ADAMTS4 is involved in the production of the Alzheimer disease amyloid biomarker APP669-711.

Amyloid-β (Aβ) deposition in the brain parenchyma is one of the pathological hallmarks of Alzheimer disease (AD). We have previously identified amyloid precursor protein (APP)669-711 (a.k.

Mouse Models of Alzheimer's Disease.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by memory loss and personality changes, eventually leading to dementia. The pathological hallmarks of AD are senile plaques and neurofibrillary tangles, which comprise abnormally aggregated β-amyloid peptide (Aβ) and hyperphosphorylated tau protein. To develop preventive, diagnostic, and therapeutic strategies for AD, it is essential to establish animal models that recapitulate the pathophysiological process of AD.

ddRAD-seq based phylogeographic study of Sargassum thunbergii (Phaeophyceae, Heterokonta) around Japanese coast.

Using genome-wide SNP data obtained from high-throughput techniques based on double digest restriction site-associated DNA sequencing (ddRAD-seq), we elucidated the migration history and genetic diversity of the Japanese population of the ecologically important brown seaweed Sargassum thunbergii (Mertens ex Roth) Kuntze. STRUCTURE and NeighborNet analyses showed a clear genetic differentiation among populations of four geographic regions: Kyushu (POP1); Sea of Japan (POP2); Hokkaido and Tohoku (POP3); and Pacific coast from Kyushu to Kanto (POP4). Approximate Bayesian Computation (ABC) analysis indicated that POP4 diverged first, followed by the separation between POP2 (the largest effective population size) and POP3; POP1 was the last to form, shaped by the mixture of POP2 (73%) and POP4 (27%).

2-Ethoxybenzamide stimulates melanin synthesis in B16F1 melanoma cells via the CREB signaling pathway.

Non-steroidal anti-inflammatory drugs are frequently used for the treatment of inflammation, pain, and fever. In this study, we found that 2-ethoxybenzamide (ETZ) significantly enhanced melanin synthesis in B16F1 melanoma cells, and also induced melanosome formation. Therefore, we investigated the mechanism by which ETZ up-regulated melanin synthesis.