Correlation of the expression level of C1q mRNA and the number of C1q-positive plaques in the Alzheimer Disease temporal cortex. analysis of C1q mrna and its protein using adjacent or nearby sections

• Published in: Dementia and geriatric cognitive disorders 2001-07, Vol.12 (4), p.237-242
• Main Authors: Tooyama, I, Sato, H, Yasuhara, O, Kimura, H, Konishi, Y, Shen, Y, Walker, D G, Beach, T G, Sue, L I, Rogers, J
• Format: Article
• Language: English
• Subjects: Aged; Aged, 80 and over; Alzheimer Disease - genetics; Alzheimer Disease - metabolism; Alzheimer Disease - pathology; Brain Chemistry; Case-Control Studies; Complement C1q - biosynthesis; Complement C1q - genetics; Gene Expression Profiling - methods; Gene Expression Regulation; Humans; Immunohistochemistry; In Vitro Techniques; Plaque, Amyloid - metabolism; Plaque, Amyloid - pathology; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger - analysis; Temporal Lobe - chemistry; Temporal Lobe - metabolism; Temporal Lobe - pathology
• ISSN: 1420-8008; 1421-9824
• DOI: 10.1159/000051265

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 degrees C. After cryoprotection with solutions containing 10-20% glycerol and 2% dimethylsulfoxide, 40-microm 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.