Sunday, January 1, 2012


for PWP

My hope is that this is the year of

Progress towards the elusive cure.
Progress for improved treatments and care.

Lack of progress for all who travel this journey with PD.


Saturday, November 27, 2010

swallowing help

Friday, September 10, 2010


Dear Howard,

We are at the cusp of a truly historic innovation in stem cell research.
Last year, Scripps Research rising star Kristin Baldwin made headlines when her lab successfully created live mice from mouse skin cells. If Dr. Baldwin's cell reprogramming techniques can be replicated in humans, scientists believe they will be able to grow replacement organs such as hearts and livers, or develop healthy replacement cells to treat damage done by Alzheimer's or Parkinson's Disease.

Not only is this a major scientific breakthrough, but Dr. Baldwin's method of reprogramming cells circumvents the political and moral issues of stem cell research because it does not use embryonic stem cells. And, since the cells would be derived directly from the patient, the rejection problems that plague conventional transplant therapies would be eliminated.

Sunday, September 5, 2010

Dancing Merengue Dog

Wednesday, September 1, 2010

Paul Greengard does it again and again and again.

This article appears in the New York Times of September 2, 2010.
September 1, 2010

Finding Suggests New Aim for Alzheimer’s Drugs

In a year when news about Alzheimer’s disease seems to whipsaw between encouraging and disheartening, a new discovery by an 84-year-old scientist has illuminated a new direction.
The scientist, Paul Greengard, who was awarded a Nobel Prize in 2000 for his work on signaling in brain cells, still works in his Rockefeller University lab in New York City seven days a week, walking there from his apartment two blocks away, taking his aging Bernese mountain dog, Alpha.
He got interested in Alzheimer’s about 25 years ago when his wife’s father developed it, and his research is now supported by a philanthropic foundation that was started solely to allow him to study the disease.
It was mostly these funds and federal government grants that allowed him to find a new protein that is needed to make beta amyloid, which makes up the telltale plaque that builds up in the brains of people with Alzheimer’s.
The finding, to be published Thursday in the journal Nature, reveals a new potential drug target that, according to the prevailing hypothesis of the genesis of Alzheimer’s, could slow or halt the devastating effects of this now untreatable disease.
The work involves laboratory experiments and studies with mice — it is far from ready for the doctor’s office. But researchers, still reeling from the announcement two weeks ago by Eli Lilly that its experimental drug turned out to make Alzheimer’s worse, not better, were encouraged.
“This really is a new approach,” said Dr. Paul Aisen, of the University of California, San Diego. “The work is very strong and it is very convincing.” Dr. Aisen directs a program financed by the National Institute on Aging to conduct clinical trials of treatments for Alzheimer’s disease.
Over the past few years, research on Alzheimer’s has exploded. Now, Dr. Aisen said, there are about 200 papers on the subject published each week. There are new scans and other tests, like spinal taps, to find signs of the disease early, enabling researchers to think of testing drugs before patients’ brains are so ravaged. And companies are testing about 100 experimental drugs that, they hope, will fundamentally alter the course of Alzheimer’s disease.
Most of the new drugs target an enzyme, gamma secretase, that snips a big protein to produce beta amyloid. The problem in Alzheimer’s is thought to be an overproduction of beta amyloid — the protein is made in healthy brains but, it is thought, in smaller quantities. Its normal role is not certain, but researchers recently found that beta amyloid can kill microbes, indicating it might help fight infections.
But gamma secretase has crucial roles in the body in addition to making beta amyloid. It removes stubs of proteins left behind on the surface of nerve cells and it also is needed to make other proteins, so completely blocking it would be problematic. Many scientists think that was what went wrong with the Eli Lilly drug, which, researchers say, took a sledgehammer to gamma secretase, stopping all of its functions. Other companies say their experimental drugs are more subtle and targeted, but they may still affect the enzyme’s other targets.
Dr. Greengard found, though, that before gamma secretase can even get started, the protein he discovered, which he calls gamma secretase activating protein, must tell the enzyme to make beta amyloid. And since that newly discovered protein is used by the enzyme only for beta amyloid production, blocking it has no effect on the other gamma secretase activities.
It turns out that the cancer drug Gleevec, already on the market to treat some types of leukemia and a rare cancer of the digestive system, blocks that newly found protein. As a consequence, it blocks production of beta amyloid. But Gleevec cannot be used to treat Alzheimer’s because it is pumped out of the brain as fast as it comes in. Nonetheless, researchers say, it should be possible to find Gleevec-like drugs that stay in the brain.
“You could use Gleevec as a starting molecule,” said Rudolph Tanzi, a neurology professor and Alzheimer’s researcher at Harvard Medical School. “You could change the structure a little bit and try analogs until you get one that does what Gleevec does and does not get kicked out of the brain. That’s possible.”
On a clear, cool summer day last week, Dr. Greengard told the story of his discovery. He sat in a brown chair in his office on the ninth floor of an old stone building on the meticulously landscaped grounds of the university, wearing a soft yellow V-neck sweater and thick-soled black shoes. Alpha lay quietly at his feet.
Dr. Greengard’s assistant ordered lunch — cantaloupe wrapped in prosciutto; ravioli filled with pears, mascarpone and pecorino Romano; cherries; and cookies. But Dr. Greengard, caught up in the tale of his science, asked her to hold off bringing in the food.
“I thought, this is just a horrible disease and maybe there is something I can do about it,” he said.
About a decade ago, Dr. Greengard and his postdoctoral students made their first discovery on the path to finding the new protein — they got a hint that certain types of drugs might block beta amyloid production. So they did an extensive screen of drugs that met their criteria and found that one of them, Gleevec, worked. It completely stopped beta amyloid production.
That was exciting — until Dr. Greengard discovered that Gleevec was pumped out of the brain. Still, he found that if he infused Gleevec directly into the brains of mice with Alzheimer’s genes, beta amyloid went away.
“We spent the next six years or so trying to figure out how Gleevec worked” on gamma secretase, Dr. Greengard said. He knew, though, that he was on to something important.
“I had very little doubt about it,” he said. “If I have an idea, I have faith in it, that it must be right.”
The system he discovered — the gamma secretase activating protein — made sense, Dr. Greengard said.
“Gamma secretase belongs to a family of proteins called proteases,” he explained. Proteases chop proteins into smaller molecules. But often proteases are not very specific. They can attack many different proteins. “Obviously, you can’t have that kind of promiscuity in a cell,” Dr. Greengard said. There has to be some sort of control over which proteins are cleaved, and when.
So, Dr. Greengard said, “what evolved is that proteases invariably have targeting proteins that help them decide which proteins to go after.”
That was what he had found: a targeting protein that sets in motion the activity of gamma secretase, which makes beta amyloid. To further test the discovery, he genetically engineered a strain of mice that had a gene for Alzheimer’s, but he blocked the gene for the gamma secretase activating protein. The animals appeared to be perfectly healthy. And they did not develop plaques in their brains.
For Sangram S. Sisodia, an Alzheimer’s researcher at the University of Chicago, that mouse experiment was critical.
“That was the proof of concept,” he said. It meant that Dr. Greengard was correct — the newly discovered protein, when blocked, does not seem to interfere with other crucial functions of gamma secretase.
“That is good news,” Dr. Sisodia said.
As for Dr. Greengard, he said, “I couldn’t be more excited.”
“I am sure there will be a fervor in the field.”

