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Alzheimer’s disease (AD) is the most common form of dementia, characterized by accumulation of amyloid β (Aβ) and neurofibrillary tangles. Oxidative stress and inflammation are considered to play an important role in the development and progression of AD. However, the extent to which these events contribute to the Aβ pathologies remains unclear. We performed inter-species comparative gene expression profiling between AD patient brains and the AppNL-G-F/NL-G-F and 3xTg-AD-H mouse models. Genes commonly altered in AppNL-G-F/NL-G-F and human AD cortices correlated with the inflammatory response or immunological disease. Among them, expression of AD-related genes (C4a/C4b, Cd74, Ctss, Gfap, Nfe2l2, Phyhd1, S100b, Tf, Tgfbr2, and Vim) was increased in the AppNL-G-F/NL-G-F cortex as Aβ amyloidosis progressed with exacerbated gliosis, while genes commonly altered in the 3xTg-AD-H and human AD cortices correlated with neurological disease. The AppNL-G-F/NL-G-F cortex also had altered expression of genes (Abi3, Apoe, Bin2, Cd33, Ctsc, Dock2, Fcer1g, Frmd6, Hck, Inpp5D, Ly86, Plcg2, Trem2, Tyrobp) defined as risk factors for AD by genome-wide association study or identified as genetic nodes in late-onset AD. These results suggest a strong correlation between cortical Aβ amyloidosis and the neuroinflammatory response and provide a better understanding of the involvement of gender effects in the development of AD.

Bursal cysts (bursitis) are attributed to repeated microtrauma of the connective tissue around the synovial joint and are rare in the coccygeal region. A 10-year-old boy had a subcutaneous tumor at the midline of the buttock. He could not walk and slid himself in a seated position because of psychomotor retardation. MR images showed a cystic lesion overlying the coccygeal bone, the intensity of which was identical to cerebrospinal fluid (CSF). Although meningocele was suspected, constructive interference in steady-state (CISS) MR images clearly depicted a discontinuity between the cyst and CSF space. It was conceivable that repeated friction between the coccygeal bone, which projected posteriorly, and overlying subcutaneous tissue during movement resulted in the formation of a bursal cyst. In addition to total removal of the cyst, the coccygeal bone was planed away to prevent friction. We should keep this rare clinical entity in mind in cases that appear to be sacrococcygeal meningocele.

Objective: The molecular mechanisms which contribute to the development of vascular events including cerebral vasospasm after subarachnoid hemorrhage (SAH) in cerebral artery remain to be elucidated. In this study, we investigated the time course of changes in the gene expression of cerebral artery using rabbit SAH model and performed bioinformatic analysis of differentially expressed genes. Methods: Rabbit basilar arteries were harvested on days 3, 5, and 7 after initial hemorrhage. Changes in gene expression of the rabbit basilar artery were investigated by using Agilent rabbit oligo microarrays and analyzed the data by Ingenuity Pathway Analysis (IPA). Results: Among investigated 43,623 genes, 1,121 genes were differentially expressed at least 1 time point. We found that the number, magnitude of fold change, and gene expression pattern were most dynamically changed on day 3, whereas narrowing of the basilar artery became most severe on day 5. In microarray datasets analyzed by IPA revealed that 25 biological functions identified from differentially expressed genes were significantly upregulated. Conclusion: Our findings that were based on gene expression analysis followed by bioinformatic analysis may provide a simple basis to interlink the various presumed pathogenesis of vascular events including cerebral vasospasm after SAH.