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Hindi Review Article
Cellular Transplantation as the Treatment of Alzheimer's Diseas e in Mouse Models
Noboru Suzuki*, Jun Shimizu, Naruyoshi Fujiwara and Nagisa Arimitsu
Department of Immunology and Medicine and Department of Regenerative Medicine, St. Marianna University Graduate School of Medicine, Kawasaki, Japan
- Corresponding Author:
- Noboru Suzuki
Department of Immunology and Medicine and Department of Regenerative Medicine
St. Marianna University Graduate School of Medicine
2-16-1 Sugao, Miyamae-ku, Kawasaki, Kanagawa 216-8511, Japan
Tel: +81-44-977-8111
E-mail: n3suzuki@marianna-u.ac.jp
Received date: March 01, 2016; Accepted date: March 07, 2016; Published date: March 14, 2016
Citation: Suzuki N, Shimizu J, Fujiwara N, Arimitsu N (2016) Cellular Transplantation as the Treatment of Alzheimer’s Disease in Mouse Models. J Alzheimers Dis Parkinsonism 6:219. doi: 10.4172/2161-0460.1000219
Copyright: © 2016 Suzuki N, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Acetylcholine (Ach) and N-methyl-D-aspartate (NMDA) have been two major therapeutic targets of Alzheimer’s disease (AD) for decade. However, truly effective remedy for AD has not been successfully developed.
We previously transplanted neurons derived from human induced pluripotent stem (hiPS) cells into the hippocampus of human amyloid precursor protein transgenic AD model mice.
The cell transplantation significantly improved cognitive dysfunction in the dementia model mice. Human choline acetyl transferase (ChAT) positive cholinergic neurons located throughout the cortex of the grafted mice.
Human and mouse ChAT positive neurons and alpha7 nicotinic acetylcholine receptor (α7nAChR) positive neurons significantly increased in the cortex and hippocampus of the grafted dementia mice compared with the vehicle injected dementia mice. Human and mouse vesicular GABA transporter (VGAT) positive neurons distributed mainly in the hippocampus and, though the number was small, human VGAT positive neurons located in the cortex. In the grafted mouse cortex,
the number of GABA receptor (GABAR) positive neurons of both hiPS origin and mouse origin increased significantly compared with those in the vehicle injected mouse cortex. We suggested that positive feedback loops of neurotransmitter secretion of the cortex and hippocampus induced the characteristic distribution of the transplanted neurons. In this review, we summarized current advances in stem cell therapy for dementia model mice, especially to highlight the relationships between major neurotransmitters and host/transplanted neurons.
