Roy A. E. Bakay, MD, neurosurgeon, Rush University Medical Center, used a novel approach to treat Parkinson’s disease consisting of Spheramineretinal (pigment epithelial (RPE) cells attached to tiny gelatin bead microcarriers implanted in the brain).

Six patients with moderate to advanced Parkinson’s disease were given Spheramine implants. All participants were monitored for at least 4 years and up to 6 years. Researchers report the subjects showed long-term improvement or stabilization of their symptoms for a minimum of 2 years after the Spheramine implantation. No serious Spheramine related adverse effects were reported. (Headaches were reported for 1 or 2 weeks after surgery.)

Rebecca Stowe, University of Birmingham, reports in a study, that appears in the latest issue of The Cochrane Library (published by an international organization that evaluates medical research), reports that patients taking dopamine agonists were more than twice as likely to quit treatment. She suggest that the reason is because the severe side effects from dopamine agonists diminish a patient’s quality of life and outweighs the benefit of muscle control.

In Stowe’s study she and colleagues reviewed 29 studies that included 5,247 patients who were in the early stages of Parkinson’s disease and did not show significant signs of muscle and movement problems. There appeared to be no significant difference in the death rate between dopamine agonists and those who did not take drugs.

According to researchers it remains unclear the balance of risks and benefits of dopamine agonists. Currently the researchers are tracking another issue that was raised during their preliminary research–the link of dopamine agonists and impulsive behaviors like gambling and hypersexuality.

Dr. Anita Hall, Department of Live Sciences, Imperial College, London, and colleagues, used mouse models to examine the early stages of brain formation. They knew that dopaminergic neurons cells produce and use the chemical dopamine to communicate with surrounding neurons. Researchers found that dopaminergic neurons are created by precursor cells identified as ‘radial glia-like cells’.

The importance of dopaminergic neurons, researchers found, is that they are created when a particular type of cell in the embryonic brain divides during the early stages of brain development in the womb. These radial glia-like cells contain all the information needed to create and support the young dopamine-producing neurons, which are essential for important human functions including motor activity, cognition, and some behaviors.

Halls suggest that these glia-like cells could be used to grow new neurons in the lab. Of course further research is needed before such a complex procedure of transplanting the cells into humans becomes clinically possible.

Dr. Xuemei Huang, medical director of Movement Disorder Clinic, University of North Carolina, Chapel Hill, NC, believes he has found a way to establish the association of low LDL levels with Parkinson’s. A group of 3,233 men of Japanese ancestry had participated in the Honolulu-Asia Aging Study between 1991 – 1993. During the study fasting lipids were measured and at that time statin therapy to lower LDL levels was not widely used. The men in the study were followed for about 10 years and the correlation between decreasing levels of LDL cholesterol and increased incidents of Parkinson’s disease emerged.

After adjusting for age, smoking, coffee intake, and other factors, the researchers calculated that the relative odds of Parkinson’s for men with lower LDL levels (85 mg per deciliter) was about twice that of those with higher LDL levels ((135 mg per deciliter).

Low levels of LDL cholesterol are associated with good cardio vascular health and people taking statins to lower their LDL are advised not to stop taking the medication simply to avoid Parkinson’s.

Lorenz Studer, MD, Head of Stem Cell and Tumor Biology Laboratory, Sloan-Kettering Cancer Center, feels that their latest study reduces the chances that somatic-cell nuclear transfer (SCNT)–or therapeutic cloning–reduces transplant rejection and enhances recovery in diseases and organ systems.

In SCNT the nucleus of a donor subject’s somatic cell is inserted into an egg, which has had the nucleus removed. This cell then develops into a blastocyst from which embryonic stem cells can be harvested for therapeutic purposes. Since the genetic information in the resulting stem cells comes from the donor subject the SCNT has a greater chance of being accepted by the immune system.

Scientist demonstrated the process on mice genetically designed to have Parkinson’s disease. They began by taking skin cells from the tails of mice and generated the missing dopamine neurons–the cause of Parkinson’s–but because they did not attempt to genetically match the transplanted cells, from donor to recipient, the cells did not survive and the mice did not recover.

Using SCNT, where the transplanted stem cells were from the same subject, the immune system accepted the transplanted cells and the mice showed signs of recovery.

Studer’s article appears in the March 23, 2008 online journal edition of Nature Medicine.

Diagnosis of Parkinson’s is done solely based on the patient’s symptoms. Unfortunately, conditions such as multi-system atrophy or progressive suprancuclear palsy look a lot like Parkinson’s. As a result approximately 10% of those diagnosed with Parkinson’s have been misdiagnosed and prevents them from getting the treatment that is best for them.

