Antipodean Pharmaceuticals has initiated the Phase II clinical trial to test the efficacy of its lead compound MitoQ (mitoquinone) for the treatment of Parkinson’s disease in New Zealand and Australia.
MitoQ, based on a novel technology, targets lipophilic cations that transport and concentrate antioxidants into the mitochondria where they accumulate up to 1000 fold.
Patients who meet the diagnosis of Parkinson’s disease, but yet to receive any treatment to relieve symptoms, will be included in the trial, said the company.
The trial will be led by Barry Snow, MD, FRACP, FRCP, HoD of Neurology, Auckland Hospital, and will involve 10 consultant neurologists at the country’s main regional hospitals who will assess and advise potential participants.
Ken Taylor, CEO, Antipodean, said: “Initiating this Phase 2 efficacy study is a major milestone for our company. We believe MitoQ is a promising compound and the study start is testament to quality research and a very efficient drug development program.”
source:
Saturday, May 30, 2009
Friday, May 29, 2009
Keeler: Parkinson's disease does not take away Fox's love for golf
BY SEAN KEELER
He's the incurable optimist. She ruins your morning. He lights up a room. She burns a hole in your wallet. He makes you want to seize the day. She makes you want to seize a 7-iron and toss it straight into the nearest lake.
It's an odd marriage, this union between Michael J. Fox and the game of golf. He's a walking inspiration; she's a succubus with sandtraps. And yet, somehow, it works.
"It gives you a new opportunity to fail every couple minutes, but it gives you an opportunity to succeed every couple minutes, too," explained Fox, the actor/author who's slated to headline the Principal Charity Classic pro-am this morning at Glen Oaks Country Club in West Des Moines. "And if you're not a good golfer, the (feeling) of hitting it, like, 190-200 yards down the fairway with a 3-wood - it's a great feeling. 'Is it on the green? Is it on the green?' That's a great feeling."
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And if it gets people talking about Parkinson's disease, well, that's fine, too. Or as Fox referred to it, jokingly, "my permanent yips.
"I kind of stumbled onto that after the fact, that people said it meant something to them to see me out there trying," said Fox, who revealed that he had Parkinson's 11 years ago and has since become one of the most recognizable advocates in the search for a cure. "Anything I do altruistic or nice for other people, I tend to do by accident."
He's 47 now, but the eyes don't look a day over 19. The impish grin hasn't changed. While Fox takes on occasional acting roles, including an acclaimed stretch on the cable drama "Rescue Me," he retired from full-time showbiz in 2000. The golfing bug bit while in his 40s, as he looked for a way to stay active - the Canadian-born Fox was a pretty salty hockey player in his younger days - and socialize.
"At first, I wanted to get out and try it and I did and I enjoyed it," he explained. "But it isn't lost on me that people draw some inspiration from it, and that's a great feeling."
Roughly 1.5 million Americans have Parkinson's. It destroys brain cells that produce dopamine, a chemical that's crucial to the movement of muscles. Patients suffer from increasingly severe tremors and rigid limbs. Motor skills are impaired, including the ability to walk and speak.
The voice and arms fail him occasionally. The spirit doesn't. Fox's latest book, "Always Looking Up," has seen a steady run on the best-seller lists, while a companion television special on ABC-TV earlier this month was a ratings hit. He even spoke to former NBA power forward Brian Grant, who recently revealed his own battle with Parkinson's, by phone last week.
"We talked about the fact that he (needs) to allow himself to go though the process of whatever - denial, anger, any of those Elisabeth-Kubler-Ross-kind-of stages that he's going to go through," Fox said. "And that's fine, he should go through them. But to be prepared, on the other side, at some point, to accept (it). Not resign yourself to it; fight tooth-and-nail if you want. Get involved with the cure and the quest to find a cure. But know that you don't have a choice about that. But around that choice, you have 1,000 other choices. Especially for someone as uniquely positioned as Brian is."
Which brings us back to golf. She chews you up, spits you out, mocks you, pulls the chair out from behind you a half-second before you were going to sit down. He loves her anyway, unconditionally.
"A couple of weeks ago, (in) Florida, at the Outback tournament, with my friend, Bill Murray," Fox said, "I don't know if you heard, but Bill took a woman out, (a woman) who specifically came out to watch him.
"Guess he went by her house and he hits it 270 yards, hooks it, and took her out. And he's perplexed that there were two wounds on her head. And I said, 'Well, one was an exit wound.' "
'Til dormie do us part.
source:
He's the incurable optimist. She ruins your morning. He lights up a room. She burns a hole in your wallet. He makes you want to seize the day. She makes you want to seize a 7-iron and toss it straight into the nearest lake.
It's an odd marriage, this union between Michael J. Fox and the game of golf. He's a walking inspiration; she's a succubus with sandtraps. And yet, somehow, it works.
"It gives you a new opportunity to fail every couple minutes, but it gives you an opportunity to succeed every couple minutes, too," explained Fox, the actor/author who's slated to headline the Principal Charity Classic pro-am this morning at Glen Oaks Country Club in West Des Moines. "And if you're not a good golfer, the (feeling) of hitting it, like, 190-200 yards down the fairway with a 3-wood - it's a great feeling. 'Is it on the green? Is it on the green?' That's a great feeling."
Advertisement
And if it gets people talking about Parkinson's disease, well, that's fine, too. Or as Fox referred to it, jokingly, "my permanent yips.
"I kind of stumbled onto that after the fact, that people said it meant something to them to see me out there trying," said Fox, who revealed that he had Parkinson's 11 years ago and has since become one of the most recognizable advocates in the search for a cure. "Anything I do altruistic or nice for other people, I tend to do by accident."
He's 47 now, but the eyes don't look a day over 19. The impish grin hasn't changed. While Fox takes on occasional acting roles, including an acclaimed stretch on the cable drama "Rescue Me," he retired from full-time showbiz in 2000. The golfing bug bit while in his 40s, as he looked for a way to stay active - the Canadian-born Fox was a pretty salty hockey player in his younger days - and socialize.
"At first, I wanted to get out and try it and I did and I enjoyed it," he explained. "But it isn't lost on me that people draw some inspiration from it, and that's a great feeling."
