
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Brain Stem / metabolism
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Brain Stem / pathology
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Cerebellum / metabolism
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Cerebellum / pathology
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Cerebral Cortex / metabolism
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Cerebral Cortex / pathology
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Choline O-Acetyltransferase / metabolism
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Hippocampus / metabolism
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Hippocampus / pathology
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Immunohistochemistry
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Mice
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Mice, Transgenic
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Neurites / metabolism
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Neurites / pathology
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Neurons / metabolism
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Neurons / pathology
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Neurotransmitter Agents / metabolism*
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Olfactory Bulb / metabolism
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Olfactory Bulb / pathology
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Plaque, Amyloid / metabolism
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Plaque, Amyloid / pathology
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Somatostatin / metabolism
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Substance P / metabolism
Substances
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Amyloid beta-Protein Precursor
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Neurotransmitter Agents
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Substance P
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Somatostatin
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Choline O-Acetyltransferase