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Stromal cell-derived factor 1α decreases β-amyloid deposition in Alzheimer's disease mouse model.
Brain Res. 2012 Jun 12; 1459:15-26.BR

Abstract

β-amyloid (Aβ) aggregates are known to induce neuronal and synaptic dysfunction, and thus are involved in learning and memory deficits in Alzheimer's disease (AD), making Aβ deposits a potential target for prevention or treatment. Microglia, especially bone marrow-derived microglia (BMDM), has been recently thought to play important roles in internalizing and phagocytozing Aβ. BMDM originate in the bone marrow, migrate into the blood as hematopoietic progenitor cells (HPCs) and enter the brain in a chemokine-dependent manner. An effective chemoattractant for HPCs is stromal cell-derived factor 1 (SDF-1), which is also involved in regulating HPCs differentiation. Therefore, we hypothesize that SDF-1 might have influence on the migration of BMDM from peripheral cycle to brain. To explore whether treatment with SDF-1α can decrease Aβ burden, APP/PS1 double transgenic mice were given intracerebroventricular injection of SDF-1α weekly from the age of 28 to 32 weeks (4 weeks of injections) or from 28 to 36 weeks (8 weeks of injections). The results of our study showed that SDF-1α treatment decreased the area and the number of Aβ deposits, increased the level of Iba-1, a marker of microglia, and increased the number of plaque associated microglia in the parenchyma of APP/PS1 transgenic mice. These results suggest that SDF-1 could provide a novel and promising target for the purpose of lowering Aβ pathology in AD.

Authors+Show Affiliations

Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Avenue, Wuhan, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22560596

Citation

Wang, Qi, et al. "Stromal Cell-derived Factor 1α Decreases Β-amyloid Deposition in Alzheimer's Disease Mouse Model." Brain Research, vol. 1459, 2012, pp. 15-26.
Wang Q, Xu Y, Chen JC, et al. Stromal cell-derived factor 1α decreases β-amyloid deposition in Alzheimer's disease mouse model. Brain Res. 2012;1459:15-26.
Wang, Q., Xu, Y., Chen, J. C., Qin, Y. Y., Liu, M., Liu, Y., Xie, M. J., Yu, Z. Y., Zhu, Z., & Wang, W. (2012). Stromal cell-derived factor 1α decreases β-amyloid deposition in Alzheimer's disease mouse model. Brain Research, 1459, 15-26. https://doi.org/10.1016/j.brainres.2012.04.011
Wang Q, et al. Stromal Cell-derived Factor 1α Decreases Β-amyloid Deposition in Alzheimer's Disease Mouse Model. Brain Res. 2012 Jun 12;1459:15-26. PubMed PMID: 22560596.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Stromal cell-derived factor 1α decreases β-amyloid deposition in Alzheimer's disease mouse model. AU - Wang,Qi, AU - Xu,Yi, AU - Chen,Jin-Cao, AU - Qin,Yuan-Yuan, AU - Liu,Mao, AU - Liu,Yang, AU - Xie,Min-Jie, AU - Yu,Zhi-Yuan, AU - Zhu,Zhou, AU - Wang,Wei, Y1 - 2012/04/17/ PY - 2011/10/02/received PY - 2012/03/21/revised PY - 2012/04/07/accepted PY - 2012/5/8/entrez PY - 2012/5/9/pubmed PY - 2012/9/19/medline SP - 15 EP - 26 JF - Brain research JO - Brain Res VL - 1459 N2 - β-amyloid (Aβ) aggregates are known to induce neuronal and synaptic dysfunction, and thus are involved in learning and memory deficits in Alzheimer's disease (AD), making Aβ deposits a potential target for prevention or treatment. Microglia, especially bone marrow-derived microglia (BMDM), has been recently thought to play important roles in internalizing and phagocytozing Aβ. BMDM originate in the bone marrow, migrate into the blood as hematopoietic progenitor cells (HPCs) and enter the brain in a chemokine-dependent manner. An effective chemoattractant for HPCs is stromal cell-derived factor 1 (SDF-1), which is also involved in regulating HPCs differentiation. Therefore, we hypothesize that SDF-1 might have influence on the migration of BMDM from peripheral cycle to brain. To explore whether treatment with SDF-1α can decrease Aβ burden, APP/PS1 double transgenic mice were given intracerebroventricular injection of SDF-1α weekly from the age of 28 to 32 weeks (4 weeks of injections) or from 28 to 36 weeks (8 weeks of injections). The results of our study showed that SDF-1α treatment decreased the area and the number of Aβ deposits, increased the level of Iba-1, a marker of microglia, and increased the number of plaque associated microglia in the parenchyma of APP/PS1 transgenic mice. These results suggest that SDF-1 could provide a novel and promising target for the purpose of lowering Aβ pathology in AD. SN - 1872-6240 UR - https://www.unboundmedicine.com/medline/citation/22560596/Stromal_cell_derived_factor_1α_decreases_β_amyloid_deposition_in_Alzheimer's_disease_mouse_model_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(12)00682-8 DB - PRIME DP - Unbound Medicine ER -