Surgery can increase one's chances to get Alzheimer's disease?

Patients who undergo major hospital operations could be at greater risk of developing Alzheimer's disease, scientists believe.

Laura Donnelly (28 Aug 2010) Alzheimer's risk 'could be increased by surgery' Telegraph.co.uk

Alexei Koudinov: interesting article! Reprinted for scholar information. Dear reader, please follow this link to visit original publication and read a number of thoughful comments, and thus appreciate this interesting article!

Tests carried out on mice have revealed changes in their brains, similar to those observed in humans with dementia, when the animals are operated on.
The researchers suspect the same effect could occur in humans after surgical procedures and are now to start a new study to further explore the theory.

Many doctors already suspect there may be a link between surgery and the onset of Alzheimer's.

Previous studies have suggested that between 10 and 30 per cent of elderly people who undergo surgery suffer memory problems afterwards, but it has not been established whether these are a short-term response to physical trauma, or the beginnings of dementia.

Cognitive problems, ranging from memory loss to delirium, have been found most commonly when elderly people have undergone heart surgery, but also following other operations.

It is not known if the procedures themselves, or the body's response to major trauma, spark changes in the brain.

The latest research, conducted at Imperial College London and due to be published in the journal Critical Care Medicine next month, shows that the brains of mice who underwent a surgical procedure showed the presence of protein "tangles" in the brain which are associated with Alzheimer's disease in humans.

Because normal mice do not develop Alzheimer's disease, the new two-year study, also being led by Imperial College, will examine genetically modified mice, in an attempt to see whether the tangles – clusters of protein that form in nerve cells – which are present after surgery go on to trigger the onset of dementia.

The study will also examine whether the use of certain drugs – such as statins, used to protect against heart disease – and the active ingredient of a herbal remedy called Celastrol, could reduce the risks for those undergoing surgery.

In the recent study on mice, Celastrol was seen to reduce inflammation in the brain.
Researchers said if either drug appeared to lower the risks of dementia in modified mice undergoing surgery, further trials would be required to see if this worked in humans, and also to see if it could protect the brains of the wider population, not just those undergoing operations.

Dr Daqing Ma, the lead investigator on the research said: "The data has shown for some time that some elderly people who undergo surgery, especially heart surgery, can develop cognitive dysfunction, which can mean memory loss, and a loss of focus but it isn't clear how much of that is short-term, and how much long-term.

"Some people go on develop dementia, which can damage lives and mean an early death, but we don't know if there is a link with the cognitive dysfunction suffered post-surgery."

Previous studies had examined the extent of dementia within groups who had experienced surgery.

But given that an increasing number of elderly people now undergo operations, it has so far proved impossible to demonstrate that the procedures themselves triggered the dementia.

Anecdotally, many doctors believe they have seen cases which might have been triggered by surgery, said Dr Ma.

He cited the example of former US President Ronald Reagan, who underwent several surgical operations in the course of his life, including emergency brain surgery in 1989, after falling from a horse, five years before he was diagnosed with Alzheimer's.

His wife Nancy has said she believes the incident hastened the onset of the disease. Mr Reagan also underwent emergency surgery following an assassination attempt in 1981, and several surgical procedures for cancer.

Doctor Suzanne Sorensen, head of research at the Alzheimer's Society, which is sponsoring the research along with the Bupa Foundation, said the study was important, because of the high numbers of elderly people who undergo one sort of surgery or another.
She said: "We know from what previous studies have shown that between 10 and 30 per cent of elderly people suffer some kind of cognitive problems after surgery, and the numbers are highest in the most elderly people.

"The problem is all the evidence is anecdotal, we know of people who went in for a hip operation, and went home with dementia, but we cannot prove the link."
Alzheimer's disease is the most common form of dementia and affects around 500,000 people in Britain.

This is expected to double by 2050 as the population ages and many have warned that the NHS will not be able to cope with the nursing needs of so many patients unless better medicines are developed.

No Success of Alzheimer's Research field debated by a Major Clinical Journal Lancet

Please visit original publication at: Debating The Success Of Alzheimer's Research, medicalnewstoday.com (29 Aug 2010)

Excerpt: An editorial in the journal Lancet debates the problems of drug development for Alzheimer's disease.

The feature questions why so many trials are failing at the phase 3 clinical trial stage and asks whether the animal models used prior to this are the most effective way to test the drugs. It also suggests treatments should perhaps start to focus more on the changes in the brain that happen before symptoms like memory loss start to appear. However, it notes that these are difficult to replicate in animal models.

Alzheimer's Society comment:

'Scientific research is essential in the search for a cure and treatments for Alzheimer's disease and we must not be too disheartened that many drug trials fall at the final hurdle. The fact only one in five clinical trials across all diseases will be successful highlights the need for more investment so we can defeat dementia.'

'Every day scientists are learning more about the early stages of Alzheimer's disease and this is an important area for further study and development. '

Dr Susanne Sorensen
Head of Research

Source: Alzheimer's Society

Full Article: Looking for Alzheimer Answers in All the Wrong Places

As seen 2010-08-28 pm time at huffingtonpost.com.

Reprinted for scholar and public information only.

Alex Koudinov: Dear reader, please make a visit to the web site of original publication, so, this interesting article original web page gets proper recognition, thanks!

*****

The news about Alzheimer's is dismal. A new Eli Lilly drug to treat Alzheimer's has failed big-time. After investing hundreds of millions of dollars in the drug, Semagacestat, the company announced it made patients worse.