Roughly 1.5 million Americans have Parkinson's. It destroys brain cells that produce dopamine, a chemical that's crucial to the movement of muscles. Patients suffer from increasingly severe tremors and rigid limbs. Motor skills are impaired, including the ability to walk and speak.
The voice and arms fail him occasionally. The spirit doesn't. Fox's latest book, "Always Looking Up," has seen a steady run on the best-seller lists, while a companion television special on ABC-TV earlier this month was a ratings hit. He even spoke to former NBA power forward Brian Grant, who recently revealed his own battle with Parkinson's, by phone last week.
"We talked about the fact that he (needs) to allow himself to go though the process of whatever - denial, anger, any of those Elisabeth-Kubler-Ross-kind-of stages that he's going to go through," Fox said. "And that's fine, he should go through them. But to be prepared, on the other side, at some point, to accept (it). Not resign yourself to it; fight tooth-and-nail if you want. Get involved with the cure and the quest to find a cure. But know that you don't have a choice about that. But around that choice, you have 1,000 other choices. Especially for someone as uniquely positioned as Brian is."
Which brings us back to golf. She chews you up, spits you out, mocks you, pulls the chair out from behind you a half-second before you were going to sit down. He loves her anyway, unconditionally.
"A couple of weeks ago, (in) Florida, at the Outback tournament, with my friend, Bill Murray," Fox said, "I don't know if you heard, but Bill took a woman out, (a woman) who specifically came out to watch him.
"Guess he went by her house and he hits it 270 yards, hooks it, and took her out. And he's perplexed that there were two wounds on her head. And I said, 'Well, one was an exit wound.' "
'Til dormie do us part.
source:
Ceregene Presents Additional Clinical Data from Phase 2 Trial of CERE-120 for Parkinson's Disease
Ceregene, Inc. today reported additional clinical data from a double-blind, controlled Phase 2 trial of CERE-120 in 58 patients with advanced Parkinson's disease. CERE-120 uses AAV-based gene therapy to deliver the neurotrophic factor, neurturin, to Parkinson's disease patients in order to restore the function and protect degenerating nigrostriatal neurons. The company previously announced that the Phase 2 trial did not meet its primary endpoint of improvement in the Unified Parkinson's Disease Rating Scale (UPDRS) motor off score at 12 months of follow-up, although several secondary endpoints suggested a modest clinical benefit.
The additional, protocol-prescribed analyses reported today focused on further analyses of the data from the 30 subjects who continued to be evaluated under double-blind conditions for up to 18 months which indicate increasing effects of CERE-120 over time. A clinically modest but statistically significant treatment effect in the primary efficacy measure (UPDRS motor off; p=0.025), as well as similar effects on several more secondary motor measures (p<0.05), were seen at the 18 month endpoint. Not a single measure similarly favored sham surgery at either the 12 month or 18 month time points. Additionally, CERE-120 appears safe when administered to advanced Parkinson's disease patients, with no significant concerns related to the neurosurgical procedure, the gene therapy vector, or the expression of neurturin in the Parkinson's disease brain.
The company also reported the results of analyses of neurturin gene expression in the brains from two CERE-120 treated subjects who died of causes unrelated to treatment. These analyses revealed that CERE-120 produced clear evidence of neurturin expression in the targeted putamen but no evidence for transport of this protein to the cell bodies of the degenerating neurons, located in the substantia nigra. In addition to the known cell loss in Parkinson's disease, these findings suggest that deficient axonal transport in degenerating nigrostriatal neurons in advanced Parkinson's disease impaired transport of CERE-120 and/or neurturin from putaminal terminals to nigral cell bodies, reducing the bioactivity of CERE-120. The data were presented today at the American Society of Gene Therapy Meeting in San Diego, CA by Raymond T. Bartus, Ph.D., Ceregene's executive vice president and chief scientific officer.
"While we were disappointed that our initial analysis of the data from this trial did not demonstrate a benefit of CERE-120 in the primary endpoint at 12 months, we are greatly encouraged by both the results of these protocol-prescribed analyses in patients who remained blinded for up to 18 months, as well as by the insight we gained," stated Dr. Bartus. "Collectively, these data suggest that CERE-120 is indeed exerting a unique and potentially important biological effect on the degenerating dopamine neurons in moderately advanced Parkinson's disease patients but that the inability of these neurons to efficiently transport neurturin back to their cell bodies compromises and delays the neurotrophic effects of neurturin in a manner that had not been anticipated. Importantly, we believe that we can overcome the transport problems of these degenerating neurons by modifying the dosing paradigm to also directly target their cell bodies in the substantia nigra with CERE-120."
"We remain optimistic that CERE-120 has the potential to significantly improve the treatment of advanced Parkinson's disease patients," stated Jeffrey M. Ostrove, Ph.D., president and chief executive officer of Ceregene. "The information gained from this initial controlled Phase 2 trial in advanced Parkinson's disease patients has been invaluable, and we can now incorporate these insights in a follow-on clinical trial that we are planning to initiate later this year. Our goal remains to significantly improve the symptoms of Parkinson's patients and also to provide the opportunity to delay further disease progression."
About Phase 2 Trial of CERE-120
Ceregene's Phase 2 trial was a double-blind, controlled clinical trial that completed enrollment of 58 patients with advanced Parkinson's disease in October 2007. This study was launched after successful execution of an extensive nonclinical program and preliminary evidence of safety and efficacy in advanced Parkinson's patients via an open-label Phase 1 trial in 12 patients. Patients in the Phase 2 trial were enrolled across nine leading academic medical centers in the United States, with two thirds of patients receiving CERE-120 and one third enrolled into a control group. Patients received a single administration of CERE-120 via stereotactic neurosurgery to deliver the drug into the putamen region of the brain and were followed for a minimum of 12 months for safety and efficacy, with over half the subjects followed for 15 to 18 months under blinded conditions, allowing longer-term analyses of the therapeutic effects of CERE-120. Ceregene gratefully acknowledges the financial support received from the Michael J. Fox Foundation for Parkinson's Research to help defray some of the costs of the CERE-120 Phase 1 and Phase 2 clinical trials.
