"Parkinson's Disease: Working Towards a Cure": Part 2-- Current Treatments

This is the second post from a three part series written by Andrew Greene, a graduate student at McGill University studying Parkinson's Disease.  

While a number of worthwhile treatments exist for Parkinson’s, they all target the symptoms rather than the root cause of the disease, the death of substantia nigra neurons. This is because, at least in most cases, we still don’t understand exactly why those neurons die. We’re getting closer every year though, and some of the cutting edge research that’s bringing us towards a cure will be discussed in Part 3. For now we’re limited to symptom-targeting treatments, but as we’ll see below, some of them can be quite effective.

In Part 1 we saw that the major symptoms of Parkinson’s disease are caused by the death of neurons that emit a chemical called dopamine. It’s not surprising then, that the gold standard in Parkinson’s treatment is the administration of dopamine supplements. Unfortunately dopamine taken by mouth does not reach the brain, but scientists have circumvented this problem by using a chemical called Levodopa, or L-dopa for short. L-dopa is a natural molecule found in both animals and plants. In humans and other animals, L-dopa taken by mouth can easily reach the brain, where it is converted into dopamine. Supplementing a patient’s brain with dopamine in this manner allows them to move much more readily than they could without treatment, but there are side effects. Whereas the brain administers dopamine to itself in a carefully regulated manner, the levels of dopamine produced from L-dopa are much less finely tuned. A frequent side effect of the treatment is ‘too much movement,’ with patients making involuntary movements such as writhing or jerking. Fortunately these can usually be minimized by reducing the L-dopa dose.

When medications aren't cutting it, eligible patients can opt for various types of surgery. Like the currently available medications, the surgeries do little to block the root cause of the disease, but they can be very effective in eliminating many of the more debilitating symptoms. An increasingly common option is the implantation of a deep brain stimulation device. Somewhat counter intuitively, the net effect of the deep brain stimulation used to treat Parkinson’s is actually to block the neural activity in a certain section of the brain. This effectively inhibits the indirect pathway, which, as mentioned in Part 1, is involved in inhibiting movement and is overactive in Parkinson’s disease. Deep brain stimulation is effective against symptoms such as rigidity and slowness of movement, and is less prone to causing involuntary movements than L-dopa is. Unfortunately it’s expensive and demands a tremendous amount of expertise in medical imaging, surgery, neurophysiology, and postoperative management, thus limiting its widespread availability. Moreover, because neither deep brain stimulation nor L-dopa treatment target the cause of Parkinson’s, neurons continue to die as the disease progresses. This means that symptoms that don’t respond to the above therapies, such as cognitive problems and frequent falls, continue to worsen. For this reason, Parkinson’s disease remains an active field of research in neuroscience.

Stay tuned for Part 3: Towards a Cure. Coming soon!