Archive for July 2007

Hope for new Parkinson’s therapy

July 15, 2007 by mike.

Scientists have discovered a protein which may help to slow, or even reverse symptoms of Parkinson’s disease.

Parkinson’s destroys nerve cells that produce the brain chemical dopamine, causing movement and balance problems.

Finnish researchers found the new molecule can prevent degeneration of these cells - and help damaged cells start to recover.

Their paper, featured in Nature, showed symptoms eased in rats given injections of the protein…

BBC NEWS

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UAB receives grants to investigate novel approaches to treat Parkinson’s disease

July 15, 2007 by mike.

Medical Research News

Published: Sunday, 15-Jul-2007

The Michael J. Fox Foundation (MJFF) has awarded two research grants to UAB (University of Alabama at Birmingham) researchers to investigate novel approaches to treat Parkinson’s disease.

UAB scientists will collaborate with researchers from the University of Alabama (UA) on one of the two grants, part of the Foundation’s 2007 Target Validation initiative.

The first award, $250,000 over two years, will be split between Dr. David Standaert, M.D., PhD, professor of neurology and Director of the UAB Center for Neurodegeneration and Experimental Therapeutics, and Guy Caldwell, Ph.D., and Kim Caldwell, Ph.D., faculty members in biological sciences at UA.

The project is based on previous work by the Caldwells. Using a worm known as C. elegans, the Caldwell lab discovered that a protein called VPS41 prevented neurons which produce dopamine from dying. In Parkinson’s patients, the death of dopamine neurons leads to the disease’s cardinal symptoms: tremor, slowness of movement and rigidity.

In the new study, Standaert’s lab will investigate whether the neuroprotective ability of VPS41 seen in the C. elegans worms will translate to human cell lines and mammalian animal models, which are more biologically advanced than the worm model.

The Caldwells at UA will continue to work in C. elegans, seeking to determine which specific components of the protein are neuroprotective and what regions of the protein might best be targeted for enhancement through drug therapy.

“This is an exciting collaboration between UAB and UA, combining the strengths of both laboratories and institutions to help find new answers in the treatment of Parkinson’s,” said Standaert. “We’re pleased to be able to work with The Michael J. Fox Foundation on these truly innovative approaches to the disease.”

The second UAB grant, also for $250,000 over two years, goes to Jianhua Zhang, Ph.D., assistant professor of neuropathology. Zhang will investigate an enzyme called Cathepsin D, which also seems to have a protective effect in brain cells.

Researchers have long known that an overabundance of a certain protein in brain cells is associated with Parkinson’s. Zhang’s previous work, in collaboration with the Caldwells and Kevin Roth, M.D./PhD., professor of neuropathology at UAB, indicated that Cathepsin D seems to have a role in the removal of this protein from brain cells and protection of neurons from death induced by its overabundance.

With the MJFF funding, Zhang will collaborate with Standaert to examine in mouse models for Parkinson’s the effects on dopaminergic neuron death by the reduction of Cathepsin D as well as the protective effects of adding the enzyme against Parkinson’s.

“It’s very gratifying to know that our efforts to promote neuroscience research in Alabama are paying dividends,” said Standaert. “Alabama is truly on the cutting edge of this important work.”

The Michael J. Fox Foundation for Parkinson’s Research is dedicated to ensuring the development of a cure for Parkinson’s disease through an aggressively funded research agenda. To date, the Foundation has funded over $94 million in research directly or through partnerships.

http://www.uab.edu/

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Cigarette Smoking May Reduce Parkinson’s Risk

July 13, 2007 by mike.

By Steven Edwards

Complementing today’s Wired story on the pharmaceutical benefits of nicotine, a study published in July’s Archives of Neurology reports that smoking may reduce the risk of developing, or delay the onset of, Parkinson’s disease. Smaller benefits were detected in former smokers.

The authors found that smokers were less likely to get Parkinson’s, and those who smoked more seemed to have greater protection. These findings indicate that smoking may delay rather than prevent the onset of Parkinson’s, but that would have to be confirmed by a larger study.

“Current smokers and those who had continued to smoke to within five years of Parkinson’s disease diagnosis exhibited the lowest risk, [but] a decrease in risk [of] 13 to 32 per cent was also observed in those who had quit smoking up to 25 years prior,” said Dr Beate Ritz, of the UCLA School of Public Health in Los Angeles, and her co-authors.

Reductions were not seen in Hispanic or African-American patients, but this didn’t discourage the researchers. They suggest that a substance in cigarette smoke may protect dopaminergic neurons, whose loss causes the tremors associated with Parkinson’s disease.

The logical extension of the cigarette smoke assumption is that non-smokers who regularly interact or live with smokers may also show a reduced risk of developing Parkinson’s disease as they would be exposed to cigarette smoke as well.

Of course, smoking cigarettes carries risks, so taking it up to protect against Parkinson’s may not be a good idea

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Enzyme Damage Could Be Key to Parkinson’s

July 6, 2007 by mike.

HealthDay

By Madeline Vann

Thursday, July 5, 2007

THURSDAY, July 5 (HealthDay News) — Disruption of a key cellular enzyme may be a root cause of Parkinson’s disease, a new study finds.

Parkinson’s disease occurs when neurons that produce dopamine die. Dopamine is a neurochemical that allows the body to move with smooth coordination. When 80 percent of the neurons that produce dopamine die off, the motor symptoms of Parkinson’s disease appear.

Now, a Canadian team has found evidence that neuronal death occurs when a cellular enzyme called Prx2 is injured. The enzyme plays a key role in eliminating the potentially damaging products of mitochondria, the cells’ power plants. Without the enzyme, these products build up and threaten the cell.