About CERE-120 and its Application to Treating Parkinson's Disease
CERE-120 is composed of an adeno-associated virus (AAV) vector carrying the gene for neurturin, a naturally occurring protein known to repair damaged and dying dopamine-secreting neurons, keeping them alive and restoring normal function. Neurturin is a member of the same protein family as glial cell-derived neurotrophic factor (GDNF). The two molecules have similar pharmacological properties, and both have been shown to benefit the midbrain dopamine neurons that degenerate in Parkinson's disease. Degeneration of these neurons is responsible for the major motor impairments of Parkinson's disease. CERE-120 has been delivered by stereotactic injection to the terminal fields (i.e., the ends of the degenerating neurons), located in an area of the brain called the putamen. The cell bodies for these same neurons are located in a different area of the brain, called the substantia nigra. Once CERE-120 is delivered to the brain, it provides stable, long-lasting expression of neurturin in a highly targeted fashion. Genzyme Corporation (Nasdaq: GENZ) has licensed the ex-North American rights for the development and commercialization of CERE-120 from Ceregene, an agreement that was announced in June 2007.
About Parkinson's Disease
Parkinson's disease is a progressive movement disorder that affects a million people in the United States. Its main symptoms, stiffness, tremors and slowed movements and gait, are caused by a loss of dopamine-containing nerve cells in the substantia nigra, which project their axons to the putamen. Dopamine is a neurotransmitter involved in controlling movement and coordination, so Parkinson's patients exhibit a progressive inability to initiate and control physical movements. There is currently no treatment that can reverse the degeneration of these neurons, let alone cure Parkinson's disease.
About Ceregene
Ceregene, Inc. is a San Diego-based biotechnology company focused on the delivery of nervous system growth (neurotrophic) factors for the treatment of neurodegenerative and retinal disorders using gene delivery. Ceregene's clinical programs include CERE-110, an AAV2 based vector expressing nerve growth factor that is currently in a multi-center, controlled Phase 2 study for the treatment of Alzheimer's disease, and CERE-120 (AAV2-Neurturin) for Parkinson's disease. CERE-135 and CERE-140 are in preclinical development for ALS (Lou Gehrig's disease) and ocular disorders, respectively. Ceregene was launched in January 2001. The company's investors include Alta Partners, MPM Capital, Investor Growth Capital and Cell Genesys, Inc. (Nasdaq: CEGE) as well as Hamilton BioVentures and California Technology Partners.
source:
The additional, protocol-prescribed analyses reported today focused on further analyses of the data from the 30 subjects who continued to be evaluated under double-blind conditions for up to 18 months which indicate increasing effects of CERE-120 over time. A clinically modest but statistically significant treatment effect in the primary efficacy measure (UPDRS motor off; p=0.025), as well as similar effects on several more secondary motor measures (p<0.05), were seen at the 18 month endpoint. Not a single measure similarly favored sham surgery at either the 12 month or 18 month time points. Additionally, CERE-120 appears safe when administered to advanced Parkinson's disease patients, with no significant concerns related to the neurosurgical procedure, the gene therapy vector, or the expression of neurturin in the Parkinson's disease brain.
The company also reported the results of analyses of neurturin gene expression in the brains from two CERE-120 treated subjects who died of causes unrelated to treatment. These analyses revealed that CERE-120 produced clear evidence of neurturin expression in the targeted putamen but no evidence for transport of this protein to the cell bodies of the degenerating neurons, located in the substantia nigra. In addition to the known cell loss in Parkinson's disease, these findings suggest that deficient axonal transport in degenerating nigrostriatal neurons in advanced Parkinson's disease impaired transport of CERE-120 and/or neurturin from putaminal terminals to nigral cell bodies, reducing the bioactivity of CERE-120. The data were presented today at the American Society of Gene Therapy Meeting in San Diego, CA by Raymond T. Bartus, Ph.D., Ceregene's executive vice president and chief scientific officer.
"While we were disappointed that our initial analysis of the data from this trial did not demonstrate a benefit of CERE-120 in the primary endpoint at 12 months, we are greatly encouraged by both the results of these protocol-prescribed analyses in patients who remained blinded for up to 18 months, as well as by the insight we gained," stated Dr. Bartus. "Collectively, these data suggest that CERE-120 is indeed exerting a unique and potentially important biological effect on the degenerating dopamine neurons in moderately advanced Parkinson's disease patients but that the inability of these neurons to efficiently transport neurturin back to their cell bodies compromises and delays the neurotrophic effects of neurturin in a manner that had not been anticipated. Importantly, we believe that we can overcome the transport problems of these degenerating neurons by modifying the dosing paradigm to also directly target their cell bodies in the substantia nigra with CERE-120."
"We remain optimistic that CERE-120 has the potential to significantly improve the treatment of advanced Parkinson's disease patients," stated Jeffrey M. Ostrove, Ph.D., president and chief executive officer of Ceregene. "The information gained from this initial controlled Phase 2 trial in advanced Parkinson's disease patients has been invaluable, and we can now incorporate these insights in a follow-on clinical trial that we are planning to initiate later this year. Our goal remains to significantly improve the symptoms of Parkinson's patients and also to provide the opportunity to delay further disease progression."
About Phase 2 Trial of CERE-120
Ceregene's Phase 2 trial was a double-blind, controlled clinical trial that completed enrollment of 58 patients with advanced Parkinson's disease in October 2007. This study was launched after successful execution of an extensive nonclinical program and preliminary evidence of safety and efficacy in advanced Parkinson's patients via an open-label Phase 1 trial in 12 patients. Patients in the Phase 2 trial were enrolled across nine leading academic medical centers in the United States, with two thirds of patients receiving CERE-120 and one third enrolled into a control group. Patients received a single administration of CERE-120 via stereotactic neurosurgery to deliver the drug into the putamen region of the brain and were followed for a minimum of 12 months for safety and efficacy, with over half the subjects followed for 15 to 18 months under blinded conditions, allowing longer-term analyses of the therapeutic effects of CERE-120. Ceregene gratefully acknowledges the financial support received from the Michael J. Fox Foundation for Parkinson's Research to help defray some of the costs of the CERE-120 Phase 1 and Phase 2 clinical trials.
