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Correlation of the Expression Level of C1q mRNA and the Number of C1q-Positive Plaques in the Alzheimer Disease Temporal Cortex
We compared the expression level of C1q mRNA and the number of C1q-positive plaques in adjacent or nearby brain sections from Alzheimer disease (AD) and control cases. Small blocks of temporal cortex were fixed with 4% paraformaldehyde for 2 days at 4°C. After cryoprotection with solutions containin...
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Published in: | Dementia and geriatric cognitive disorders 2001, Vol.12 (4), p.237-242 |
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container_title | Dementia and geriatric cognitive disorders |
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creator | Tooyama, Ikuo Sato, Haruhisa Yasuhara, Osamu Kimura, Hiroshi Konishi, Yoshinori Shen, Yong Walker, Douglas G. Beach, Thomas G. Sue, Lucia I. Rogers, Joseph |
description | We compared the expression level of C1q mRNA and the number of C1q-positive plaques in adjacent or nearby brain sections from Alzheimer disease (AD) and control cases. Small blocks of temporal cortex were fixed with 4% paraformaldehyde for 2 days at 4°C. After cryoprotection with solutions containing 10–20% glycerol and 2% dimethylsulfoxide, 40-µm sections were cut from the tissue blocks. A section from each case was stained by immunohistochemistry using a C1q antibody, while RNA was purified from adjacent or nearby sections using a combination of proteinase K pretreatment followed by extraction using Trizol reagent. The expression of C1q B chain mRNA was analyzed in these samples by the reverse-transcription polymerase chain reaction (RT-PCR). The intensities of the PCR products were measured by an image analyzer. The expression of C1q B chain mRNA was significantly more abundant in AD than in control cases (p < 0.05). Immunohistochemical analysis showed that C1q protein was localized in senile plaques in the AD brain. The number of C1q-positive plaques correlated with the expression level of C1q gene (p < 0.05). The present results suggest that C1q protein in senile plaques originates is endogenously produced in the AD brain. |
doi_str_mv | 10.1159/000051265 |
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Small blocks of temporal cortex were fixed with 4% paraformaldehyde for 2 days at 4°C. After cryoprotection with solutions containing 10–20% glycerol and 2% dimethylsulfoxide, 40-µm sections were cut from the tissue blocks. A section from each case was stained by immunohistochemistry using a C1q antibody, while RNA was purified from adjacent or nearby sections using a combination of proteinase K pretreatment followed by extraction using Trizol reagent. The expression of C1q B chain mRNA was analyzed in these samples by the reverse-transcription polymerase chain reaction (RT-PCR). The intensities of the PCR products were measured by an image analyzer. The expression of C1q B chain mRNA was significantly more abundant in AD than in control cases (p < 0.05). Immunohistochemical analysis showed that C1q protein was localized in senile plaques in the AD brain. The number of C1q-positive plaques correlated with the expression level of C1q gene (p < 0.05). 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Small blocks of temporal cortex were fixed with 4% paraformaldehyde for 2 days at 4°C. After cryoprotection with solutions containing 10–20% glycerol and 2% dimethylsulfoxide, 40-µm sections were cut from the tissue blocks. A section from each case was stained by immunohistochemistry using a C1q antibody, while RNA was purified from adjacent or nearby sections using a combination of proteinase K pretreatment followed by extraction using Trizol reagent. The expression of C1q B chain mRNA was analyzed in these samples by the reverse-transcription polymerase chain reaction (RT-PCR). The intensities of the PCR products were measured by an image analyzer. The expression of C1q B chain mRNA was significantly more abundant in AD than in control cases (p < 0.05). Immunohistochemical analysis showed that C1q protein was localized in senile plaques in the AD brain. The number of C1q-positive plaques correlated with the expression level of C1q gene (p < 0.05). 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Small blocks of temporal cortex were fixed with 4% paraformaldehyde for 2 days at 4°C. After cryoprotection with solutions containing 10–20% glycerol and 2% dimethylsulfoxide, 40-µm sections were cut from the tissue blocks. A section from each case was stained by immunohistochemistry using a C1q antibody, while RNA was purified from adjacent or nearby sections using a combination of proteinase K pretreatment followed by extraction using Trizol reagent. The expression of C1q B chain mRNA was analyzed in these samples by the reverse-transcription polymerase chain reaction (RT-PCR). The intensities of the PCR products were measured by an image analyzer. The expression of C1q B chain mRNA was significantly more abundant in AD than in control cases (p < 0.05). Immunohistochemical analysis showed that C1q protein was localized in senile plaques in the AD brain. The number of C1q-positive plaques correlated with the expression level of C1q gene (p < 0.05). The present results suggest that C1q protein in senile plaques originates is endogenously produced in the AD brain.</abstract><cop>Basel, Switzerland</cop><pmid>11351134</pmid><doi>10.1159/000051265</doi><tpages>6</tpages></addata></record> |
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title | Correlation of the Expression Level of C1q mRNA and the Number of C1q-Positive Plaques in the Alzheimer Disease Temporal Cortex |
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