And the latest idea from an elite circle of Alzheimer's researchers is to torture us with diagnostic spinal taps and brain scans, so we can know ten years in advance if we are heading lickety split into Alzheimer's even though specialists admit they have no treatment to stop it and are even losing faith in their long-held theories of what causes it. "This is a time of major soul-searching in the field," lamented Duke University researcher, Dr. P. Murali Doraiswamy, in the New York Times.

As a person who carries the major gene, ApoE4 for Alzheimer's, I am intensely tuned into and disturbed by this public conversation. The gene triples my risk of ending up with Alzheimer's. Some 77 million other Americans also carry ApoE4 (25 percent of the population), but few know it, and doctors are reluctant to test and tell, supposedly because they don't want to scare us. I accidentally discovered my gene via a blood test for cholesterol factors several years ago, and I'm glad I did, because it energized me to search for answers other than those from Big Pharma and its philosophical collaborators.

I have discovered a large contingent of Alzheimer's researchers who are extremely positive about prevention and not counting on an elusive drug to stymie the growing Alzheimer's epidemic of aging baby boomers. Investigators Gregory Cole and Sally Frautschy at UCLA's Center for Alzheimer's Research and Gary W.Arendash, PhD, at the Florida Alzheimer's Research Center, for example, are all focusing on prevention. There is a plethora of upbeat dialogue in the scientific community that does not grab headlines because it's not about big money and a magic cure. It's primarily about what people can do to change their own trajectory toward Alzheimer's.

Contrast the recent disturbing headlines in the New York Times about Alzheimer's drugs and diagnosis with the June, 2010 issue of the Journal of Alzheimer's Disease. It is a special issue devoted to finding ways to prevent Alzheimer's. Editors in chief George Perry, University of Texas at San Antonio and Mark A. Smith, Case Western Reserve, (who predicted the failure of Lilly's drug and others like it,) and guest editor, Jack de la Torre at the Center for Alzheimer's Research, Banner Sun Health Research Institute in Arizona all endorse the science showing how this disease can be cut off at the pass earlier in life.

Dr. de la Torre boldly asserts that finding a cure for Alzheimer's is a delusionary quest unlikely to happen in a hundred years and most probably, never. He argues that even if you could replace dead neuronal networks, bringing a shrunken Alzheimer's brain back to life, the persona and intellect of the individual would be so altered as to create a different personality. "Alzheimer's is incurable, but it is preventable," he says. "We need to identify and lower Alzheimer's risk factors in people when they are still cognitively normal and long before irreversible symptoms appear."

While the search for a pharmaceutical cure plays front and center, quietly in the background countless neuroscientists worldwide have concluded that Alzheimer's, as well as memory decline and other age-related dementias are actually slow-developing chronic diseases, like heart disease and cancer, partly dependent on lifestyle and other treatable diseases.

De la Torre, for example, is convinced that Alzheimer's and dementia are particularly tied to cardiovascular factors, notably, constricted blood flow to brain cells, and that midlife screening to detect and correct such heart-related deficits would help prevent much brain degeneration during aging. The special journal issue produced by de la Torre, called "Basics of Alzheimer's Disease Prevention," also included new research on the relationship between Alzheimer's and diabetes, high blood pressure, triglycerides, cholesterol and cholesterol- lowering drugs, (statins), a Mediterranean diet, exercise, fish oil, B vitamins and antioxidants.

This special issue of JAD is but the latest example of a shifting paradigm toward prevention. Other leading medical journals are full of studies, often funded by your tax dollars, filtered through the National Institutes of Health, revealing the dangers of alcohol, smoking, toxic chemicals, head injuries, infections, certain forms of anesthesia, excess copper, low vitamin B, excess calories, obesity, diabetes, thyroid problems, sleep deprivation, and depression in raising your risk of dementia and Alzheimer's.

The wisdom of Alzheimer's prevention, derived from the famous Nun Study at the University of Minnesota, and the Religious Orders Study, at Rush University in Chicago, has been piling up for a decade or two, but is rarely put into practice. Comparing brains at autopsy with lifestyle and cognitive status allows investigators to proclaim the value of mental, social and physical stimulation in building a brain more resistant to Alzheimer's. Best time to start: when you are young, but even activity in old age can make a huge difference.

Prolific research from the U.S. Department of Agriculture, UCLA, Tufts University and Columbia University College of Physicians and Surgeons, as well as dozens of other institutions, reveals a reduced Alzheimer's risk from consuming berries, nuts, curry powder, fruits and vegetables, fatty fish, olive oil and the Mediterranean diet, and various supplements, including folic acid, alpha lipoic acid, Vitamin B12, multivitamins and vitamin D.

We are missing the boat when we allow a small fragment of the scientific conversation about Alzheimer's, centered on ineffective pharmaceuticals and frightening diagnostic methods, drown out the momentous message coming from another research perspective: that we can take action right now to delay the progression and onset of Alzheimer's which happens over decades. The good news is that we know now how to detect and lessen many midlife lifestyle problems that may otherwise lead to irreversible dementia. The approach is much the same, Dr. De la Torre points out, as we now use extensively to prevent heart disease, cancer, diabetes and other chronic diseases of aging.

Obviously, this doesn't mean we should stop searching for treatments for the underlying causes and symptoms of Alzheimer's and other dementias or spare funding to relieve those already suffering.

But it is urgent that we have a vigorous dialogue about how to rescue the multitudes now racing at breakneck speed toward Alzheimer's. Unless we intervene, Alzheimer's cases in the United States will nearly triple. A May Alzheimer's Association report, "Changing the Trajectory of Alzheimer's Disease," predicts that cases will jump from 5.1 million to 13.5 million by 2050 with costs during that period exceeding $20 trillion in today's dollars.

