title: Curcumin improves bone microarchitecture and enhances mineral density in APP/PS1 transgenic mice.
abstract: Alzheimer's disease and osteoporosis are often observed to co-occur in clinical practice. The present study aimed to evaluate the bone microarchitecture and bone mineral density (BMD) of the proximal tibia in APP/PS1 transgenic mice by micro-computed tomography (micro-CT), and to search for evidence that curcumin can be used to reduce bone mineral losses and treat osteoporosis after senile dementia in these transgenic mice. Three-month-old female mice were divided into the following groups (n=9 per group): wild-type mice (WT group); APP/PS1 transgenic mice (APP group); and APP/PS1 transgenic mice with curcumin treatment (APP+Cur group). Between 9 and 12 months of age, the APP+Cur group were administered curcumin orally (600ppm). CT scans of the proximal tibia were taken at 6, 9 and 12 months. At 6 months, there were little differences in the structural parameters. At 9 months, the APP groups displayed loss of bone volume ratio (BV/TV), trabecular thickness (Tb.Th), trabecular number (Tb.N) and connectivity density (Conn.D) and increases in trabecular separation (Tb.Sp) and geometric degree of anisotropy (DA) (P<0.05 or P<0.01), with significant changes in the BMD parameters. At 12 months, curcumin treatment led to constant increases in the trabecular bone mass of the metaphysis and clearly improved the BMD. By the same time, we measured the TNF-α and IL-6 in the serum among the different groups at 6, 9 and 12 months by enzyme-linked immunoassay(ELISA). These results suggest that APP/PS1 transgenic mice are susceptible to osteoporosis, and that curcumin can prevent further deterioration of the bone structure and produce beneficial changes in bone turnover. The change of inflammation cytokine, including TNF-α and IL-6, may play an important role in the mechanisms of action of curcumin, but the detail mechanism remains unknown.
authors.affiliation: Department of Orthopedics, First Affiliated Hospital, China Medical University, Shenyang 110001, PR China. ymw69@sohu.com
authors.forename: Mao-Wei
authors.initials: MW
authors.lastname: Yang
authors.forename: Tong-Hao
authors.initials: TH
authors.lastname: Wang
authors.forename: Pei-Pei
authors.initials: PP
authors.lastname: Yan
authors.forename: Li-Wei
authors.initials: LW
authors.lastname: Chu
authors.forename: Jiang
authors.initials: J
authors.lastname: Yu
authors.forename: Zhi-Da
authors.initials: ZD
authors.lastname: Gao
authors.forename: Yuan-Zhou
authors.initials: YZ
authors.lastname: Li
authors.forename: Bao-Lei
authors.initials: BL
authors.lastname: Guo
mesh_terms: D000544:Alzheimer Disease / Q000097:blood / Q000150:complications*; D016564:Amyloid beta-Protein Precursor / Q000235:genetics; D000818:Animals; D015519:Bone Density / Q000187:drug effects*; D001842:Bone and Bones / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000473:pathology; D030024:Curcuma / Q000737:chemistry; D003474:Curcumin / Q000494:pharmacology / Q000627:therapeutic use*; D005260:Female; D015850:Interleukin-6 / Q000097:blood; D051379:Mice; D008815:Mice, Inbred Strains; D008822:Mice, Transgenic; D010024:Osteoporosis / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use; D013977:Tibia / Q000000981:diagnostic imaging; D014057:Tomography, X-Ray Computed; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D016564:Amyloid beta-Protein Precursor; D015850:Interleukin-6; D010936:Plant Extracts; D014409:Tumor Necrosis Factor-alpha; D003474:Curcumin