A randomized trial of mesenchymal stem cells in multiple system atrophy

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Posted May 7, 2013
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Neuroprotective or regenerative strategies are invaluable in multiple system atrophy (MSA) due to its rapid progression with fatal prognosis. We evaluated the efficacy of autologous mesenchymal stem cells (MSC) in patients with MSA-cerebellar type (MSA-C).


Thirty-three patients with probable MSA-C and baseline unified MSA rating scale (UMSARS) scores ranging from 30 to 50 were randomly assigned to receive MSC (4 × 10(7) /injection) via intra-arterial and intravenous routes or placebo.

The primary outcome was change in the total UMSARS scores from baseline throughout a 360-day follow-up period between groups. Secondary outcomes were changes in the UMSARS part II scores, cerebral glucose metabolism, gray matter density, and cognitive performance over a 360-day period.


The mixed model analysis of neurological deficits revealed a significant interaction effect between treatment group and time, suggesting that the MSC group had a smaller increase in total and part II UMSARS scores compared with the placebo group (p = 0.047 and p = 0.008, respectively).

Cerebral glucose metabolism and gray matter density at 360 days relative to the baseline were more extensively decreased in the cerebellum and the cerebral cortical areas, along with greater deterioration of frontal cognition in the placebo group compared with the MSC group. We found no serious adverse effects that were directly related to MSC treatment. However, intra-arterial infusion resulted in small ischemic lesions on magnetic resonance imaging.


MSC therapy could delay the progression of neurological deficits in patients with MSA-C, suggesting the potential of MSC therapy as a treatment candidate of MSA.

Source: PubMed

Comment this news or article

  • Rick Anderson

    I am a 70 years old male. I have recently [May 7, 2013] been
    diagnosed with Multiple System Atrophy [MSA].

    One of my MSA discoveries is there exists only palliative
    treatment of MSA symptoms [MSA syndrome]: speech and physical therapy, swallow
    tests, postural balance, et cetera. That
    is, only MSA symptom clusters are treated, not the cerebellar degenerative
    disease itself. Perhaps that is due to the rarity of MSA. Only 2-3 mostly
    seniors develop it out of 100,000 people.

    Are you a progressive investigator who is trying to correct
    that syndrome treatment approach and cure the actual disease itself? I’d like
    to find a neurologist who thinks “out of the box” and is willing to
    prescribe clinical test procedures for me like stem cells.

    I have researched autologous bone marrow-derived mesenchymal
    stem cell MSA therapy

    I live in northern Virginia, near Washington, DC.

    I am retired and can travel the MSA treatment of the stem
    cells medical provider.

    I have a good general physician Dr. Sandra Ratterman near me
    at Inova Fair Oaks Hospital

    I will travel to your medical examinations.

    Email me if you are interested in guiding my return to
    strenuous bicycling and exercise.


    Rick Anderson

    Rick Anderson, Ph.D.

    Principal, state of the heart computing, Inc.

    Professor Emeritus



    Categories of MSA


    MSA is a progressive, fatal disorder characterized by
    autonomic failure and parkinsonism and/or cerebellar involvement. Neuropathologically,
    MSA is characterized by glial cytoplasmic inclusions (GCI) of abnormally
    aggregated α-synuclein (α-syn).

    MSA SYMPTOMS reflect the dysfunction and eventual loss of
    nerve cells in several different areas in the brain and spinal cord that control
    the autonomic nervous system and coordinate muscle movements. The loss of nerve cells may be due to the
    buildup of a protein called alpha-synuclein in the cells that produce dopamine,
    a neurotransmitter that relays motor commands in the brain. The buildup also occurs in other cells called
    oligodendroglia, which help transmit nerve signals. MSA, along with Parkinson’s disease and some
    other neurodegenerative conditions, are called SYNUCLEINOPATHIES because they
    share a buildup of alpha-synuclein in brain cells.

    MSA differs from Parkinson’s disease and other
    synucleinopathies in that the troublesome protein aggregates appear
    predominantly in OLIGODENDROCYTES rather than neurons.

    The formation of α-synuclein fibrils and disaggregate
    fibrils already formed will delay progression or reverse neurologic and
    autonomic functions and symptoms in MSA. This approach has been proposed as a
    potential approach to treat parkinsonism and, specifically, MSA.

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