Thursday, May 27, 2010


Just a fleeting thought, my wife and I have devised a food and restaurant rating that we use from time to time.
Perhaps it is time to institute a PD guide for our good days and bad days. We could save a lot of time and energy by using a day rating code. Just to communicate to whomever and the world how we feel on any  particular day. We  could keep a log and chart our feelings, sort of a doctor visit sheet. "Hi, GG" or " Hi, GB "




I hope it is GG for you today.

Sunday, April 25, 2010


I got a call a few days ago from a friend of an old friend of mine. It seems this ladie's husband has had PD for ten years.
He is not doing well and the rate of progression is of a concern. He cannot walk by himself anymore and has other advanced problems associated with PD.
His only treatment is Carbadopa/Levadopa 25/100 four times a day. He is depressed and cannot find himself in an upbeat mood anymore.
I am not a doctor just a PD patient with 13 year on the journey and not offering medical advice, just my observation.
As I understand the situation as described via the telephone, this person's neurologist thinks he is overmedicated.
April is Parkinson's awareness month.
With all the advancement in treatments in the last few years, you might wonder why so many PWP are not aware of the various alternatives and do not get that comprehensive and all inclusive care that is so vital to the quality of life of the whole person. Parkinson's is a fickel disease, ever changing with many surprises. Those who provide medical care should be addressing the whole person and learn from their patients how and when changes occur. There is ample research to show and share, teaching us that PD affects us in different ways and cannot be treated with a rubber stamp philosophy.

I have empathy for the person I first mentioned.
Hoping for better days ahead.

Zebrafish model to understand Parkinson’s developed | TheMedGuru

Zebrafish model to understand Parkinson’s developed | TheMedGuru

Friday, April 16, 2010



Now, a voice test to predict Parkinson's!

Now, a voice test to predict Parkinson's! (Getty Images)
In what could be called a major breakthrough, scientists claim to have developed a voice test which can predict Parkinson's disease years earlier in people.

Parkinson's is normally only diagnosed once symptoms show -- meaning it's already at an advanced stage and patients have lost a significant number of brain cells. Now, an Israeli team has devised a test to predict the neurological disorder.

In their research, the team from Haifa University have discovered that by measuring tiny changes in speech patterns, undetectable to human ear, they can tell whether a seemingly healthy person is a sufferer.

Accordingly, they developed a computer programme that can identify a Parkinson's "voice", which they claim could be used for screening those who are at the hereditary risk of the disease or as part of a national screening programme, British newspaper the Daily Mail reported.

Speech is affected by the disorder because it causes a deterioration of muscles in the neck and mouth -- giving some sufferers a husky voice. But the change is apparent to human ear after the disease has been diagnosed through symptoms such as rigid muscles, tremors, slow movement, and loss of balance.

The new test needs only a couple of sentences from patients, say the scientists.

Sunday, April 11, 2010


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