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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.

Adipocyte enhancer binding protein 1 (AEBP1) activates inflammatory responses via the NF‐κB pathway in macrophages and regulates adipogenesis in preadipocytes. Up‐regulation of AEBP1 in the hippocampi of patients with Alzheimer's disease (AD) has been revealed by microarray analyses of autopsied brains from the Japanese general population (the Hisayama study). In this study, we compared the expression patterns of AEBP1 in normal and AD brains, including in the hippocampus, using immunohistochemistry. The subjects were 24 AD cases and 52 non‐AD cases. Brain specimens were immunostained with antibodies against AEBP1, tau protein, amyloid β protein, NF‐κB, GFAP and Iba‐1. In normal brains, AEBP1 immunoreactivity mainly localized to the perikarya of hippocampal pyramidal neurons, and its expression was elevated in the pyramidal neurons and some astrocytes in AD hippocampi. Although AEBP1 immunoreactivity was almost absent in neurons containing neurofibrillary tangles, AEBP1 was highly expressed in neurons with pretangles and in the tau‐immunopositive, dystrophic neurites of senile plaques. Nuclear localization of NF‐κB was also observed in certain AEBP1‐positive neurons in AD cases. Comparison of AD and non‐AD cases suggested a positive correlation between the expression level of AEBP1 and the degree of amyloid β pathology. These findings imply that AEBP1 protein has a role in the progression of AD pathology.

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.

We found that mRNA of MET, the receptor of hepatocyte growth factor (HGF), is significantly decreased in the hippocampus of Alzheimer's disease (AD) patients. Therefore, we tried to determine the cellular component-dependent changes of MET expressions. In this study, we examined cellular distribution of MET in the cerebral neocortices and hippocampi of 12 AD and 11 normal controls without brain diseases. In normal brains, MET immunoreactivity was observed in the neuronal perikarya and a subpopulation of astrocytes mainly in the subpial layer and white matter. In AD brains, we found marked decline of MET in hippocampal pyramidal neurons and granule cells of dentate gyrus. The decline was more obvious in the pyramidal neurons of the hippocampi than that in the neocortical neurons. In addition, we found strong MET immunostaining in reactive astrocytes, including those near senile plaques. Given the neurotrophic effects of the HGF/MET pathway, this decline may adversely affect neuronal survival in AD cases. Because it has been reported that HGF is also up-regulated around senile plaques, β-amyloid deposition might be associated with astrocytosis through the HGF signaling pathway.