Replies to post #63534 on Biotech Values

[blackcat]

There will be more data at ICAD which will answer some of the current questions.

[DewDiligence]

Good article. Yes, there are lots of questions but, overall, these phase-2 data can’t be awful or the companies would not have embarked on a very expensive phase-3 program. (As stated in a prior post, Zebra’s Law does not apply nearly as strongly to Big Pharma as it does to small biotech companies.) Regards, Dew

[DewDiligence]

Vaccine Failure Deepens Alzheimer's Mystery

http://www.msnbc.msn.com/id/25722244

›Experimental shot stopped plaque, but not dementia

The Associated Press
Thurs July 17, 2008, 7:00 p.m. ET

LONDON - Some doctors have long suspected that if the plaque that builds up in the brains of patients with Alzheimer's disease could be removed, they could be saved. But a new vaccine that did just that suggests the theory is wrong.

British researchers gave 64 patients with moderate Alzheimer's disease an experimental vaccine designed to eliminate plaque from their brains. Some patients were followed for up to six years.

Autopsies on seven patients who died of Alzheimer's during the study showed that nearly all of the sticky beta-amyloid protein thought to be dangerous had been removed. But all patients still had severe dementia.

"It may be that these toxic plaques trigger the neurodegeneration, but don't have an ongoing role," said Clive Holmes of the University of Southampton, lead author, in a press statement. The study was published Friday in the medical journal, The Lancet. It was paid for by the Alzheimer's Research Trust, a British charity.

Alzheimer's disease is the most common cause of dementia and affects about 25 million people worldwide.

Experts said that the study's findings pointed to a major gap in our understanding of the disease. Doctors have never been sure whether the brain plaques are the cause of Alzheimer's disease or just a side effect.

"We still don't have enough understanding of what we should target," said Dr. Bengt Winblad, director of the Alzheimer's Centre at Sweden's Karolinska Institute. Winblad was not connected to the study.

Brain tangles may play a role

Aside from the plaque build-up, scientists also think that tangles of another brain protein called tau play a major role in Alzheimer's. Because those tangles form later than the plaque, some experts think they should be the focus instead.

"It may be harder to get a response from targeting plaque because that forms years before people actually have Alzheimer's," said Dr. Simon Lovestone, professor of Old Age Psychiatry at King's College in London. "By the time you do something, it may be too late."

Winblad said there was a better connection between brain tangles and Alzheimer's symptoms, but that no studies so far had looked at whether removing tangles might improve or even reverse Alzheimer's disease in patients.

Still, experts say that attacking toxic plaque in the brain shouldn't be abandoned just yet, since the formation of such plaques might be what sparks Alzheimer's disease in the first place.

"Removal of the initial motor for the disease might slow progression," wrote Peter H. St. George-Hyslop and John C. Morris of the University of Cambridge and the University of Toronto in an accompanying commentary in the Lancet.‹

[Preciouslife1]

Rapid Alzheimer's Improvement After New Immune-based Treatment

http://www.sciencedaily.com/releases/2008/07/080720212354.htm

(July 21, 2008) — New research into the treatment of Alzheimer's disease reports improvement in language abilities using a novel immune-based approach. A video accompanying the research, published in the open access journal BMC Neurology, documents rapid language improvement within minutes of using this new treatment.

Building on previous work by the same authors, published in BioMed Central's Journal of Neuroinflammation, this study focuses on the effect of the anti-tumor necrosis factor--alpha (TNF-alpha) drug, etanercept, on measures of verbal ability.

TNF-alpha, a critical component of the brain's immune system, normally finely regulates the transmission of neural impulses in the brain. The authors hypothesize that elevated levels of TNF-alpha in Alzheimer's disease interfere with this regulation. To reduce elevated TNF-alpha, the authors utilized a unique perispinal delivery method to administer etanercept.

The new BMC Neurology article provides preliminary evidence that the disrupted neural communication seen in Alzheimer's disease may be reversible.

According to the lead author of the study, Edward Tobinick, "There are limitations to the data presented; the clinical trial was open label, and not controlled. These caveats notwithstanding, the scientific rationale for the further investigation of anti-TNF-alpha treatment of Alzheimer's disease is compelling. In addition, family members, independent neurologists, and other independent observers have confirmed the clinical, cognitive, and behavioral improvement noted".

Disruption of language function, such as the ability to find words, is a common symptom in advancing Alzheimer's disease, and this BMC Neurology article is one of the first to suggest the possibility of a new therapeutic approach that may address these symptoms.

The lead author of the study, Edward Tobinick MD, is Director of the Institute for Neurological Research, a private medical group, inc., in Los Angeles. Dr. Tobinick has been investigating the role of TNF in neurological disorders for a decade. His research has provided new potential insight into the way immune molecules, such as TNF, may influence the function of the nervous system.



Journal reference:

Edward L. Tobinick and Hyman Gross. Rapid improvement in verbal fluency and aphasia following perispinal etanercept in Alzheimer's disease. BMC Neurology, July 21, 2008