Dr. M. Flint Beal, Chairman of Neurology, and Anne Parrish Titzell, Professor of Neurology, both of Weill Cornell  Medical College, collected blood from 66 Parkinson’s patients who were either receiving–or not receiving–treatment for the disease. The blood from the 2 groups was compared for metabolomic patterns, then the blood from both groups was compared to blood from a control group who did not have Parkinson’s. What emerged was a pattern of 160 different compounds that were specific to the Parkinson’s patients.

The significance of many individual compounds to the disease remains unknown, but changes in a few metabolites are linked to oxidative stress and linked to Parkinson’s. These included low levels of the antioxidant uric acid; an increase in blood levels of another antioxidant, glutathione; and increased levels of a marker for oxidative damage called 8-OHdG.

The researchers are increasing the number subjects involved in the study and also have begun to take periodic samples of their blood to serve as a benchmark for the progression of Parkinson’s disease.

Using the ‘metabolomic’ alterations of small molecules in the serum, researchers hope to develop an unique pattern that identifies individuals that either have developed–or are vulnerable to–Parkinson’s disease. This will lead to an accurate diagnostic blood test for Parkinson’s disease.

Nicholas Muzyczka, PhD, professor of molecular genetics and microbiology, College of Medicine, University of Florida, believes that his research group have found one more piece of information about what might be causing the toxicity in Parkinson’s disease; specifically, what the protein alpha-synuclein does in the brain.

Alpha-synuclein is located at the synapses of nerve cells and believed to aid in brain function by controlling the release of neurotransmitters–such as dopamine. The rare inherited form of Parkinson’s disease may be caused by a mutation of alpha-synuclein.

Researchers used gene transfer to enhance the production of 3 versions of alpha-synuclein in the substantia nigra region in rats’ brains. For comparison the other side of the rats’ brains were left untreated. All 3 forms simulated phosphorylation. One form of the phosphorylation was non-toxic, but the remaining 2 forms created a toxin protein that caused significant loss of dopamine neurons.

About the smallest thing that can happen in biology is to add a phosphate group, which researchers did when they used gene transfer to enhance the production of alpha-synuclein. Although a relatively minor change the result was that everything got switched around and an innocuous problem became a huge problem. The researchers hope that continuing research in this area will help them get a handle on some of the common diseases and eventually to a drug discovery program.

Peter Sadler, Professor, University of Warwick, and Sandeep Verma, Professor, Indian Institute of Technology, found that that by taking the protein that is responsible for transporting iron in the bloodstream and letting it dry out will form tendrils, or worm like fibrils. Even more interesting was that the iron that had been wrapped inside the transporting protein now formed bands that plated the fibrils. This process could leave iron dangerously exposed and available to interact in ways that could cause cell damage.

Deposits of iron exposed in this way could be responsible for some forms of Parkinson’s, Alzheimer’s, and Huntington’s diseases. Until now there had been no real idea as to how iron becomes deposited in brain in such a dangerous way. It is essential for the brain to have iron safely delivered to it; this observation could provide the first real clue as to how that iron comes to be deposited in such a dangerous way.

Paul Greengard, Rockefeller University, and colleagues in Sweden, have found evidence that serotonin also plays a crucial role in Parkinson’s disease. Using a mouse model of the disease the researchers were able to block the side effects of L-DOPA by manipulating a specific serotonin receptor.

The neuro transmitter dopamine has several functions in the brain, including the regulation of movement. Parkinson’s disease is characterized by a progressive degeneration of dopamine-producing neurons, causing the tremors and other disease characteristics. These neurons project from the midbrain to an area of the brain called the corpus striatum. Although dopamine signaling is impaired in Parkinson’s patients, serotonin production remains strong.

Christoph R. Meier, PhD, MSc, University Hospital Basel, Switzerland, studied 7,374 men and women over the age of 40. One-half of the group had Parkinson’s disease, the other half–the control group–had no signs of the disease. In each group approximately one-half used high blood pressure medications, such as calcium channel blockers, AT II antagonists, ACE inhibitors, and beta blockers.

Researchers are not certain why calcium channel blockers appear to protect against Parkinson’s disease and feel additional research is needed to rule out a causal association. Also, they would like to better understand why the other types of high blood pressure medications do not appear to reduce the risk of Parkinson’s.

The complete article appears in the current issue of the American Academy of Neurology.