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29th-Apr-2007 11:25 pm(no subject)
1
Neurochem announces the launch of North American Phase III clinical trial on Alzhemed™ for the treatment of Alzheimer's Disease.

- Neurochem Inc. (NASDAQ: NRMX; TSX: NRM) announced today that it has launched its North American Phase III clinical trial on Alzhemed™, following an investigators' meeting attended by more than 200 clinicians and clinical monitors held in Montreal from June 18 to June 20, 2004. Alzhemed™ is the Company's investigational product candidate for the treatment of Alzheimer's Disease (AD). The trial will be conducted by 50 U.S. and 20 Canadian clinical centers across North America.

The multi-center, randomized, double-blind, placebo-controlled and parallel design North American Phase III clinical trial will investigate the safety and efficacy of Alzhemed™ for the treatment of AD in approximately 950 mild-to-moderate patients. The patients will be randomized to receive either placebo or one of two different dose levels of Alzhemed™ for a period of 18 months. The Company anticipates launching its Alzhemed™ European Phase III clinical trial early in 2005.

"We are on schedule for the launch of our Phase III clinical trial program on Alzhemed™," said Dr. Francesco Bellini, Chairman and CEO of Neurochem. "We are encouraged by the interest shown by the medical community in this Phase III trial and by the attendance at the investigators meeting by clinicians from all 70 sites to ensure that the trial protocol is well harmonized throughout all of North America. The results of our Phase II clinical trial and our on-going open-label Phase II extension study appear to indicate that Alzhemed™ addresses not only the symptoms, but also has the potential to affect the progression of the disease, especially in mild AD patients," he added.

Alzhemed™ is an orally administered, small organic molecule that has been specifically designed to modify the course of AD by binding to amyloid ß (Aß) protein and keeping it in a non-fibrillar form. As part of a "disease modifying" class of product candidates, Alzhemed™ is expected to act at two levels: in preventing and stopping the formation and deposit of amyloid fibrils in the brain and in inhibiting the inflammatory response associated with amyloid build-up in AD.

"The most promising target in AD therapeutics is the amyloid peptide," said Dr. Paul Aisen, Alzhemed™ principal investigator for the U.S. clinical sites and Professor of Neurology and Medicine, and Director, Memory Disorders Program, at Georgetown University Medical Center in Washington, D.C. "This investigational product candidate has been shown in preclinical development to target the amyloid peptide. Neurochem's Phase II study demonstrated that Alzhemed™ is well tolerated in individuals with AD. Furthermore, the majority of patients receiving Alzhemed™ for a very long period in the open-label extension study, that is, for up to 16 months, have shown stable cognitive function tests, especially in the mild population."

Results of the Phase II trial demonstrated that there were no apparent safety findings of concern in patients treated with Alzhemed™ and that the investigational product candidate was well tolerated in individuals with mild-to-moderate AD. Furthermore, Alzhemed™ was detected in the cerebrospinal fluid of the patients, suggesting its ability to cross the blood-brain-barrier and its potential to act on amyloid, the underlying pathology of AD. The patients with the greatest decrease of amyloid protein, as measured by immunoassays, were on Alzhemed™ and the majority of mild AD patients on the highest dose showed stable or improved results on cognitive function tests even after 16 months of follow-up.

"Neurochem's study on Alzhemed™ could offer new hope for the thousands of people afflicted with Alzheimer's disease", said Dr. Serge Gauthier, Alzhemed™ principal investigator for the Canadian sites and Professor of Neurology and Neurosurgery, Psychiatry, Medicine and Associate Member of Pharmacology and Therapeutics at McGill University in Montreal, Canada. "The outcome measures during treatment with Alzhemed™ will accurately evaluate the daily life of participants and their families, as well as the biological changes associated with the disease."

[Source: here]


I'm still looking around to find some more, updated information.

I'd like to really get this community active. I really want to encourage everyone to share stories, pictures, art, anything. (Keeping to the topic of Alzheimer's, or loved ones suffering with Alzheimer's, please.)

The difficulty with support groups is the overwhelming pessimism (and unfortunately, more often than not--justified pessimism). Right now, there is no cure for Alzheimer's. There are some drugs that can cause temporary relief, but for people suffering from late stages of Alzheimer's, there is really nothing that can be done. But Alzheimer's doesn't just effect the person suffering--it effects their entire family.
For people currently suffering with Alzheimer's, we have to remember those clear days, where your loved one is lucid and almost seems normal, or well. Cling to those days, and make them something wonderful.
For people who have dealt with Alzheimer's, who's loved ones have passed on, remember the days before Alzheimer's, before the dazed looks and struggle to remember insignificant things.

Again, I'd like to really encourage everyone to share stories, pictures, art, whatever.
24th-Nov-2006 01:39 am(no subject)
1
22nd November 2006
By Staff Writer
Researchers at the Stanford University School of Medicine have discovered a possible cause of how humans may develop Alzheimer's disease from a molecule found in the immune system.
The researchers discovered that, when a molecule responsible for dialing down the immune system malfunctions in the brain cells of mice, the rodents develop symptoms of Alzheimer's disease.

