MULTIPLE SYSTEM ATROPHY

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

My incredible discovery is there exists only palliative treatment of MSA symptoms [syndrome]: speech and physical therapy, swallow tests, postural balance, et cetera. MSA symptom clusters are treated, not the 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 one of the progressive investigators who are trying to correct that approach? I'd like to find a neurologist who thinks "out of the box" and is willing to prescribe drugs for a personal clinical test.

I live in northern Virginia, near Washington, DC, although I do not need to be near the medical provider.

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

I will travel to your first medical examination.

I have been researching clinical trials and FDA-approved, off-label, "compassionate use" drugs that attack the disease itself and synuclein buildup, including:
- minocycline
- rasagiline mesylate
- rifampicin
- terazosin [Diana Perez, PhD, at the Cleveland Clinic]
- nilotinib and bosutinib [Dr. Moussa, Georgetown University School of Medicine]
- fluoxetine (aka by the tradename Prozac)

I also have researched:
- autologous bone marrow-derived mesenchymal stem cell MSA therapy
- intravenous immunoglobulin [Dr. Peter Novak, University of Massachusetts Medical School]
U Mass]

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

Thanks!

Rick Anderson


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TECHNICAL DATA

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.