Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2020 Jan 27;27(1):29.
doi: 10.1186/s12929-020-0622-x.

Effects of neural stem cell transplantation in Alzheimer's disease models

Yoshihito Hayashi  1   2 , Huan-Ting Lin  3 , Cheng-Che Lee  1 , Kuen-Jer Tsai  4   5   6
Affiliations
Review

Effects of neural stem cell transplantation in Alzheimer's disease models

Yoshihito Hayashi et al. J Biomed Sci. .

Abstract

Currently there are no therapies for treating Alzheimer's disease (AD) that can effectively halt disease progression. Existing drugs such as acetylcholinesterase inhibitors or NMDA receptor antagonists offers only symptomatic benefit. More recently, transplantation of neural stem cells (NSCs) to treat neurodegenerative diseases, including AD, has been investigated as a new therapeutic approach. Transplanted cells have the potential to replace damaged neural circuitry and secrete neurotrophic factors to counter symptomatic deterioration or to alter lesion protein levels. However, since there are animal models that can recapitulate AD in its entirety, it is challenging to precisely characterize the positive effects of transplanting NSCs. In the present review, we discuss the types of mouse modeling system that are available and the effect in each model after human-derived NSC (hNSC) or murine-derived NSC (mNSC) transplantation. Taken together, results from studies involving NSC transplantation in AD models indicate that this strategy could serve as a new therapeutic approach.

Keywords: Alzheimer’s disease; Cell therapy; Cognitive impairment; Inflammation; Neural stem cell; Neurogenesis; Synaptogenesis.

PubMed Disclaimer

Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
The mechanisms of the respective drugs. Acetylcholinesterase inhibitors (galantamine, rivastigmine and donepezil) enhance the activity of neuro-message transduction by preventing acetylcholine degradation (1,2,3). NMDA receptor antagonists (memantine) compete with glutamate in binding to the NMDA receptor to inhibit Ca2+ influx into the postsynapse (4,5). These drugs have little effect on amyloid-beta production and aggregation, synaptogenesis, and neurogenesis yet they rescue cognitive impairment
Fig. 2
Fig. 2
Routes for neural stem cell transplantation and mechanisms of cognitive impairment restoration. Transplantation of neural stem cells triggers (1) endogenous synaptogenesis and (2) endogenous neurogenesis to influence behavioral performance. (3) The limited causal relationship between amyloid-beta and neural stem cells contraindicates any link between behavioral performance and amyloid-beta aggregation
See this image and copyright information in PMC

References

    1. Ryan NS, Rossor MN, Fox NC. Alzheimer's disease in the 100 years since Alzheimer's death. Brain. 2015;138(Pt 12):3816–3821. doi: 10.1093/brain/awv316. - DOI - PubMed
    1. Wenk, G.L., Neuropathologic changes in ALzheimers Disease. The Journal of Clinical Psychiatry, 2003. 64(Suppl 9:7–10). - PubMed
    1. Guan R, et al. Trends in Alzheimer's disease research based upon machine learning analysis of PubMed abstracts. Int J Biol Sci. 2019;15(10):2065–2074. doi: 10.7150/ijbs.35743. - DOI - PMC - PubMed
    1. Gerwin Roksa BD, Heutinkc P, Julliamsb A, Backhovensb H, Van de Broeckb M, Serneelsb S, Hofmana A, Van Broeckhovenb C, van Duijna CM, Crutsb M. Mutation screening of the tau gene in patients with early-onset. Neurosci Lett. 1999;277:137–139. doi: 10.1016/S0304-3940(99)00861-7. - DOI - PubMed
    1. Radde R, et al. Abeta42-driven cerebral amyloidosis in transgenic mice reveals early and robust pathology. EMBO Rep. 2006;7(9):940–946. doi: 10.1038/sj.embor.7400784. - DOI - PMC - PubMed