About CERE-120 and its Application to Treating Parkinson's Disease
CERE-120 is composed of an adeno-associated virus (AAV) vector carrying the gene for neurturin, a naturally occurring protein known to repair damaged and dying dopamine-secreting neurons, keeping them alive and restoring normal function. Neurturin is a member of the same protein family as glial cell-derived neurotrophic factor (GDNF). The two molecules have similar pharmacological properties, and both have been shown to benefit the midbrain dopamine neurons that degenerate in Parkinson's disease. Degeneration of these neurons is responsible for the major motor impairments of Parkinson's disease. CERE-120 has been delivered by stereotactic injection to the terminal fields (i.e., the ends of the degenerating neurons), located in an area of the brain called the putamen. The cell bodies for these same neurons are located in a different area of the brain, called the substantia nigra. Once CERE-120 is delivered to the brain, it provides stable, long-lasting expression of neurturin in a highly targeted fashion. Genzyme Corporation (Nasdaq: GENZ) has licensed the ex-North American rights for the development and commercialization of CERE-120 from Ceregene, an agreement that was announced in June 2007.
About Parkinson's Disease
Parkinson's disease is a progressive movement disorder that affects a million people in the United States. Its main symptoms, stiffness, tremors and slowed movements and gait, are caused by a loss of dopamine-containing nerve cells in the substantia nigra, which project their axons to the putamen. Dopamine is a neurotransmitter involved in controlling movement and coordination, so Parkinson's patients exhibit a progressive inability to initiate and control physical movements. There is currently no treatment that can reverse the degeneration of these neurons, let alone cure Parkinson's disease.
About Ceregene
Ceregene, Inc. is a San Diego-based biotechnology company focused on the delivery of nervous system growth (neurotrophic) factors for the treatment of neurodegenerative and retinal disorders using gene delivery. Ceregene's clinical programs include CERE-110, an AAV2 based vector expressing nerve growth factor that is currently in a multi-center, controlled Phase 2 study for the treatment of Alzheimer's disease, and CERE-120 (AAV2-Neurturin) for Parkinson's disease. CERE-135 and CERE-140 are in preclinical development for ALS (Lou Gehrig's disease) and ocular disorders, respectively. Ceregene was launched in January 2001. The company's investors include Alta Partners, MPM Capital, Investor Growth Capital and Cell Genesys, Inc. (Nasdaq: CEGE) as well as Hamilton BioVentures and California Technology Partners.
source:
Thursday, May 28, 2009
Former Trail Blazer opens up about Parkinson's diagnosis
After the diagnosis of early onset Parkinson's disease made Brian Grant and his wife, Gina, stop and think, he's taken a positive approach and decided to be upbeat "because that's who I am."
Ex-Trail Blazer Brian Grant is taking his battle against Parkinson's disease public. Following the example of Muhammad Ali's family and Michael J. Fox, Grant tells The Oregonian in a front page story today that he hopes talking about his diagnosis helps others.
Like a lot of folks who just lost a job, Brian Grant was feeling down.
After 12 seasons in the National Basketball Association, three with the Trail Blazers, the well-liked forward and center retired in 2006. He hoped to relax in Miami with his wife and four kids, resting from a bruising career battling bigger centers. Instead, depression settled on Grant, a gloom enhanced by an unsettling and uncontrollable shaking in his left hand.
Grant moved from Miami to the Portland area, hoping to find a job and raise his spirits. But he was afraid to go on interviews, unable to explain his tremors.
"I had a rough time," Grant says. "I kind of sat at home, wasn't exercising and picked up more weight. The more weight I put on, the worse my tremor got."
In January, Oregon Health & Science University neurologist Dr. John Nutt delivered a diagnosis that knocked Grant for a loop: Parkinson's disease, a brain disorder that slowly saps a person's ability to control their movements. While the disease is usually seen around age 60, Grant was just 36 when diagnosed.
source:
Ex-Trail Blazer Brian Grant is taking his battle against Parkinson's disease public. Following the example of Muhammad Ali's family and Michael J. Fox, Grant tells The Oregonian in a front page story today that he hopes talking about his diagnosis helps others.
Like a lot of folks who just lost a job, Brian Grant was feeling down.
After 12 seasons in the National Basketball Association, three with the Trail Blazers, the well-liked forward and center retired in 2006. He hoped to relax in Miami with his wife and four kids, resting from a bruising career battling bigger centers. Instead, depression settled on Grant, a gloom enhanced by an unsettling and uncontrollable shaking in his left hand.
Grant moved from Miami to the Portland area, hoping to find a job and raise his spirits. But he was afraid to go on interviews, unable to explain his tremors.
"I had a rough time," Grant says. "I kind of sat at home, wasn't exercising and picked up more weight. The more weight I put on, the worse my tremor got."
In January, Oregon Health & Science University neurologist Dr. John Nutt delivered a diagnosis that knocked Grant for a loop: Parkinson's disease, a brain disorder that slowly saps a person's ability to control their movements. While the disease is usually seen around age 60, Grant was just 36 when diagnosed.
source:
Conejo team to ride in LA Bike Tour for Parkinson's disease research
By Rachel McGrath
Conejo Valley residents Jessica Chadbourn and Debbie Jew are gearing up for a 22-mile ride on a bicycle made for two at this year’s L.A. Marathon.
The pair has registered to take part in the Acura LA Bike Tour, which is part of the L.A. Marathon and begins at 5 a.m. in downtown Los Angeles onMonday, Memorial Day, ahead of the big race.
The women will be raising money for Team Parkinson, a nonprofit organization that raises funds for research to find a cure for Parkinson’s disease.
The idea of riding a tandem in the event came after Chadbourn and Jew learned how research showed that the use of a two-seater bicycle can help people suffering from Parkinson’s disease.
“Research showed that by having a person in front and a person with Parkinson’s in the back, (riding a tandem) reduced symptoms and reduced the sufferer’s shakiness,” Chadbourn said.
“We also saw it as a metaphor for going through life,” she said. “Everybody needs a little help, and there’s power in numbers.”
Chadbourn, 46, a freelance writer who lives in Westlake Village, and Jew, 48, an accountant from Thousand Oaks, acknowledge a 22-mile tandem bike ride is a fairly daunting challenge. They’ve been preparing by spending their Saturday and Sunday mornings training along the Ventura-to-Ojai bike path. They say it’s taken some time to get used to being a two-person team.
