Similar discoveries followed about losses of specific subsets of neurons in Huntington's disease and Alzheimer's disease, creating specific neurochemical deficits. The pharmacological substitution therapy provided by L-dopa revolutionized the treatment of Parkinson's disease. It turned out that the solution wasn't so simple. As is now well known, the patients experienced severe fluctuations in the drug effect, despite relatively constant levels of the drug in the blood and the brain. At such times, the patient freezes up momentarily and loses mobility.
Symptoms can fluctuate wildly with L-dopa treatment or analog drugs.
Moreover, it is reasonable to assume that one of the reasons L-dopa becomes less effective is that it cannot be taken up by the decreased number of surviving dopaminergic neurons to create some form of regulated release of the transmitter. This has led a number of scientists to question whether pharmacological drug substitution therapy will be effective for the age-related neurodegenerative diseases. To many of my colleagues, however, the idea of further damaging circuitry to remove a problem due to the loss of nerve cells, is counter-intuitive. We have, instead, explored the possibility that the very adaptive mammalian brain can integrate new cells into places where they have died. This type of reintegration of neuronal elements is also known as neural transplantation.