Unfortunately, the only two researchers that I have discovered who are
publishing stem cell research on multiple system atrophy are still
working with rat models, and haven't progressed in their research to
humans. So, while the basic answer to your question is "yes", for all
practical purposes for your father, the answer is "no." I'm including
below the citations and abstracts to two papers published by these
research groups, one of which is at the Veterans Administration
Hospital in San Diego, CA, and the other is at the University of
These articles were found in the PubMed MEDLINE database
(http://www.pubmed.gov) using the search statement: "multiple system
atrophy AND stem cell".
1: Neuroreport. 2002 Jul 19;13(10):1305-8.
Oligodendrocytes from neural stem cells express alpha-synuclein: increased
numbers from presenilin 1 deficient mice.
Culvenor JG, Rietze RL, Bartlett PF, Masters CL, Li QX.
Department of Pathology, The University of Melbourne and Mental Health Research
Institute of Victoria, Parkville, Victoria 3010, Australia.
alpha-Synuclein normally a synaptic vesicle-associated cytoplasmic protein is
the major component of filamentous inclusions of neurons in Parkinson's disease
and dementia with Lewy bodies. It is also the major component of glial
inclusions of multiple system atrophy. In characterizing cells derived from
embryonic neural stem cells we found all oligodendrocytes had strong cytoplasmic
expression of alpha-synuclein. Comparison of cells from presenilin 1
(PS1)-deficient mice with wild type revealed a 7-fold increase in
oligodendrocytes. Western blotting analysis indicated the cells contained
alpha-synuclein monomers and SDS-stable dimers and trimers. This cell system of
oligodendroglial alpha-synuclein expression is a useful system to study
alpha-synuclein metabolism in the cell type affected in multiple system atrophy.
Increased oligodendroglial cell numbers from PS1-deficient cells provides
further evidence for a role of PS1-dependent Notch signalling in cell fate
PMID: 12151792 [PubMed - indexed for MEDLINE]
2: Brain Res. 2000 Nov 17;883(2):192-204.
Fibroblast growth factor-2-producing fibroblasts protect the nigrostriatal
dopaminergic system from 6-hydroxydopamine.
Shults CW, Ray J, Tsuboi K, Gage FH.
Neurology Service, Veterans Affairs San Diego Healthcare System, VA Medical
Center, 3350 La Jolla Village Drive, San Diego, CA 92161, USA.
We tested the hypothesis that fibroblasts, which had been genetically engineered
to produce fibroblast growth factor-2 (FGF-2), can protect nigrostriatal
dopaminergic neurons. Three groups of rats received either a burr hole only
(n=5) or implantation of fibroblasts, which had been genetically engineered to
produce beta-galactosidase (beta-gal) (n=8) or FGF-2 (n=8), at two sites in the
right striatum. Two weeks later, the animals received an injection of 25 microg
of 6-hydroxydopamine hydrobromide (6-OHDA) midway between the two implant sites.
The group that received FGF-2-fibroblasts had significantly fewer
apomorphine-induced rotations than the groups that received a burr hole only or
beta-gal-fibroblasts at weeks 2 and 3 following lesioning with 6-OHDA. Testing
for amphetamine-induced rotation revealed a mild reduction in rotation in the
beta-gal-fibroblast group compared to the burr hole only group, but a striking
attenuation of amphetamine-induced rotation in the FGF-2-fibroblast group. There
was also preservation of TH-IR neurons on the lesioned side relative to both
control groups. The size of the grafts and the gliosis surrounding the injection
sites did not differ between the FGF-2-fibroblast and beta-gal-fibroblast
groups. To further characterize the production of FGF-2 by the
FGF-2-fibroblasts, we implanted FGF-2-fibroblasts and beta-gal-fibroblast into
the striatum of rats but did not lesion the animals with 6-OHDA. The animals
were then sacrificed at 1, 2 and 5 weeks following implantation. Prior to
implantation the FGF-2 fibroblasts contained 148 ng/mg of FGF-2-immunoreactive
(FGF-2-IR) material per mg of protein of cell lysate. After implantation
FGF-2-IR material was noted in the grafts of FGF-2-fibroblasts, most
conspicuously at 1 and 2 weeks following implantation. We also noted FGF-2-IR
material in the nuclei of reactive astrocytes adjacent to the implants, and
OX-42-immunoreactive (OX-42-IR) cells adjacent and occasionally within the
implants. Our work indicates that fibroblasts genetically engineered to produce
FGF-2 and implanted in the striatum can protect the nigrostriatal dopaminergic
system and may be useful in the treatment of Parkinson's disease.
PMID: 11074048 [PubMed - indexed for MEDLINE]
There have been a number of clinical trials involving MSA, many of
which compare it to Parkinson's Disease (which, apparently, is
similar). If you'd like me to give you some citations to those I'd be
happy to - just put in a clarification request (preferably before you
rate the answer).
In addition, you may have already found these websites, but I'd like
to give them to you just in case and for your information. I got them
all by doing a search of the MedlinePlus consumer health database for
"multiple system atrophy":
ClinicalTrials.gov lists currently recruiting clinical trials, one of
which your father may qualify for, if you're interested:
The MedlinePlus encyclopedia article for MSA:
WE MOVE Multiple System Atrophy page: http://www.wemove.org/msa/
The NINDS MSA Information Page: http://www.ninds.nih.gov/disorders/msa/msa.htm
You may be frustrated with the relative shortness of these pages -
this is largely because this disease is still being studied.
Researchers aren't quite sure what causes it, or how to cure it. I'm
very sorry for you and your father, and hope that the above
information will be of some help. Again, please do not hesitate to
ask for more information if you would like it.
The Mayo Clinic information page on Shy-Drager Syndrome (a special
case of MSA): http://www.mayoclinic.com/invoke.cfm?id=AN00616