“I’m the front person,” Chadbourn said, “but she, Debbie, is a back seat driver. I go where she tells me.”
Jew says communication is the key to a successful tandem ride.
“We motivate each other,” she said.
Chadbourn began raising awareness and money for Parkinson’s research about eight years ago after her uncle and her brother-in-law were diagnosed with the disease. She says that while cancer and AIDS have huge fundraising and research efforts behind them, Parkinson’s disease received less attention until actor Michael J. Fox revealed he had it and “unwittingly became the poster boy for it.”
Chadbourn and Jew met at a Parkinson’s fundraiser in Westlake Village two years ago and immediately hit it off. Jew says she’s in awe of Chadbourn’s advocacy for the disease. Chadbourn says she’s in awe of Jew’s dynamism and motivation.
Together, “The Dynamic Duo,” as they call themselves, have raised almost $12,000 in pledged sponsorship for the LA Bike Tour and are hoping to increase that during this last week before the event.
“We’re still working hard to raise more, and we’re just knocking on doors,” Jew said.
source:
Conejo Valley residents Jessica Chadbourn and Debbie Jew are gearing up for a 22-mile ride on a bicycle made for two at this year’s L.A. Marathon.
The pair has registered to take part in the Acura LA Bike Tour, which is part of the L.A. Marathon and begins at 5 a.m. in downtown Los Angeles onMonday, Memorial Day, ahead of the big race.
The women will be raising money for Team Parkinson, a nonprofit organization that raises funds for research to find a cure for Parkinson’s disease.
The idea of riding a tandem in the event came after Chadbourn and Jew learned how research showed that the use of a two-seater bicycle can help people suffering from Parkinson’s disease.
“Research showed that by having a person in front and a person with Parkinson’s in the back, (riding a tandem) reduced symptoms and reduced the sufferer’s shakiness,” Chadbourn said.
“We also saw it as a metaphor for going through life,” she said. “Everybody needs a little help, and there’s power in numbers.”
Chadbourn, 46, a freelance writer who lives in Westlake Village, and Jew, 48, an accountant from Thousand Oaks, acknowledge a 22-mile tandem bike ride is a fairly daunting challenge. They’ve been preparing by spending their Saturday and Sunday mornings training along the Ventura-to-Ojai bike path. They say it’s taken some time to get used to being a two-person team.
“I’m the front person,” Chadbourn said, “but she, Debbie, is a back seat driver. I go where she tells me.”
Jew says communication is the key to a successful tandem ride.
“We motivate each other,” she said.
Chadbourn began raising awareness and money for Parkinson’s research about eight years ago after her uncle and her brother-in-law were diagnosed with the disease. She says that while cancer and AIDS have huge fundraising and research efforts behind them, Parkinson’s disease received less attention until actor Michael J. Fox revealed he had it and “unwittingly became the poster boy for it.”
Chadbourn and Jew met at a Parkinson’s fundraiser in Westlake Village two years ago and immediately hit it off. Jew says she’s in awe of Chadbourn’s advocacy for the disease. Chadbourn says she’s in awe of Jew’s dynamism and motivation.
Together, “The Dynamic Duo,” as they call themselves, have raised almost $12,000 in pledged sponsorship for the LA Bike Tour and are hoping to increase that during this last week before the event.
“We’re still working hard to raise more, and we’re just knocking on doors,” Jew said.
source:
Wednesday, May 27, 2009
Man-made polymer promises Parkinson's palliative
Researchers at ANSTO have discovered that a protein, Alpha-Synuclein, which plays a role in the development of Parkinson’s disease when it behaves abnormally, can be controlled with a man-made polymer, dendrimer, also known as a ‘dense star’ polymer.
ANSTO Researcher, Dr Agata Rekas, said that past research had shown the dendrimer – called a PAMAM dendrimer and made by Dendirtech Inc - had positively affected a peptide involved in Alzheimer’s disease (ABeta) and a prion peptide. So Dr Rekas and Dr Seok Il Yun, an ANSTO Post Doctoral fellow, decided to see if it had a similar effect on Parkinson’s disease, which affects around one in 250 Australians.
“As all these diseases affect the brain and neuronal pathways in the body we anticipated the dendrimer’s effect would be similar, and we were right,” said Rekas.
“The Alpha-Synuclein protein is a natural protein in the body but when it aggregates into fibrils, long insoluble strings of protein molecules stuck together, it affects transmissions to the brain, resulting in Parkinson’s disease,” Dr Rekas said. “No one is sure of the protein’s normal role but we believe it assists cognitive function.
“It is thought that the aggregation is triggered by a dopamine3 deficiency and causes deposits in the brain to occur, however this could be just a factor, not the complete cause, of the disease,” she said. “There is still much to find out, but it’s all part of the puzzle. The exciting part of our results is that it most definitely provides further information as to how this dendrimer can contribute to developing better therapeutics for Parkinson’s disease,” she said.
A dendrimer is spherical in shape and contains chemical groups similar to those of proteins, which start branching out in the middle so the dendrimer increased in size as each layer was added, similar to the branch-like structures seen in snow flakes.
“The more layers in the dendrimer the more effective it was due to the larger surface area. In the experiments we put certain amounts of these dendrimers and a control, with no dendrimers, into a protein solution for over 120 hours and stimulated aggregation with heat and shaking,” she explained. “The control measured a lot of fibrils and different dendrimers reduced this fibrillar growth to various extents.
“We used an electron microscope to look at what was physically happening and verified the results using small angle neutron scattering, where a neutron beam passes through the sample onto a detector giving information as to what’s occurring at the molecular level," she said.
“The results clearly showed that the larger dendrimer inhibited the abnormal activity of the protein best. This information can now be used by drug companies focussed on treating Parkinson’s so the next stage would be for such companies to develop this research further,” said Rekas.
source:
ANSTO Researcher, Dr Agata Rekas, said that past research had shown the dendrimer – called a PAMAM dendrimer and made by Dendirtech Inc - had positively affected a peptide involved in Alzheimer’s disease (ABeta) and a prion peptide. So Dr Rekas and Dr Seok Il Yun, an ANSTO Post Doctoral fellow, decided to see if it had a similar effect on Parkinson’s disease, which affects around one in 250 Australians.