If we could delay the onset of Alzheimer's by only five years, according to the report, some 1.6 million Americans expected to get Alzheimer's by 2015 and nearly 6 million scheduled to get it by 2050 would remain free of it while Medicare savings would be $33 billion in 2020 and $283 billion by mid century.

The only way to make that happen is to start talking as loudly about preventing Alzheimer's -- and listening to the researchers who can tell us how to do that -- as we do about trying to cure it.

Jean Carper is the author of 100 Simple Things You Can Do to Prevent Alzheimer's and Age-Related Memory Loss (Little, Brown & Company, September 2010).

New book review: Renoved scientist calls for a change in Alzheimer's disese direction

Press release: A Call For Major Reform In The Direction Of Alzheimer's Treatment And Patient Care As The Boomer Generation Ages:

New Book review: The Alzheimer's solution: How today's care is failing millions - and how we can do better (Prometheus Books, $19)

Article Date: 28 Aug 2010 - 1:00 PDT

by Kenneth S. Kosik, MD (Santa Barbara, CA)

Although a new surge of scientific research has uncovered telltale signs of Alzheimer's disease that show up in brain scans and spinal taps, many questions remain unanswered about the clinical value of early testing and the overall direction of patient care, according to Dr. Kenneth S. Kosik, Harriman Professor of Neuroscience Research at the University of California and co-director of UCSB's Neuroscience Research Institute.

Kosik, also formerly a longtime neurologist at the Brigham and Women's Hospital memory clinic in Boston, cautioned that such "biomarker" tests for Alzheimer's do not address the most devastating issues presented by the disease. Indeed, he said, without substantial reforms in the treatment of Alzheimer's, the advent of early testing may only increase the anxiety of patients and their families.

"Suppose you test positive, then what?" Kosik said in a recent interview. "The test doesn't tell you when you might be likely to get the disease, for example. Patients and families will inevitably have many questions about what lies ahead. Unfortunately, the medical system is not set up to answer them."

In his new book, THE ALZHEIMER'S SOLUTION: HOW TODAY'S CARE IS FAILING MILLIONS - AND HOW WE CAN DO BETTER (Prometheus Books, $19) Kosik and co-author Ellen Clegg, a former journalist and science communication specialist at the Broad Institute of MIT and Harvard, provide a bold vision for reforming Alzheimer's disease treatment, and outline an array of simple preventive measures that patients can take to delay the onset of symptoms.

The average time from diagnosis to death in patients with Alzheimer's disease is ten years, Kosik said, a time when interest in the patient's welfare by the medical establishment wanes rapidly. Patients and their families are left in a desperate search for information about treatment, experimental leads and clinical trials, and basic support.

While recent news reports have highlighted stepped-up collaboration among scientists in government agencies, universities, and private industry to develop new Alzheimer's drugs, there is certainly no cure on the immediate horizon. Indeed, the drugs currently on the market are not effective as the disease takes its devastating course. "We have no satisfactory treatment for Alzheimer's disease," Kosik said. "If you have a problem for which neither surgery nor pills will work, then the medical system is really more of an obstacle than a help." He explained that people don't generally know this and they think that if they have a medical problem, they should seek help within the medical system. "It need not work that way," he said.

New ethical guidelines are needed to address how testing is handled and for end-of-life care, Kosik argues. The authors recommend clear discussion of medical wishes at the earliest possible stage among patients, families, and physicians. In his clinical work, Kosik found that many patients say they would rather not go on living than accept an illness that will rob their life of dignity.

The time to act is now, the authors write in THE ALZHEIMER'S SOLUTION. With the aging of nearly 80 million baby boomers, Alzheimer's disease is an impending epidemic. To meet this challenge, Kosik and Clegg propose that a network of one-stop centers should be established to provide expertise and reliable information on a range of topics, including diet, physical and cognitive exercise programs that may help reduce the risk for dementia, and palliative measures to reduce suffering. The centers they describe would take a family-oriented, personalized approach to care and prevention, creating an atmosphere conducive to adult learning, and facilitating personal growth in areas that patients have enjoyed over a lifetime, including the arts, dance, socializing, and a host of other possibilities.

Kosik recently launched a pilot clinic in Santa Barbara called The Center for Cognitive Fitness and Innovative Therapies (CFIT) to put these preventive measures into practice.

About the Co-Authors:

Kenneth S. Kosik, MD (Santa Barbara, CA), is the Harriman Chair in Neurosciences, co-director of the Neuroscience Research Institute, and professor in the Department of Molecular, Cellular and Developmental Biology at the University of California, Santa Barbara. Previously, Dr. Kosik was professor of neurology and neuroscience at Harvard Medical School. Ellen Clegg (Boston, MA) is Managing Editor for Communications Platforms at the Broad Institute of MIT and Harvard, a genetic research center in Cambridge, Massachusetts. Previously, she was Deputy Managing Editor/News Operations of the Boston Globe. Her prior positions at the Globe include Sunday editor and health and science editor. She is the author of "ChemoBrain: How Cancer Therapies Can Affect Your Mind".

Source:
Jill Maxick
Prometheus Books

as seen at medicalnewstoday 2010/08/28

Star Tribune: Aging boomers will strain families, State

Aging boomers will strain families, state

There will be fewer people to care for the aged, and tax-supported nursing home costs will bust budgets.

By WARREN WOLFE, Star Tribune Last update: August 21, 2010 - 11:08 PM

Excerpt:

Lynn and Steve Halverson saved taxpayers about $175 yesterday -- the cost of a nursing home room -- and they'll do it again today as they start their third year of caring for Lynn's 80-year-old mother in their Apple Valley home.

