Targeting alpha-synuclein in Parkinson's
While clinicians have long been using dopamine agonists to treat Parkinson's disease, Joseph Jankovic, MD, of Baylor College of Medicine in Houston, and his colleagues have been trying to fix what they think may be the underlying problem in the disease: the accumulation of alpha-synuclein. In this exclusive video, Jankovic details how his center is treating Parkinson's patients with an experimental monoclonal antibody to remove the protein from the brain.
A transcript follows:
Parkinson's disease is a progressive neurological disorder, the cause of which is really still not full understood. The major hypothesis right now is that there is an accumulation of a protein called alpha-synuclein in the brain cells of patients with Parkinson's disease. This alpha-synuclein can cause interference with the normal function of the cells, as a result of which there's a deficiency of dopamine in the middle part of the brain called the substantia nigra.
As a result of the damage by this toxic protein, alpha synuclein, there's a degeneration of these nerve cells in the various parts of the brain, including the midbrain, but other parts of the brain may be involved, and as a result patients develop Parkinson's symptoms. They can be manifested by tremor, slowness of movement, trouble with gait and balance. But many Parkinson's patients have a variety of non-motor symptoms as well, such as loss of smell; they may have trouble with their sleep; they have fluctuations in their blood pressure, and eventually many of them develop cognitive deficit.
So, one of the leading hypotheses currently is that alpha-synuclein causes damage in these cells, and therefore alpha-synuclein is an ideal therapeutic target for the treatment of Parkinson's disease, particularly in our effort to alter the natural history of the disease. So one of the medications that we are currently testing at Baylor College of Medicine is a monoclonal antibody against alpha-synuclein. We infuse the monoclonal antibody once a month through an infusion and we hope that with prolonged treatment, we will favorably alter the natural progression of the disease.