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Increased host neuronal survival and motor function in BMT Parkinsonian mice: involvement of immunosuppression.

Increased host neuronal survival and motor function in BMT Parkinsonian mice: involvement of immunosuppression. Research Abstract Details 

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  • Increased host neuronal survival and motor function in BMT Parkinsonian mice: involvement of immunosuppression. Abstract Text:

    gilmor i keshetGilmor I Keshet,ravi j tolwaniRavi J Tolwani,angelica trejoAngelica Trejo,peggy kraftPeggy Kraft,regis doyonnasRegis Doyonnas,carol claybergerCarol Clayberger,james m weimannJames M Weimann,helen m blauHelen M Blau,gilmor i keshetGilmor I Keshet,ravi j tolwaniRavi J Tolwani,angelica trejoAngelica Trejo,peggy kraftPeggy Kraft,regis doyonnasRegis Doyonnas,carol claybergerCarol Clayberger,james m weimannJames M Weimann,helen m blauHelen M Blau,

    We examined the potential of bone marrow transplantation (BMT) to rescue dopaminergic neurons in a mouse model of Parkinson's disease (PD). A BMT from mice transgenic for green fluorescent protein (GFP(+)) given either before or after administration of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) led to the accumulation of transplanted adult GFP(+) bone-marrow-derived cells (BMDC) in the substantia nigra, where dopaminergic neurodegeneration occurs in PD. Post-BMT, mice exposed to MPTP had substantially greater numbers of endogenous tyrosine hydroxylase-positive neuronal cell bodies in the substantia nigra and increased dopamine transporter-positive projections into the striatum compared to controls. Moreover, motor function was restored to normal within 1 month post-MPTP in BMT-treated mice assayed by a rotarod behavioral test. The effect of BMT on PD was indirect, as no evidence of BMDC fusion with or transdifferentiation into dopaminergic neurons was observed. BMDC activated by BMT or associated factors could play a trophic role in rescuing damaged cells. Alternatively, the beneficial effects of BMT are due to immunosuppression reflected by a reduction in the proportion of T-cells and a reduction of T-cell proliferation in BMT mice. These findings highlight that when immunosuppression is required for transplantation studies, the amelioration of symptoms may not be due to the transplant itself. Further, they suggest that the immune system plays a role in the development of characteristics typical of PD.

    Increased host neuronal survival and motor function in BMT Parkinsonian mice: involvement of immunosuppression. Publishing Authors By Initials

    gi keshetGI Keshet,rj tolwaniRJ Tolwani,a trejoA Trejo,p kraftP Kraft,r doyonnasR Doyonnas,c claybergerC Clayberger,jm weimannJM Weimann,hm blauHM Blau,gi keshetGI Keshet,rj tolwaniRJ Tolwani,a trejoA Trejo,p kraftP Kraft,r doyonnasR Doyonnas,c claybergerC Clayberger,jm weimannJM Weimann,hm blauHM Blau,

    For similar abstracts research abstracts see: abstracts research

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    Increased host neuronal survival and motor function in BMT Parkinsonian mice: involvement of immunosuppression. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: The Journal of comparative neurology

    VOLUME: 504

    Page Numbers: 690-701

    Journal Abbreviation: J. Comp. Neurol.

    ISSN: 0021-9967

    DAY: 20

    MONTH: Oct

    YEAR: 2007

    Increased host neuronal survival and motor function in BMT Parkinsonian mice: involvement of immunosuppression. Information

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    LANGUAGE: eng

    NlmUniqueID: 406041

    Increased host neuronal survival and motor function in BMT Parkinsonian mice: involvement of immunosuppression. Keywords Mesh Terms:

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    Grant and Affiliation Information for Increased host neuronal survival and motor function in BMT Parkinsonian mice: involvement of immunosuppression.

    AFFILIATION: Baxter Laboratory for Genetic Pharmacology, Stanford University School of Medicine, Department of Microbiology and Immunology, Stanford University, Stanford, California 94305, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NCRR

    GRANT: K01-RR00129

    ACRONYM: RR

    MEDLINETA: J Comp Neurol

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