"It's what you do -- you take care of family," said Steve Halverson, who was laid off as a Schwan's manager the same month that an increasingly frail Joan Anderson moved to their house from Eau Claire, Wis.

"We get by, but some days it's not easy," he said. "It's about caring -- loving, I guess you'd say.''

Across Minnesota about 650,000 caregivers -- one in five adults -- are deeply involved with the joys and frustrations of helping aging relatives. Many help with chores, arrange doctor visits, shop for groceries or simply check in by phone every day. But for others, the care is far more intense and intimate -- feeding, bathing, dressing, monitoring chronic diseases and answering a million repeated questions.

The need for that sort of help -- whether from paid staff or families -- is about to explode. About 680,000 Minnesotans are 65 and older now. That number will soar to 950,000 in a decade, then to 1.3 million by 2030, when baby boomers start turning 85.

It's an amazing success story in longevity, but it's tempered by a worrying problem: There are far fewer young people behind them to provide care -- or finance it -- as this "silver tsunami" gains force. One measure, the age dependency ratio, shows that compared to people of working age, the proportion of seniors will almost double over the next 20 years -- from 21 per 100 workers to 39.

That will be offset slightly by a drop in the ratio of children to working-age people -- but caring for children is cheaper than caring for the frail aged.

...Continue reading at Star Tribune

A New Look At Alzheimer's, Forbes says. Well, long overdue, Dr.Koudinov adds!

Robert Langreth. A New Look At Alzheimer's (09.16.09, 06:00 PM EDT) Forbes Magazine Dated October 05, 2009

Have researchers been barking up the wrong tree?

Excerpt: "...Alzheimer's disease is a bit like a murder mystery with numerous possible culprits and only a few vague clues. For years the prime suspect has been a protein fragment called beta-amyloid, which forms clumps inside the brains of dementia patients. Big drug companies since the 1990s have bet heavily on the concept that amyloid poisons brain cells and that blocking it will halt a patient's devastating decline.

But even as their drugs move into final human trials, the evidence implicating amyloid is starting to look a little shaky. An amyloid-lowering drug from Myriad Genetics ( MYGN - news - people ) did nothing in a giant trial. Wyeth ( WYE - news - people ) and Elan ( ELN - news - people )'s amyloid-clearing antibody, called bapineuzumab, showed mixed results in a midstage human trial last year. It clearly helped only a subset of patients who lacked a certain gene mutation, and it had side effects such as fluid leakage in the brain.

Stranger yet, this summer researchers from the Mount Sinai School of Medicine in New York City examined an old allergy drug from Russia that recently showed promising results in Alzheimer's victims. They wanted to know whether it lowered amyloid. To their surprise, it boosted short-term amyloid levels in animal and lab experiments, according to results reported at a big Alzheimer's conference. Pfizer ( PFE - news - people ) licensed comarketing rights for the Russian antihistamine from the biotech company Medivation ( MDVN - news - people ) in 2008 for $225 million plus milestone payments, and the companies are conducting large trials. Results are due next year.

All of this has some scientists wondering if they are targeting the wrong chemical. "People inside and outside the amyloid field are trying to think what are we doing wrong. Either we are treating the wrong thing or using the wrong drug or treating it in the wrong way," says Mount Sinai's Samuel Gandy, who led the research into the Russian drug and still thinks amyloid is involved. Adds Merck ( MRK - news - people ) Vice President Richard Hargreaves: "There has been a sort of a narrow-minded approach to Alzheimer's disease. Amyloid deposition is only one of the features."

Some go much further. "I think amyloid is a complete nothing," says University of Aberdeen (Scotland) researcher Claude Wischik. "One day someone has to write a book about how a whole field can get suckered into this for so long." ...read on full article at forbes.com

Alex Koudinov-Sheffer note: Well... www.alclub.org is all about shoing the public, not just field insiders, ethically corrupted for one reason (stock shares) or another (grant support for amyloid theory or a need to support amyloid because of tenure promotion)))

More Alzheimer's anti-amyloid therapy failures of the recent past

As seen 20 August 2010 14:00 at bloomberg.com, Lilly Halts Development of Alzheimer's Disease Drug, by Elizabeth Lopatto and Meg Tirrell - Aug 17, 2010 10:20 PM GMT+0200, excerpt:

"...Researchers have announced setbacks with experimental treatments from GlaxoSmithKline Plc and AstraZeneca Plc, both of London; Martek Biosciences Corp., of Columbia, Maryland; New Brunswick, New Jersey-based J&J; Abbott Laboratories of Abbott Park, Illinois; New York-based Pfizer, Medivation Inc. of San Francisco, and Myriad Genetics Inc. of Salt Lake City, Utah, in the past several years, many targeting amyloid.

One of the drugs, Pfizer and J&J’s bapineuzumab, reduced the buildup of amyloid plaque in the brains of patients with Alzheimer’s disease, according to a study published March 1. Patients getting the medicine in the trial, though, didn’t show a clear improvement in mental function.

Elan Product

On Aug. 9, Dublin-based Elan Corp. and Transition Therapeutics Inc. of Toronto said their experimental Alzheimer’s disease drug, ELND005, will move into the final stage of human tests, even though the drug failed to meet an interim study’s main goals of improving patients’ mental status or daily living activities.

The drugs from Pfizer and Elan are in the final stage of testing usually required by the Food and Drug Administration to approve the marketing of new treatments..."