Alzheimer's disease is characterized by an excessive buildup of proteins into plaques that are likely to cause brain cells to die and lose their connections to other neurons. However, the underlying biological problems behind Alzheimer's are not yet understood.

Researchers in the university's department of neurology examined slices of the brains of Alzheimer's patients who had died, and discovered abnormally low levels of the molecule involved in the body's response to infection. That molecule allows the brain to detect and respond to TGF-beta, a protein teeming through human bodies and involved in fighting infection.

Scientists attempted to investigate the effects of TGF-beta on neurons that could help prevent Alzheimer's. "We tried to see what happens if we block neurons from getting this beneficial signal," explained Tony Wyss-Coray, associate professor of neurology at Stanford University.

The mice were genetically engineered with a defect similar to the one they found in the brains of Alzheimer's patients and had brain cells that could no longer respond to TGF-beta's signal. Unable to receive the beneficial TGF-beta signal, the rodents showed signs of Alzheimer's disease. Brain cells died as the mice grew older, and the cells failed to make connections to other brain cells.

In the past, researchers have tried using molecules that work like TGF-beta to provide protection against Alzheimer's, but the proteins are too large to enter the brain through the bloodstream. To sidestep that problem, the researchers are working to identify small molecules that can boost the TGF-beta pathway in neurons.

[Source: here]

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The community has gotten a face lift. :]
3rd-Jun-2006 12:36 am(no subject)
1
This is a paper written by my older sister, for her English class. I thought I'd share it.

     Thursday, October 13, 2005 at 1 in the morning, I received the call I had been dreading and anticipating for nearly 4 years. My grandpa had passed from complications of end-stage Alzheimer's. He was now completely taken from me. I say completely because 4 years ago he was diagnosed with Alzheimer's. Seemingly overnight, everything changed. It was like watching the mightiest being I had ever known lose everything important in his life. I watched month after month, as his mind, memories, dignity, and eventually his body, were taken from him. He had been in stedy decline until that early Thursday morning. My grandpa, Willie "Foy" P------, was the strongest, bravest, and most noble person I ever knew, and I miss him dearly.
     In the early years, it was the little things that slipped away from him. Things like, where his keys were or where his glasses were. Sometimes he would tell me funny stories that did not seem to make sense. He would always use humor to cover up his forgetfulness. When he did not remember your name, he would intentionally call you by a silly made-up name. The names he most often used were Leroy and George. I did not realize then what was really happening. As it worsened, he began to forget more. He was finally diagnosed with Alzheimer's around 2002. He could not continue working and was granted early disability. Soon after that, he was forced to give up on his favorite hobbies. One of his favorite past times was woodworking. This became a very dangerous and difficult hobby for him. He no longer spent hours restoring cars or creating beautiful furniture. He was physically able to do these things, but mentally incapable. He just could not remember how. I think this was much more difficult for him to accept because he was still in such great shape.
     By the time I was 20, about 2 years into the disease, my grandpa no longer knew my name or who I was. Grandpa still lived at home with my grandmother, which proved very difficult. As with most Alzheimer's patients, they tend to become mean, confused, and even violent to their closest loved ones. Because he was still in good physical shape, he would often wander off and walk for hours before being picked up by police officers and brought back home. Some days, he would leave because he was mad at us; others, he would not realize where he was and would just want to "go home". He had become a prisoner in his own home. All doors, windows, and gates were eventually locked to prevent him from getting out. He would still try to remove, dissemble, or even break the locks to get out again. This continue to worsen over the next 18 months.
     Finally 3 months ago, due to the difficulty of providing him care and safety, grandpa was placed in a nursing home. He was no longer able to feed or bathe himself. The man who gave me a car he had restored himself, when I was 16 years old, now had to be cared for like an infant. It was heart-breaking to watch someone so strong and so proud to be unable to speak. The last time I saw him he was wasting away, having lost nearly 80 pounds. When I saw him that way I decided, it hurt too much to see the greatest person I knew suffering so terribly. The man before me was not grandpa anymore. This was just a shell of a man that resembled him. I could not stand to see him this way and wanted it to end.
     In those early hours when I recieved the call, I was so sad that he was gone. I laid in bed and sobbed that morning, feeling saddened and relieved at the same time. Even though a wonder drug was not discovered in enough time to save my grandpa, he was no longer suffering. I know that he would never have wanted to live those years the way he did; he was too proud of a man for that. I miss who I called my "Old-Grandpa", the man that he was before the disease took him. The man who taught me how to swim, and how to catch a fly ball. The one who taught me never to back down and never to give up. I miss the grandpa that was the proudest fan at the softball fields, cheering me on. I will always remember how B's were never as good as A's in school to him. I miss the grandpa who, when I looked into his eyes and he beamed back at me, I knew he was proud of me and loved me to no end. That grandpa was lost long before that early Thursday morning. So on that morning, in a way, he was given back to me. He is now able to be with me, in my heart, and watch me from above. I know now without a doubt, that he remembers my name and so much more. I love you, Grandpa.

© Brandy S.
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