Reporting in the July issue of Neuron, researchers at the Ottawa Health Research Institute, in Ontario, studied mice in which a mitochondria-affecting toxin is used to create a condition similar to Parkinson’s disease.

They found a chain of events in which the toxin turns on a cellular switch, which then turns off Prx2. They also found that they could reverse this chain of events by turning Prx2 back on in the toxin-treated mice — preventing the loss of dopamine-making neurons.

The team also noted lower-than-normal Prx2 activity in the brain tissue of humans with Parkinson’s disease.

The researchers theorize that managing Prx2 activity may be a viable approach to the treatment of Parkinson’s disease.
HealthDay

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“Ceregene and Genzyme Announce Partnership for the Development and Commercialization of Cere-120 for Parkinson’s Disease”.

July 4, 2007 by mike.

“Ceregene, Inc. and Genzyme Corporation today announced that they have entered into a partnership for the development and commercialization of CERE-120, Ceregene’s proprietary lead program for the treatment of Parkinson’s disease.

Under the terms of the agreement, Genzyme will pay Ceregene a $25 million up-front payment in exchange for certain partnership-related expenses. Ceregene will also be entitled to development-related milestone payments of up to $125 million and 50 percent reimbursement of the worldwide Phase 3 development costs. Genzyme will gain marketing rights in all markets outside of the US and Canada, and Genzyme will pay Ceregene tiered royalties based on sales in markets where it has rights. Ceregene will retain exclusive rights to CERE-120 in the US and Canada.

“We are pleased to be partnering CERE-120 with Genzyme-a company with a strong international presence and marketing expertise that will enable us to maximize the worldwide commercialization of CERE-120,” stated Jeffrey M. Ostrove, Ph.D., president and chief executive officer of Ceregene. “CERE-120, which is currently undergoing a controlled Phase 2 trial in the United States that is being partially funded by the Michael J. Fox Foundation, has demonstrated strong clinical and preclinical data to date and may have the ability to both improve Parkinson’s disease symptoms and slow the disease progression. The resources provided by our new partnership with Genzyme, together with the greater than $27 million initial closing of our Series C financing, which was led by Investor Growth Capital and closed in the first quarter, provides the funding we currently need to advance CERE-120 toward commercialization.”

“We are very enthusiastic about the potential that CERE-120 may have to improve the lives of people with Parkinson’s disease, which currently affects at least one million Americans,” said David Meeker, president, Lysosomal Storage Disorders unit, Genzyme Corporation. “We look forward to helping further the development of this exciting approach, building on our long-term commitment to gene therapy and neurodegenerative diseases. This program - which is focused on preserving neuronal function - will complement our existing Parkinson’s clinical trial that is currently underway.”

“We look forward to working with Genzyme to accelerate the development of CERE-120 in Europe and other areas outside North America,” stated Raymond T. Bartus, Ph.D., Ceregene’s senior vice president of clinical and preclinical R&D and chief operating officer, as well as chairman of the partnership’s joint steering committee. “Strong synergies and complementary skills and experience exist between Ceregene and Genzyme. Their deep infrastructure in developing and commercializing innovative therapeutic products and their experience working with international regulatory agencies will be invaluable as we expand the development of CERE-120.”

In a complementary program, Genzyme is conducting a separate Phase 1-2 clinical trial of a gene therapy for Parkinson’s disease designed to restore the therapeutic effectiveness of levo-Dopa by enhancing the brain’s ability to convert it into dopamine. In addition, Genzyme has an extensive gene therapy portfolio that includes two additional ongoing clinical trials.”

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Pioneering gene therapy for Parkinson’s shows early progress - Lancet

July 4, 2007 by mike.

PARIS (Thomson Financial) - The first attempt at gene therapy against Parkinson’s disease has yielded promising results and is safe, according to early data to appear in the British journal The Lancet on Saturday.

The pilot study among 11 men and one woman with Parkinson’s disease in New York involved a ‘Trojan horse’ technique. This entailed taking a gene and placing it inside a disabled cold virus, which is then injected into a key area of the brain.

The harmless virus ‘infects’ the local cells and thus stealthily delivers the corrective piece of genetic code.

The 12 volunteers showed significant improvement in trembling, jerkiness and other symptoms, and none had any side effects, according to an assessment carried out a year after the operation.

Parkinson’s is an incurable, degenerative disease of the central nervous system that causes uncontrollable shaking, along with impaired speech and movement. In approximately one third of cases it also results in dementia. The disease affects at least 1 pct of people over the age of 65.

Researchers led by Matthew During, a professor at Cornell University’s Weill Medical College, aimed at part of the brain called the subthalamic nucleus, which becomes hyperactive as a result of Parkinson’s and ‘blocks’ signals to the nervous system, thus hampering motor control.

Using a magnetic resonance imaging (MRI) scanner to pinpoint their operations, the team delicately delivered a gene that controls an enzyme, glutamic acid decarboxylase (GAD), into the volunteers’ subthalamic nucleus.

The idea was to use the gene as a switch to reverse the subthalamic nucleus’ activity, turning it into an inhibitor rather than exciter of motor output signals.

None of the patients suffered any ill-effects from the surgery, or from the transplanted gene. Within three months of the operation, they reported substantial improvements in the side of the body that was opposite to the brain hemisphere where the gene was delivered, and the improvement continued until 12 months, the endpoint of the trial.

The researchers say the results, while preliminary, are encouraging, especially as US health watchdogs only gave them cautious authorisation for a gene transplant on one side of the brain, not both.

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