Stress in mid-life increases chances of dementia, research by Swedish scientists says

Excerpt: As per a new study conducted by Swedish scientists, the mid-life stress in women can give way to Alzheimer's disease in them.

The research concluded that women with frequent and high-level of stress and anxiety during their middle ages are more threatened to get affected by dementia, as compared to those who don’t.

The results were published in the journal Brain...

Continue reading original publication

Eli Lilly’s semagacestat targeted amyloid beta plaques but patients got worse

Eli Lilly’s semagacestat targeted amyloid beta plaques but patients got worse, excellent Senior Journal article says

As seen at: www.seniorjournal.com 29 August 2010 AM Jerusalem time:

Alzheimer's, Dementia & Mental Health: Battle Against Alzheimer’s Disease Hits Wall as Drug Test Stopped; Maybe Plaque Not Cause seniorjournal.com

Note by Alexei Koudinov: Please make a visit to the original publication to appreciate this excellent report, thanks!

Eli Lilly’s semagacestat targeted amyloid beta plaques but patients got worse

Aug. 19, 2010 – The efforts to prevent or successfully treat Alzheimer’s disease – the disease most feared by senior citizens - with drugs has never advanced very far, but these efforts suffered a major setback this week when Eli Lilly and Company announced it was halting development of semagacestat. This potential treatment for AD was in advanced clinical trials when it was discovered to be making patients worse instead of better. Many see this failure as a major blow to the most popular theory on the cause of the disease.

The Lilly announcement said, “Studies showed it did not slow disease progression and was associated with worsening of clinical measures of cognition and the ability to perform activities of daily living.”

"This is disappointing news for the millions of Alzheimer's patients and their families worldwide who anxiously await a successful treatment for this devastating illness," said Jan M. Lundberg, Ph.D., Executive Vice President, Science and Technology, and President, Lilly Research Laboratories. "This is a setback, but Lilly's commitment to beating Alzheimer's will not waver."

Lilly is instructing clinical trial investigators for all semagacestat studies to contact study participants as soon as possible and tell them to immediately stop taking the study drug. Study participants or caregivers should call their study physician to schedule their next appointment. Lilly has also informed regulatory agencies and is providing instructions to investigators outlining the process for finalizing the studies.

In two pivotal Phase III trials, semagacestat was compared with placebo in more than 2,600 patients with mild-to-moderate Alzheimer's disease.

Semagacestat was designed to reduce the body's production of amyloid beta plaques, which scientists believe play an important role in causing Alzheimer's disease. Semagacestat is believed to block the activity of gamma secretase, an enzyme that is essential to the body's production of amyloid beta plaques, according to the company. It was being tested in two Phase III clinical trials called IDENTITY and IDENTITY-2.

Lilly’s interim analysis showed that, as expected, cognition and the ability to complete activities of daily living of placebo-treated patients worsened. However, by these same measures, patients treated with semagacestat worsened to a statistically significantly greater degree than those treated with placebo.

In addition, data showed semagacestat is associated with an increased risk of skin cancer compared with those who received placebo.

Semagacestat was one of many drugs being tested that focus on amyloid-beta proteins, which are believed to play a critical role in Alzheimer's disease. Lilly actually has another amyloid-beta compound, solanezumab, in Phase III trials and says this testing will continue.

The company says these two compounds have “different mechanisms of action.” Lilly also has two other compounds in earlier stages of clinical development that will also continue.

Lilly's clinical team will continue to gather and evaluate data from these studies, and will publish the results for the benefit of future Alzheimer's research.

Although dosing with semagacestat is being stopped, Lilly plans to continue collecting safety data, including cognitive scores, for at least six months through regularly scheduled follow-up visits with study physicians and modifications of the existing Phase III protocols.

These additional follow-up visits are expected to help answer a number of important questions, including whether the differences between patients who received semagacestat and those who received placebo will continue after semagacestat has been discontinued. Other smaller short-term studies will be stopped and participants will receive appropriate follow-up.

"We are clearly disappointed by the results," said John C. Lechleiter Ph.D., Lilly's chairman and chief executive officer. He said, however, that the company has nearly 70 molecules currently in clinical development.

"Pharmaceutical research always carries risk, as these results show. But it offers as well the potential for tremendous reward for millions of patients who await new medicines. Despite this and other recent setbacks, Eli Lilly and Company remains financially strong and is even more determined to prevail in our quest to provide new treatments for Alzheimer's and other serious diseases," added Lechleiter.

About Alzheimer's disease

Alzheimer's disease is a fatal form of dementia that causes progressive decline in memory and other aspects of cognition. It occurs when billions of neurons in the brain begin dying prematurely. Researchers don't know exactly what causes it, but the leading hypothesis is that amyloid beta plaques play an important role.

About the IDENTITY trials

IDENTITY (Interrupting Alzheimer's Dementia by EvaluatiNg Treatment of AmyloId PaThologY) and IDENTITY-2 are Lilly's Phase III placebo-controlled trials studying semagacestat, a gamma-secretase inhibitor being investigated as a potential treatment to slow the progression of mild to moderate Alzheimer's disease. Both Phase III trials are fully enrolled, with more than 2,600 patients from 31 countries, and include a treatment period of approximately 21 months. An open-label extension study (IDENTITY-XT) is available to all participants completing either study.

All study participants had to be at least 55 years old and meet the National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer's Disease and Related Disorders Association (NINCDS/ADRDA) criteria for probable Alzheimer's disease, with certain assessment scores indicating mild to moderate Alzheimer's disease. Patients with more advanced Alzheimer's disease were not included in the studies.

