Parkinson's progression with times? Open Forum

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teokimhoeJoined: 03 Mar 2007Posts: 23Location: Malaysia
Posted: Sat Oct 13, 2007 8:29 pm Post subject: parkinson's progression with times

Do you agree that Parkinson's progression with time?

Despites there are new medications i.e one, second and third lines for Parkinson's treatment there are still no way to stop it's progression with time. Is it a shame for the medical world? Yes ,Parkinson's progression with times is individual and some come earlier or later. Nobody could tell you even doctors themselve could not .

The Parkinson's progression aggravates any part of body movement and emotional mood.

Exercise is not the treatment and the medication too. Both are helpful to relieve your muscles stiffness and emotional disorders i.e motor and non motor symdome. Do you agree?

TEOKIMHOE

to help the PD patients aware the diseases and encourage to set up support groups to educate the patients and their immediate families
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cowboyJoined: 03 Oct 2007Posts: 68
Posted: Sun Oct 14, 2007 11:45 am Post subject:

Yes, I agree with you Teokimhoe. It is a shame. There is, lately though, some promising treatment and new diagnostic aids on the horizon. I believe Altropane SPECT will allow physicians to more accurately diagnose Parkinson's much quicker and at a fraction of the cost compared to PET. I believe some of the new non-dopamine type drugs that are now gaining excitement among scientists will all but cure Parkinson's in the next 20 years. Asridipine (spelling?) alone has had really great results for some during it's testing (still in progress). Exercise and "mind activity" certainly help.
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Joe or BobJoined: 12 Aug 2007Posts: 38
Posted: Sun Oct 14, 2007 12:19 pm Post subject:

The primary fault in Parkinson's Disease is the insufficient formation of dopamine. That is why L-dopa initially relieves it. Parkinson's Disease gets progressively worse because the drugs used to treat it cause it to get worse. No substance lowers somebody's capacity to produce their own L-dopa as L-dopa does. So although L-dopa helps at first, in the long term it is a cause of Parkinson's Disease. Although dopamine agonists stimulate the dopamine receptors at first, they eventually cause the dopamine receptors to become progressively less sensitive. They make the problem worse. Unless any method increases dopamine formation it has no chance of relieving Parkinson's Disease. So none of the methods in development that don't increase dopamine have any chance of ridding it. Isradipine certainly won't be of any use. Isradipine has never benefited or been tested in Parkinson's Disease. Israpidine doesn't even in theory raise dopamine levels. It claims that it rejuvenates the cells involved in forming dopamine. However, they are being very misleading by claiming this. Israpidine alters only one aspect of the biochemistry of those cells. It doesn't rejuvenate their activity, which should be the primary aim of any treatment. Parkinson's Disease : http://viartis.net/parkinsons.disease
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cowboyJoined: 03 Oct 2007Posts: 68
Posted: Sun Oct 14, 2007 12:58 pm Post subject:

Joe or Bob, I will research Isradipine more. If you have anything more current than the information below, please provide to me. I would certainly appreciate it. Does your Viartis site discuss this in detail? I know Northwestern has a grant to complete studies. You may find some reference in the forum "Patients Like Me". One individual in this forum is taking it with great success. Additionally, one individual in our local support group has been taking for two months in trial participation and reports good results. I do not want to spew false statements though. Anything you have is appreciated. Please read below: Isradipine shown to slow down Parkinson's disease Medical Studies/Trials Published: Thursday, 14-Jun-2007 Printer Friendly Email to a Friend Northwestern University researchers have discovered a drug that slows and may even halt the progression of Parkinson's disease. The drug rejuvenates aging dopamine cells, whose death in the brain causes the symptoms of this devastating and widespread disease. D. James Surmeier, the Nathan Smith Davis Professor and chair of physiology at Northwestern University's Feinberg School of Medicine, and his team of researchers have found that isradipine, a drug widely used for hypertension and stroke, restores stressed-out dopamine neurons to their vigorous younger selves. The study is described in a feature article in the international journal Nature, which will be published on-line June 10. Dopamine is a critical chemical messenger in the brain that affects a person's ability to direct his movements. In Parkinson's disease, the neurons that release dopamine die, causing movement to become more and more difficult. Ultimately, a person loses the ability to walk, talk or pick up a glass of water. The illness is the second most common neurodegenenerative disease in the country, affecting about 1 million people. The incidence of Parkinson's disease increases with age, soaring after age 60. "Our hope is that this drug will protect dopamine neurons, so that if you began taking it early enough, you won't get Parkinson's disease, even if you were at risk. " said Surmeier, who heads the Morris K. Udall Center of Excellence for Parkinson's Disease Research at Northwestern. "It would be like taking a baby aspirin everyday to protect your heart." Isradipine may also significantly benefit people who already have Parkinson's disease. In animal models of the disease, Surmeier's team found the drug protected dopamine neurons from toxins that would normally kill them by restoring the neurons to a younger state in which they are less vulnerable. The principal therapy for Parkinson's disease patients currently is L-DOPA, which is converted in the brain to dopamine. Although L-DOPA relieves many symptoms of the disease in its early stages, the drug becomes less effective over time. As the disease progresses, higher doses of L-DOPA are required to help patients, leading to unwanted side-effects that include involuntary movements. The hope is that by slowing the death of dopamine neurons, isradipine could significantly extend the time in which L-DOPA works effectively. "If we could double or triple the therapeutic window for L-DOPA, it would be a huge advance," Surmeier said. The work by Surmeier's group is particularly exciting because nothing is known to prevent or slow the progression of Parkinson's disease. "There has not been a major advance in the pharmacological management of Parkinson's disease for 30 years," Surmeier said. Surmeier, who has researched Parkinson's disease for 20 years, had long been frustrated because it wasn't known how or why dopamine cells die in the disease. "It didn't seem like we were making much progress in spite of intense study on several fronts," he said. Because he's a physiologist, Surmeier decided to investigate whether the electrical activity of dopamine neurons might provide a clue to their vulnerability. All neurons in the brain use electrical signals to do their job, much like digital computers. First, Surmeier observed that dopamine neurons are non-stop workers called pacemakers. They generate regular electrical signals seven days a week, 24 hours a day, just like pacemaker cells in the heart. This was already known. But then he probed more deeply and discovered something very strange about these dopamine neurons. Most pacemaking neurons use sodium ions (like those found in table salt) to produce electrical signals. But Surmeier found that adult dopamine neurons use calcium instead. Sodium is a mild mannered ion that does its job without causing a whit of trouble to the cell. Calcium ions, however, are wild and rambunctious. Remember when Marlon Brando rode into town with his motorcycle gang in "The Wild One" Those guys were like calcium ions. "The reliance upon calcium was a red flag to us," Surmeier said. Calcium ions need to be chaperoned by the cell almost as soon as they enter to keep them from causing trouble, he noted. The cell has to sequester them or keep pumping them out. This takes a lot of energy. "It's a little like having a room full of two year olds you have to watch like a hawk so they don't get into trouble," Surmeier said. "That's really going to stress you." With three boys under age eleven, he can relate to the stressed dopamine neuron. Surmeier theorized that the non-stop stress on the dopamine neurons explains why they are more vulnerable to toxins and die at a more rapid rate as we age. But these findings still didn't offer him a new therapy. Then, serendipity struck when he was working on a different problem. He discovered that young dopamine neurons and adult ones have an entirely different way of operating. When the neurons are young, Surmeier found they actually use sodium ions to do their work. But as the neurons age, they become more and more dependent on the troublesome calcium and stop using sodium. This calcium dependence and the stress it causes the neurons --is what makes them more vulnerable to death. What would happen, Surmeier wondered, if he simply blocked the calcium's route into the adult neuron cells" Would the neurons revert to their youthful behavior and start using sodium again" "The cells had put away their old childhood tools in the closet. The question was if we stopped them from behaving like adults would they go into the closet and get them out again", Surmeier asked. "Sure enough, they did." When he gave the mice isradipine, it blocked the calcium from entering the dopamine neuron. At first, the dopamine neurons became silent. But within a few hours, they had reverted to their childhood ways, once again using sodium to get their work done. "This lowers the cells stress level and makes them much more resistant to any other insult that's going to come along down the road. They start acting like they're youngsters again," Surmeier said. The next step will be launching a clinical study. "This animal study suggests that calcium channel blockers, drugs currently used to reduce blood pressure, might someday be used to slow the steady progression of Parkinson's disease," said Walter J. Koroshetz, M.D., deputy director of the NINDS. http://www.northwestern.edu/
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Joe or BobJoined: 12 Aug 2007Posts: 38
Posted: Sun Oct 14, 2007 1:37 pm Post subject:

Somebody asked about this quite some time ago on the Viartis site. I have basically repeated the response that was made at the time. The article you have added provides everything of significance concerning Israpidine. Even if Israpidine was fully developed it couldn't get rid of Parkinson's Disease. Right now, there are a lot of non-dopamine methods being developed. Israpidine is one of them. Biochemically, the approaches these drugs use are so removed from the primary problem in Parkinson's Disease, that they have no chance of being of any long term use. The biochemistry involved is usually so complicated that most people, including even biochemists, don't understand it well enough to realise that that it will never lead to anything. In the meantime, the researchers and pharmaceutical companies are able to hype these drugs, raising more funding in the process. We always seem to hear from them "This could lead to....." but of course it never does.
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cowboyJoined: 03 Oct 2007Posts: 68
Posted: Sun Oct 14, 2007 4:13 pm Post subject:

Thanks for your take on this. I am a little skeptical too. Will do more study on this.
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johnball20Joined: 09 Mar 2007Posts: 96Location: Whittier, California
Posted: Sun Oct 14, 2007 7:14 pm Post subject: Isradipine and other treatments

Viartis and Cowboy, I am surprised at the assertion that Isradipine won't do anything to help slow or stop Parkinson's disease progression, You say "they have no chance of being of any long-term use." That assumes that we already know exactly why we have PD. i don't believe we as patients, or the doctors who treat us, or the scientists who are studying the underlying disease process are all that certain that there is one cause or one process at work. I believe that the underlying disease pocess affects far more than just the dopamine-producing cells or the dopamine receptors or even the dopamine transport system. It seems to me that it is a cellular decay that begins in the brain stem and moves selectively through the brain geography and will eventually reach the outer cortical layers if given sufficient time. It may result from cellular stress such as prolonged periods of anxiety, or emotional stress; from toxic stress, such as paraquat, rotennone or other biological contaminants; from misfolded proteins, from faulty genetic coding as in alpha-synuclein, or perhaps a combination of these toxic insults...At any rate there are so many varied symptoms and so many different reactions to the medications that I don't think we should rule out any potential strategy. Perhaps calcium-based processes could be replaced with sodium-based and re-invigorate the neurons. This will take time to figure out. Let's not shut off potential avenues of new thought just because it doesn't agree with our particular belief about the nature of the disease. John_________________We are working to raisea wareness and find a cure.
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Joe or BobJoined: 12 Aug 2007Posts: 38
Posted: Sun Oct 14, 2007 7:53 pm Post subject:

There's no great mystery about Parkinson's Disease. It is primarily due to a lack of dopamine. That is why L-dopa (which forms dopamine) can relieve the symptoms so readily. When they speak of calcium-based processes changing to sodium-based in order to reinvigorate the neurons they are talking biochemical nonsense. Even in theory, let alone practice, that would have no direct effect on dopamine formation. The amount of dopamine that is formed is not dependent on whether the process is calcium based or sodium based. Both processes exist anyway. People don't change from one to the other as they have claimed. Unfortunately, it is now almost the norm that drugs and methods are being hyped that fail to have a scientific basis.
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cowboyJoined: 03 Oct 2007Posts: 68
Posted: Sun Oct 14, 2007 8:42 pm Post subject:

JohnBall20, thanks for your take on this. My primary skepticism comes from the blood pressure lowering aspects of Isradipine and whether or not this can be neutralized and provide the same benefit to those without blood pressure problems. Northwestern has a great reputation for having a first class Neurology Sciences Team so I am taking this seriously with some degree of hope. That, and the fact that I know it is already being prescribed for certain individuals. Admittedly, I tread lightly because of my ignorance in brain chemistry and the fact I am neither physician or neuro-scientist. I am an Engineer by trade.
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teokimhoeJoined: 03 Mar 2007Posts: 23Location: Malaysia
Posted: Thu Oct 18, 2007 3:08 am Post subject: parkinson's progression survival with times

Dear Mr Teo For an incurable illness such as PD, it is certainly hoped that there should be at least a way to slow down the progression of illness, i.e. the rate of brain cell loss. Unfortunately, so far, no medication has been unequivocably proven to be able to slow down the progression of PD. The good news is that dopamine agonists (Pramipexole, Ropinirole) have been shown to have potential neuroprotective effect - the ability to slow down the rate of brain cell loss. Experimental studies have shown that dopamine agonists can protect nerve cells from the damage caused by poison. The ability of dopamine agonists to protect the brain cells (if it is true) can help Parkinson's patients to have additional several years of relatively good quality of life, and without motor complications (the involuntary movement). Despite this, I still think that there is a potential neuroprotective property of dopamine agonists. I still prefer to use dopamine agonists as the first-line medications for my PD patients. I am happy that Pramipexole and Ropinirole have recently arrived in Malaysia, and I am already prescribing them to my patients. Dr Chew Nee Kong, Kuala Lumpur, Malaysia._________________to help the PD patients aware the diseases and encourage to set up support groups to educate the patients and their immediate families
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