“As all these diseases affect the brain and neuronal pathways in the body we anticipated the dendrimer’s effect would be similar, and we were right,” said Rekas.
“The Alpha-Synuclein protein is a natural protein in the body but when it aggregates into fibrils, long insoluble strings of protein molecules stuck together, it affects transmissions to the brain, resulting in Parkinson’s disease,” Dr Rekas said. “No one is sure of the protein’s normal role but we believe it assists cognitive function.
“It is thought that the aggregation is triggered by a dopamine3 deficiency and causes deposits in the brain to occur, however this could be just a factor, not the complete cause, of the disease,” she said. “There is still much to find out, but it’s all part of the puzzle. The exciting part of our results is that it most definitely provides further information as to how this dendrimer can contribute to developing better therapeutics for Parkinson’s disease,” she said.
A dendrimer is spherical in shape and contains chemical groups similar to those of proteins, which start branching out in the middle so the dendrimer increased in size as each layer was added, similar to the branch-like structures seen in snow flakes.
“The more layers in the dendrimer the more effective it was due to the larger surface area. In the experiments we put certain amounts of these dendrimers and a control, with no dendrimers, into a protein solution for over 120 hours and stimulated aggregation with heat and shaking,” she explained. “The control measured a lot of fibrils and different dendrimers reduced this fibrillar growth to various extents.
“We used an electron microscope to look at what was physically happening and verified the results using small angle neutron scattering, where a neutron beam passes through the sample onto a detector giving information as to what’s occurring at the molecular level," she said.
“The results clearly showed that the larger dendrimer inhibited the abnormal activity of the protein best. This information can now be used by drug companies focussed on treating Parkinson’s so the next stage would be for such companies to develop this research further,” said Rekas.
source:
Learning to live with life-changing illness
DETERMINED Jeanette Sharp has refused to let Parkinson’s Disease stop her from living a normal life – despite being diagnosed at just 42.
The mother-of-two, now 49, discovered she had the condition following a brain scan and, together with her husband, family and friends, has fought back.
She takes 17 tablets a day to control the disease, but has refused to let it beat her.
Jeanette still works at Eastwood Primary School, where she used to help children with their handwriting as a learning support assistant.
She said: “My handwriting was getting smaller and smaller and I couldn’t do this anymore.
“I tried to leave the school, but they have been really supportive and I now work in the office.
“If I had given up work, it would have done more harm than good. You have to live a normal life.
“It is still difficult to do some things.
“You really have to concentrate when you walk, thinking left, right, left, right.
“The tablets help a lot, but I couldn’t be doing this without the support of my family. “ Jeanette, of Dulverton Avenue, Westcliff, admits there have been some tough times.
She said: “It was a shock when I was diagnosed. I had gone to see my GP with a problem with my arm and he referred me to a specialist.
“I have never been ill all my life, but this isn’t an illness, it is a condition.
“People can’t see anything wrong with you and sometimes don’t understand when you can’t do something.
“I don’t like going to the supermarket because you have to stand in queues and my face often looks stiff and vacant.
“It’s silly things like that which get to you.”
About 10,000 people are diagnosed each year with the condition, but it is more common in people over 50.
Parkinson’s affects nerve cells which produce a chemical called dopamine. This chemical allows messages to be sent to co-ordinate movement.
Actor Michael J Fox and boxer Muhammad Ali also both suffer with the disease. It leads to problems with movement such as writing and walking.
Husband Gary, 48, said: “Jeanette was shocked when the doctors told her. We both always thought the disease is something older people get.
“They put Jeanette on medication straight away, which helped a lot. If you took the tablets away you would notice the difference.
“She doesn’t get the tremors, but she does have a lot of stiffness. There is a noticeable change in her face as well, but really Parkinson’s restricts her movement.
“We have had a lot of support from the society. Jeanette struggles to open bottle tops and buttons.
“But I found I was helping too much to start with. I would take over and do things before she even had a chance to do them and she found that frustrating.
“I had to learn to let her lead her life and help if she asked for it.”
Because of the support the couple have had from the Parkinson’s Disease Society, they have pledged to raise funds for the organisation.
In October, Gary will be flying out to Beijing for a five-day trek along the Great Wall of China.
Gary added: “They have been terrific.”
source:
The mother-of-two, now 49, discovered she had the condition following a brain scan and, together with her husband, family and friends, has fought back.
She takes 17 tablets a day to control the disease, but has refused to let it beat her.
Jeanette still works at Eastwood Primary School, where she used to help children with their handwriting as a learning support assistant.
She said: “My handwriting was getting smaller and smaller and I couldn’t do this anymore.
“I tried to leave the school, but they have been really supportive and I now work in the office.
“If I had given up work, it would have done more harm than good. You have to live a normal life.
“It is still difficult to do some things.
“You really have to concentrate when you walk, thinking left, right, left, right.
“The tablets help a lot, but I couldn’t be doing this without the support of my family. “ Jeanette, of Dulverton Avenue, Westcliff, admits there have been some tough times.
She said: “It was a shock when I was diagnosed. I had gone to see my GP with a problem with my arm and he referred me to a specialist.
“I have never been ill all my life, but this isn’t an illness, it is a condition.
“People can’t see anything wrong with you and sometimes don’t understand when you can’t do something.
“I don’t like going to the supermarket because you have to stand in queues and my face often looks stiff and vacant.
“It’s silly things like that which get to you.”
About 10,000 people are diagnosed each year with the condition, but it is more common in people over 50.
Parkinson’s affects nerve cells which produce a chemical called dopamine. This chemical allows messages to be sent to co-ordinate movement.
Actor Michael J Fox and boxer Muhammad Ali also both suffer with the disease. It leads to problems with movement such as writing and walking.
Husband Gary, 48, said: “Jeanette was shocked when the doctors told her. We both always thought the disease is something older people get.
“They put Jeanette on medication straight away, which helped a lot. If you took the tablets away you would notice the difference.
“She doesn’t get the tremors, but she does have a lot of stiffness. There is a noticeable change in her face as well, but really Parkinson’s restricts her movement.