This article URL

I don't believe Alzheimer's Association dissapointed of Phase III clinical trial of anti-amyloid beta Semagacestat by Eli Lilly!

Comment by Alexei Koudinov:

Are they truly dissapointed at Alzheimer's association of Phase III clinical trial of Semagacestat by Eli Lilly? I doubt it! Or more precisely, I do not believe it! I mean I don't believe he is dissapointed of the development setback, as media reports. Perhaphs he is dissapointed of fundraising problem (as it will be much harder to full the public that the research funded by Alzheimer's association is just bullshit), meaning less profit personally for him? You can ask him and Alzheimer's association CEO, they should be available via Alz.Org web site. I tried myself. In April 2004 I wrote the letter to the editor of The Wall Street Journal on WSJ coverage of Alzheimer's research. There were two (plus letters to editor, and another article in late summer, after Alzheimer's Global convention) articles, and the person behind that research by WSJ's Sharon begley was myself: I brought the story to them, described facts, provided contacts, you will learn all this at Alzheimer's Code History web site. My letter to WSJ editor responded on Alzheimer's Association letter (by Sheldon Goldberg, President and CEO, Alzheimer’s Association, 16 April 2004) to The Wall Street Journal editor on April 16 WSJ article "Scientists World-Wide Battle a Narrow View of Alzheimer's Cause" by Sharon Begley. In this letter I provided facts why Alzheimer's asscoation is a part of narrow amyloid view on Alzheiemr's. And now Dr.Thies says he is dissapointed. I don't believe him, period.

Source: Alzheimer's Association

All or excerpts from the following statement can be attributed to William Thies, Ph.D., Alzheimer's Association Chief Medical and Scientific Officer:

The Alzheimer's Association is disappointed to learn of the negative interim results from the Phase III clinical trial of Semagacestat. People with Alzheimer's urgently need more and better treatment options for this devastating, fatal brain disease. That said, the Alzheimer's Association remains optimistic about the future prospects for earlier detection of Alzheimer's, better treatments and prevention strategies.

We learn from every research study. This one was successfully launched and operated in more than 20 countries around the world. It had good site-to-site consistency in the data, which gave a signal strong enough to show a difference between the treated

group and the placebo group, though of course not in the direction that we would have hoped. It generated much valuable information for future large-scale, global trials in Alzheimer's, which are the types of trials we need to give us confidence that trials results are valid and that the tested drug works in a wide variety of people.

Dozens of other compounds are in the development pipeline for Alzheimer's disease. We are encouraged that drugs in the pipeline attack the disease from a variety of angles. Amyloid beta remains a viable target in Alzheimer's disease that should be addressed through myriad methods and mechanisms. Abnormal tau protein, inflammation, free radicals, and the connections between heart disease and Alzheimer's, among others, should also be targeted. New knowledge about the causes and progression of Alzheimer's emerges every day, and this must be fostered, discussed, and incorporated into ongoing therapy development as fast as is humanly possible.

At the same time, we are realistic in our understanding that addressing and eventually defeating brain diseases such as Alzheimer's is very challenging, and that enthusiasm must be balanced with appropriate care and caution.

The at-risk population for Alzheimer's is growing rapidly, and we need to make significant advances in early detection, treatment and prevention. Alzheimer's is an overwhelming epidemic, already claiming millions of individuals, and it is on track to deplete our healthcare resources and devastate Medicare. The current level of federal research funding for Alzheimer's is unacceptable considering the many millions of people this disease affects and the huge financial impact on our economy and society.

Alzheimer's disease is clearly the #1 public health challenge of the 21st century and research is the only way to solve this problem. In order to get better diagnosis, treatments and prevention for Alzheimer's, we must swiftly and boldly address two important issues.


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Psychiatric Drug Effects - Learn The Untold Story Of Psychotropic Drugging. Get Free DVD - CCHR.org

1) The chronic underinvestment in Alzheimer's disease research. We need to get more Alzheimer drugs in the pipeline. To do this, we must increase the research investment in Alzheimer's to levels similar to other leading causes of death, such as cancer and heart disease. Only then will we have the chance to see the same type of progress - declining death rates and viable lifestyle-based prevention strategies - and stop this epidemic.

This summer's Alzheimer's Breakthrough Ride is an example of the research community's dedication and collaborative spirit in eliminating Alzheimer's disease. Alzheimer researchers are cycling with the Alzheimer's Association to raise awareness about Alzheimer's and collect signatures for a petition urging Congress to make Alzheimer's disease a national priority. The Ride will culminate in Washington, D.C. on World Alzheimer's Day (Sept. 21), where the signatures will be presented to Congress. Follow the Ride's progress and sign the petition here.

2) More volunteers needed for Alzheimer's clinical studies. Recruiting and retaining trial participants is one of the greatest obstacles to developing the next generation of Alzheimer's treatments, perhaps second only to lack of funding. In July, the Alzheimer's Association launched Alzheimer's Association TrialMatchTM, a confidential and free interactive tool that provides comprehensive clinical trial information and an individualized trial matching service for people with Alzheimer's disease and related dementias - easily accessible via the Internet and toll free telephone (800-272-3900).

Source: Alzheimer's Association

Termination of the drug test is a major Alzheimer's field advancement, Alexei Koudinov comments on Dr. Paul Aisen explanation of the drug failure

Eli Lilly termination of the drug test is a major Alzheimer's field advancement, Koudinov comments on Paul Aisen PBS interview

Reprinted for educational Alzheimer's scholar information purpose only, original publication and video can be found here



Transcript (Accompanied by in-text comments by Alexei Koudinov, MD, PhD, DrSci)

GWEN IFILL: Now: the latest on the search for treating Alzheimer's disease.

