상위피인용논문
- 조회1,127
Abstract
Jong Kil Lee1,2,3, Hee Kyung Jin1,2,*, Shogo Endo4, Edward H. Schuchman5, Janet E. Carter6 and Jae-sung Bae1,3,*
1 Stem Cell Neuroplasticity Research Group, Kyungpook National University, Daegu, Korea
2 Department of Laboratory Animal Medicine, Cell and Matrix Research Institute, College of Veterinary Medicine, Kyungpook National University, Daegu, Korea
3 Department of Physiology, Cell and Matrix Research Institute and World Class University Program, School of Medicine and Brain Korea 21, Kyungpook National University, Daegu, Korea
4 Unit for Molecular Neurobiology of Learning and Memory, Okinawa Institute of Science and Technology, Uruma, Okinawa, Japan
5 Departments of Genetics and Genomic Sciences and Gene and Cell Medicine, Mount Sinai School of Medicine, New York, New York, U.S.
6 Department of Mental Health Sciences, Royal Free and University College Medical School, University College London, London, U.K.
*Correspondence: Jae-sung Bae, D.V.M., Ph.D., School of Medicine and Brain Korea 21, Kyungpook National University, 101 Dongindong 2Ga, Jung-Gu, Daegu 700-422, South Korea. or Hee Kyung Jin, D.V.M., Ph.D., College of Veterinary Medicine, Kyungpook National University, 1,370 Sankyuk-dong, Buk-gu, Daegu, 702-701, South Korea.
Abstract
Alzheimer's disease (AD) is characterized by the deposition of amyloid-β peptide (Aβ) and the formation of neurofibrillary tangles. Transplantation of bone marrow-derived mesenchymal stem cells (BM-MSCs) has been suggested as a potential therapeutic approach to prevent various neurodegenerative disorders, including AD. However, the actual therapeutic impact of BM-MSCs and their mechanism of action in AD have not yet been ascertained. The aim of this study was therefore to evaluate the therapeutic effect of BM-MSC transplantation on the neuropathology and memory deficits in amyloid precursor protein (APP) and presenilin one (PS1) double-transgenic mice. Here we show that intracerebral transplantation of BM-MSCs into APP/PS1 mice significantly reduced amyloid β-peptide (Aβ) deposition. Interestingly, these effects were associated with restoration of defective microglial function, as evidenced by increased Aβ-degrading factors, decreased inflammatory responses, and elevation of alternatively activated microglial markers. Furthermore, APP/PS1 mice treated with BM-MSCs had decreased tau hyperphosphorylation and improved cognitive function. In conclusion, BM-MSCs can modulate immune/inflammatory responses in AD mice, ameliorate their pathophysiology, and improve the cognitive decline associated with Aβ deposits. These results demonstrate that BM-MSCs are a potential new therapeutic agent for AD. STEM CELLS 2010;28:329?343
Keywords : Alzheimer's disease model; Bone marrow-derived mesenchymal stem cell; Amyloid-β; Transplantation; Alternatively activated microglia
논문정보
- Research article
- 2010년 02월 (BRIC 등록일 2017-03-31)
- 국내(교신)+국외 연구진
- 의약학 > 신경의학
- 120회 이상 인용된 논문
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