“We have had a lot of support from the society. Jeanette struggles to open bottle tops and buttons.
“But I found I was helping too much to start with. I would take over and do things before she even had a chance to do them and she found that frustrating.
“I had to learn to let her lead her life and help if she asked for it.”
Because of the support the couple have had from the Parkinson’s Disease Society, they have pledged to raise funds for the organisation.
In October, Gary will be flying out to Beijing for a five-day trek along the Great Wall of China.
Gary added: “They have been terrific.”
source:
Friday, May 22, 2009
Medtronic Announces FDA Approval of Two Deep Brain Stimulation Devices That Offer Programming Advances and New Tools for Patients with Movement Disord
Medtronic, Inc. (NYSE: MDT) today announced U.S. Food and Drug Administration (FDA) approval of Activa® RC and Activa PC, the most innovative deep brain stimulation (DBS) devices available for the treatment of the symptoms of advanced Parkinson’s disease and essential tremor. Medtronic DBS Therapy delivers small electrical pulses to precisely targeted areas within one or both sides of the brain to help patients achieve greater control over disabling body movements. The new devices will be available in the United States in June.
Both Activa RC and Activa PC devices provide bi-lateral stimulation (to both sides of the brain) and offer a more advanced approach to device programming, and additional tools for capturing history relevant to the patient’s therapy. New programming options provide greater ability to fine tune the stimulation field and give patients more options to optimize their settings compared to previous DBS devices. Additionally, information about patient symptoms and side effects can be stored in the device, which is helpful to physicians in determining the best programming settings for each patient.
These next generation devices also have a hand-held patient programmer, which features new advancements, including an LCD screen that provides valuable information such as the level of battery charge. The programmer allows patients to alternate between stimulation settings pre-programmed by their clinician so they can customize their therapy based on their activity.
"The Activa RC and Activa PC devices offer exciting new programming features that can further enhance the therapeutic benefit of deep brain stimulation for patients with Parkinson’s disease and other movement disorders,” said Leo Verhagen, M.D., Ph.D., medical director of the Surgery Program for Movement Disorders at Rush University Medical Center, Chicago. "This advanced technology will offer more programming features that allow doctors to optimize stimulation effects and also provide options for patients to better control and monitor their therapy settings. For appropriate patients who require high energy settings on their DBS devices, the rechargeable device (Activa RC) may eliminate the need for frequent battery changes.”
Activa PC is powered by a primary cell (non-rechargeable) battery that does not require any regular maintenance from the patient to provide continuous stimulation for multiple years. The Activa PC neurostimulator represents a 20 percent reduction in size and weight compared to previous bi-lateral devices and has similar battery life.
Activa RC is the first and only rechargeable DBS neurostimulator in the world and lasts for nine years before replacement is necessary. Patients need to recharge the device at home on a regular basis depending on their stimulation settings. Activa RC, also significantly smaller than previous bi-lateral devices, is expected to be used for select patients who have high-energy stimulation requirements.
Both Activa RC and Activa PC were approved in Europe in August 2008. Activa PC has become the most widely used device in Europe for bi-lateral DBS therapy.
"Activa RC and Activa PC expand our family of DBS therapy devices to give patients and physicians the flexibility they need to customize a successful DBS treatment program to manage the debilitating symptoms of movement disorders like Parkinson’s disease and essential tremor,” said Richard E. Kuntz, M.D., president of the Neuromodulation business and senior vice president at Medtronic. "These devices also accentuate Medtronic’s place as the long-time pioneer and leader in neuromodulation technology, represented by the only commercially available DBS therapy system in the United States, 20 years of DBS experience, and an ongoing commitment to further pursuit of technological innovations to improve the lives of patients.”
About Medtronic DBS Therapy
Medtronic launched DBS in the United States in 1997 for the treatment of essential and Parkinson’s tremor. Since the initial launch of DBS therapy, the list of indications has grown to include management of the symptoms of advanced Parkinson’s disease (approved in 2002), dystonia (approved under a humanitarian device exemption (HDE) in 2003), and obsessive compulsive disorder (approved under an HDE in 2009). To date, more than 60,000 people worldwide have received Medtronic DBS therapy.
The DBS therapy system consists of implantable and external components. Implanted components of the system include the lead, which is a thin coiled wire with electrodes on the end that are placed in a specific target in the brain; the extension wire to connect the lead to the neurostimulator; and the neurostimulator, which, similar to a pacemaker, is placed beneath the skin in the chest and produces the tiny electrical pulses that are believed to block abnormal brain function that causes disabling movements.
External components of the system:
- Physician programmer: the physician programmer (N-Vision®) is used to adjust stimulation programming settings. The electrical pulses can be non-invasively adjusted by a clinician using the physician programmer and transmitted via radio telemetry to the implanted neurostimulator.
- Patient programmer: the hand-held programmer is used by the patient to turn the neurostimulator off or on, check the battery status, or choose their stimulation settings within a range of options preset by the physician.
- Activa RC utilizes a wearable charging system which includes the patient controller, recharge antenna, and belt to hold the components in place while re-charging. A patient can move about while recharging, which typically takes a couple of hours every two weeks.
Medtronic’s Leadership in DBS
Medtronic, in collaboration with leading physicians around the world, pioneered DBS therapy. The company has been involved in more than 1,500 clinical studies and continues to pursue additional studies today to evaluate the promise of this therapy for other chronic, debilitating neurological conditions.
About Medtronic
Medtronic, Inc. (www.medtronic.com), headquartered in Minneapolis, is the global leader in medical technology – alleviating pain, restoring health and extending life for millions of people around the world.
Thursday, May 21, 2009
Deep brain stimulation advancing as a treatment for Parkinson's disease
THE SPECIALIST: DR. RON ALTERMAN ON PARKINSON’S DISEASE AND DEEP BRAIN STIMULATION
As the director of functional and restorative neuro-surgery at Mount Sinai, Alterman performs minimally invasive operations that seek to normalize brain activity. One of these surgeries, deep brain stimulation (DBS), involves implanting electrodes to treat disorders such as tremors, Parkinson’s disease and dystonia.