Judy Woodruff has the story.

JUDY WOODRUFF: The effort to develop a treatment for Alzheimer's suffered a blow yesterday when a clinical trial was halted after finding that a new drug did more harm than good. Manufacturer Eli Lilly called off the studies after data showed the drug led to a greater risk of skin cancer and more memory loss.

The setback comes on the heels of some promising news about early diagnosis of Alzheimer's. Last week, samples of spinal fluid were found to be highly accurate at predicting a patient's likelihood of eventually developing the disease. Researchers also believe that brain scans may lead to diagnosis before symptoms develop.

And to help explain the findings, we turn to a leading researcher, Dr. Paul Aisen of the University of California, San Diego, School of Medicine. For the record, Dr. Aisen was involved in the early stages of that Eli Lilly trial, and he has consulted for Lilly and several other pharmaceutical companies.

Dr. Aisen, thank you for being with us.

DR. PAUL AISEN, University of California, San Diego, School of Medicine: Thank you.

JUDY WOODRUFF: First of all, tell us a little bit more about that drug involved in these clinical trials. What was it designed to do?

DR. PAUL AISEN: Well, we think that the cause of Alzheimer's disease is a -- is the accumulation of a toxic fragment called amyloid peptide, and this drug was designed to prevent that fragment from being released and from accumulating.

Dr. Alexei Koudinov: Well, Dr. Aisen, may I ask you to talk for yourself, and avoid using "we". We means who? You, Dr.Selkoe, other shareholders of a related BioTech Stock, PIs of NIH and other Funding Bodies research grants on amyloid, or your fellow participants of NIH State-of-the-Science Conference Preventing Alzheimer's Disease 2010? Would it be practical for you to think differently, Dr. Aisen? Be specific! I and many other researchers do not think that amyloid beta causes Alzheiemer's, and we did not grant you the privelege to talk on our behalf.

JUDY WOODRUFF: And what went wrong?

DR. PAUL AISEN: Well, this was a large treatment study, with thousands of participants. And, in such a program, you follow the data. You have an independent group monitoring the trial and monitoring the data, both for safety and for impact of drug on memory. And this monitoring led to the conclusion that the drug was carrying a risk, a risk of skin cancer, and wasn't improving memory. So, that means that this dose of this particular drug is not effective at this stage of disease.

Dr. Alexei Koudinov: You are wrong! This means the whole concept and amyloid theory is wrong, Dr.Aisen! You know that, don't you?

JUDY WOODRUFF: And you said not improving memory. Is it also the case that it was making memory and other symptoms worse?

DR. PAUL AISEN: Yes. The interim analysis, the look at the data, suggested that people taking the drug had more difficulty with memory than the people on placebo.

JUDY WOODRUFF: So, now, as I understand it, this trial was at least a decade in the making. How much of a setback is that?

DR. PAUL AISEN: It's a big setback, because there are only a few drugs that are at this pivotal stage, this final stage of drug development. So, having one of the major trials fail is a significant setback for the field.

But I think the good news is that there are dozens of other drugs at earlier phases of development, and that the tools available to study and prove efficacy for these drugs are improving -- that is, the field has developed new methods that should increase the likelihood that some of these drug programs will succeed.

Dr. Alexei Koudinov: It's a major advance, Dr. Aisen! It's happened a number of years ago, Elan trial collapsed, do you remember? It should happened again, so, it happened this August 2010 with Lilly trial. it will happen again to prove simple truth: amyloid is not an enemy, amyloid beta protein is a friend of the diseased brain, aiding the function, impaired by the other primary disease cause. So, you simply can not remove it from the brain!

JUDY WOODRUFF: So, then those other trials are -- are continuing.

Meantime, as we reported a moment ago, there are some promising new developments with regard to diagnosing Alzheimer's. Tell us a little bit more about that.

DR. PAUL AISEN: Sure. The -- the basic abnormality in the Alzheimer's disease brain is, as I said, the accumulation of a toxic fragment called amyloid. And we have always been able to be sure that Alzheimer's is present after death when we can examine brain tissue and see the amyloid in brain.

Now, for the first time, we can very accurately track the accumulation of amyloid with tests in living people. We have two tests, a PET scan, a form of brain scanning, and sampling of spinal fluid, that now give a very accurate indication of amyloid buildup in brain. This is a major step forward. It allows us to identify people well before dementia has occurred, even before memory impairment has occurred.

Dr. Alexei Koudinov: Why you are not mentioning amyloid accumulation in other human brain disease states, as well is amyloid accumulation in non-demented individuals?

JUDY WOODRUFF: So, earlier diagnosis, but the question is, if you don't have a treatment yet, what good does that do?

DR. PAUL AISEN: Well, the major benefit of these advances is that it gives us a tool for drug development.

Right now, these are research tools primarily. They will allow investigators to identify people before symptoms have occurred or before symptoms are bad, at the early stage, at which the disease is likely to be treatable, identify people at this stage, and test their drugs at this stage.

So, the trial that was just stopped was conducted in the dementia stage. It may well be that the dementia stage is too late for such a drug to work. We now know that amyloid accumulates 10 or 15 years before dementia. And we think that, for anti-amyloid drugs to be effective, the earlier the better we intervene.

These tools give us a way of testing the drugs at the earliest stage, and ultimately can be used -- when we prove that these drugs work, they can be used to guide therapy in people before the onset of symptoms (AK: see related article by Dr.Aisen).

