The Journal of Experimental Medicine
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Published online May 21, 2007
doi:10.1084/jem.20062481
The Journal of Experimental Medicine, Vol. 204, No. 6, 1273-1280
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Tsai et al.
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BRIEF DEFINITIVE REPORT

 G-CSF rescues the memory impairment of animal models of Alzheimer's disease

Kuen-Jer Tsai1, Yueh-Chiao Tsai2, and Che-Kun James Shen1,2

1 Institute of Molecular Biology, Academia Sinica, Taipei 115, Taiwan, Republic of China
2 Institute of Genome Sciences, National Yang-Ming University, Taipei 112, Taiwan, Republic of China

CORRESPONDENCE Che-Kun James Shen: ckshen{at}imb.sinica.edu.tw

Most of the current clinical treatments for Alzheimer's disease (AD) are largely symptomatic and can have serious side effects. We have tested the feasibility of using the granulocyte colony-stimulating factor (G-CSF), which is known to mobilize hematopoietic stem cells (HSCs) from the bone marrow into the peripheral blood, as a therapeutic agent for AD. Subcutaneous administration of G-CSF into two different ß-amyloid (Aß)–induced AD mouse models substantially rescued their cognitive/memory functions. The rescue was accompanied by the accumulation of 5-bromo-2'deoxyuridine–positive HSCs, as well as local neurogenesis surrounding the Aß aggregates. Furthermore, the level of acetylcholine in the brains of Tg2576 mice was considerably enhanced upon G-CSF treatment. We suggest that G-CSF, a drug already extensively used for treating chemotherapy-induced neutropenia, should be pursued as a novel, noninvasive therapeutic agent for the treatment of AD.


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