THE BIG STORY:
This year, the Journal of the American Medical Association published the results of a large study done in the VA system comparing Parkinson’s patients who received the best drug treatments to patients who received deep brain stimulation. “The patients who received surgery did better than the patients who did not,” says Alterman. “This randomized, double-blind trial is the best proof we have that surgery does a better job than medicine alone when treating some PD patients.”
WHO’S AT RISK:
Upwards of 1 million Americans are living with Parkinson’s disease, a chronic, progressive illness that affects the nervous system and impairs movement. “Basically everybody in the general population is at risk,” says Alterman. “Parkinson’s is the second most common neurodegenerative disease in humans, after Alzheimer’s.” The major risk factor is age. “The average age of onset in the U.S. is 62 — though as we know from Michael J. Fox, people can develop it at a younger age,” says Alterman. Men are at a slightly higher risk than woman.
The symptoms mostly result from a lack of dopamine, a chemical messenger, in the brain. This occurs when the brain cells that make dopamine die or cease to function. No one has been able to identify the root cause, however. Parkinson’s has been associated with rural living, so some hypothesize that well water or other environmental factors may put people at risk.
SIGNS AND SYMPTOMS:
The disease develops gradually. “The cardinal features of Parkinson’s are tremor, stiffness (doctors call it rigidity) and bradykinesia, which refers to slowed movements,” says Alterman. “But one doesn’t have to have all three symptoms to be diagnosed.” As Parkinson’s progresses, it can lead to problems with walking, balance, sleeping and memory, which can look a lot like Alzheimer’s.
Patients and family members often notice that the symptoms are worse on one side of the body than the other. “The disease usually affects both sides of the body, but in an asymmetric way,” says Alterman. “It tends to start on one side, and that side typically remains worse than the other.”
Read more: "Deep brain stimulation advancing as a treatment for Parkinson's disease" - http://www.nydailynews.com/lifestyle/health/2009/05/19/2009-05-19_deep_brain_stimulation_advancing_as_a_treatment_for_parkinsons_disease.html#ixzz0G9JdJ90Q&A
Tuesday, May 12, 2009
Fish Oil Protects Against Diseases Like Parkinson's
Dr. Nicolas Bazan, Director of the Neuroscience Center of Excellence, Boyd Professor, and Ernest C. and Yvette C. Villere Chair of Retinal Degenerative Diseases Research at LSU Health Sciences Center New Orleans, will present new research findings showing that an omega three fatty acid in the diet protects brain cells by preventing the misfolding of a protein resulting from a gene mutation in neurodegenerative diseases like Parkinson's and Huntington's.
He will present these findings for the first time on April 19, 2009 at the Ernest N. Morial Convention Center, Nouvelle C Room, at the American Society for Nutrition, Experimental Biology 2009 Annual Meeting.
With funding from the National Eye Institute of the National Institutes of Health, Dr. Bazan and his colleagues developed a cell model with a mutation of the Ataxin-1 gene. The defective Ataxin-1 gene induces the misfolding of the protein produced by the gene. These misshapened proteins cannot be properly processed by the cell machinery, resulting in tangled clumps of toxic protein that eventually kill the cell. Spinocerebellar Ataxia, a disabling disorder that affects speech, eye movement, and hand coordination at early ages of life, is one disorder resulting from the Ataxin-1 misfolding defect. The research team led by Dr. Bazan found that the omega three fatty acid, docosahexaenoic acid (DHA), protects cells from this defect.
Dr. Bazan's laboratory discovered earlier that neuroprotectin D1 (NPD1), a naturally-occurring molecule in the human brain that is derived from DHA also promotes brain cell survival. In this system NPD1 is capable of rescue the dying cells with the pathological type of Ataxin-1, keeping their integrity intact.
"These experiments provide proof of principle that neuroprotectin D1 can be applied therapeutically to combat various neurodegenerative diseases," says Dr. Bazan. "Furthermore, this study provides the basis of new therapeutic approaches to manipulate retinal pigment epithelial cells to be used as a source of NPD1 to treat patients with disorders characterized by this mutation like Parkinson's, Retinitis Pigmentosa and some forms of Alzheimer's Disease."
source:
Parkinson's Partially Linked to Pesticides
UCLA researchers have provided strong new evidence linking at least some cases of Parkinson's disease to exposure to pesticides. Researchers have suspected for some time that pesticides may cause the neurodegenerative disorder, and experiments in animals have shown that the chemicals, particularly the fungicide maneb and the herbicide paraquat, can cause Parkinson-like symptoms in animals. But proving it in humans has been difficult because of problems in assessing exposure to the agents.
Parkinson's is a disorder of the central nervous system that often impairs the sufferer's motor skills, speech and other functions. It is not fatal of itself, but complications often are. The disease has been recognized since the Middle Ages but became more prevalent in the 20th century. As many as 180 of every 100,000 Americans develop it.
To explore a potential connection to pesticides, epidemiologist Beate Ritz of UCLA and her graduate student Sadie Costello, now at UC Berkeley, studied public records of pesticide applications in California's Central Valley from 1974 to 1999. Every application of pesticides to crops must be registered with the state. Working with Myles Cockburn of USC, they developed a tool to estimate pesticide exposure in areas immediately adjacent to the fields.
They then identified 368 longtime residents who lived within 500 yards of fields where the chemicals had been sprayed and compared them to 341 carefully matched controls who did not live near the fields.
They reported in the current issue of the American Journal of Epidemiology that people who lived next to fields where maneb or paraquat had been sprayed were, on average, about 75% more likely to develop the disease. But those who developed the early-onset form of the disease -- contracting it before the age of 60 -- had double the risk of contracting it if they were exposed to either maneb or paraquat alone and four times the risk if they were exposed to both. In most cases, the exposure occurred years before the onset of the disease. Exposure to other pesticides did not appreciably alter the risk.
"The results confirmed two previous observations from animal studies," Ritz said. "One, that exposure to multiple chemicals may increase the effect of each chemical. That's important, since humans are often exposed to more than one pesticide in the environment. And second, that the timing of the exposure is also important."
-- Thomas H. Maugh II
source: http://latimesblogs.latimes.com/booster_shots/2009/04/parkinsons-partially-linked-to-pesticides.html
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