Dr. Alexei Koudinov: Well, one faked tool we have for more then a decade, a so called Gold standard for testing Alzheiemr's therapies. You know what I am talking about, right? A so called Alzheimer's transgenic mouse. No wonder, assisted by faked peer review at Nature, amyloid mafia got a ticket for testing drugs in Humans.

JUDY WOODRUFF: Having said that, Alzheimer's was identified, I was reading today, in 1906, so it's been over a century. Why is this such a tough disease to make progress on?

DR. PAUL AISEN: Well, first, this is a disease that can't be directly observed.

So, if you're testing a drug for blood pressure, you measure blood pressure, you get a quick answer. If you're treating a rash, you can watch the benefits of the drug. In Alzheimer's disease, this is not a -- it's not a condition that's apparent.

We have to use indirect measures of the disease. And that creates a lot of noise, a lot of measurement difficulty. Up until now, we have relied on memory tests and similar assessments. But they're not very accurate. Memory fluctuates from day to day. It's not a very precise gauge of disease progression or the impact of drug treatment.

Now we have new, much more precise measures of disease that allow us to identify people at the very early stages, as we said, but also to much more precisely measure the impact of treatment. So, I think that clinical trial methodology has advanced, and that's going to help us demonstrate effective treatments.

Dr. Alexei Koudinov: You know, what I got in mind is a Russian (Soviets-time) anecdote of a TV appearence of a Big Professor (just like you at PBC this time) reporting the Tooth Extraction over anus. So much amazed TV reporter is asking "why" and "what for"? ...and the answer is straight forward and cristal clear: First, because all we do we do this way, and Second, because (for tooth extraction) it is for the first time ever. So, Dr.Aisen, don't oversimplify the story. As you are on the wrong pass with Alzheimer's theory, no methodology will yield the cure. Period!

JUDY WOODRUFF: Dr. Paul Aisen, we're going to leave it there. Thank you very much for talking with us.

DR. PAUL AISEN: Thank you.

Drug's Failure invalidates the Tactic in Alzheimer's Battle, New York Times article correctly implies, says Alexei Koudinov of AlzClub.org

Drug's Failure Casts Doubt on a Tactic in Alzheimer's Battle - Gina Kolata, NYTimes, commented by A Koudinov, an excerpt(summary) and full comment are available

Reprinted for educational Alzheimer's scholar information purpose only, originally seen at New York Times Online

Drug’s Failure Casts Doubt on a Tactic in Alzheimer’s Battle

Alexei Koudinov note: it was never promising, who told you that? Did you check their scientific and ethical credit history first? You should! I checked and never believed those bastards of Alzheimer's leadership, "Professors" on campuses of major Universities and Medical centers. Want a referenced proof? Here it is, United Kingdom Parliament Written Evidence for the Science and technology Committee, check it out. I would infact ban them from doing science in early 2000, I asked Office of Research Integrity and SEC to do it. No reply yet]

By Gina Kolata Published: August 18, 2010

The failure of a promising Alzheimer’s drug in clinical trials highlights the gap between diagnosis — where real progress has recently been made — and treatment of the disease.

It was not just that the drug, made by Eli Lilly, did not work — maybe that could be explained by saying the patients’ illness was too far advanced when they received it. It was that the drug actually made them worse, the company said. And the larger the dose they took, the worse were patients’ symptoms of memory loss and inability to care for themselves. Not only that, the drug also increased the risk of skin cancer.

So when Lilly announced on Tuesday that it was ending its large clinical trials of that drug, semagacestat, researchers were dismayed.

“Obviously, this is disappointing news, to say the least,” said Dr. Steven Paul, an Alzheimer’s researcher and a recently retired executive vice president at Lilly.

Beyond the setback for Lilly, the study raises questions about a leading hypothesis of the cause of Alzheimer’s and how to treat it. The idea, known as the amyloid hypothesis, says the disease occurs when a toxic protein, beta amyloid, accumulates in the brain. The idea is that if beta amyloid levels are reduced, the disease might be slowed, halted or even prevented if treatment starts early enough.

The Lilly drug, like most of the more than 100 Alzheimer’s drugs under development, blocks an enzyme, gamma secretase, needed to make beta amyloid. It was among the first shown to broach the blood-brain barrier and reduce levels of beta amyloid in the brain. And, company studies showed, it did reduce amyloid production.

“We did get enough in the brain to have an effect,” said Dr. Eric Siemers, medical director of Lilly’s Alzheimer’s disease team. “Unfortunately, the effect was not what we wanted.”

Now researchers are focused on what went wrong, and why.

Some, like Dr. Lon Schneider, an Alzheimer’s researcher at the University of Southern California, say the drug’s failure may mean the field is rushing off a cliff in its near single-minded focus on blocking the production of amyloid. Dr. Schneider, like most leading Alzheimer’s researchers, consults for a number of drug companies, including Lilly.

The Lilly study’s failure, he said, “chips away at that approach to testing the amyloid hypothesis.”

“We don’t know what the drug targets for Alzheimer’s disease are,” Dr. Schneider said. “We don’t know because we don’t know the causes of Alzheimer’s.”

At the very least, said Dr. P. Murali Doraiswamy, an Alzheimer’s researcher at Duke University, the Lilly result “clearly tells us that our current views may be too simplistic.”

Dr. Doraiswamy said he was not abandoning the amyloid hypothesis. But, he said, “this is a time of major soul searching in the field.”

“What worries me is that we don’t know if this was a toxicity unique to Lilly’s drug and this late-stage population or whether it also applies to similar anti-amyloid therapies given at earlier stages of the disease,” Dr. Doraiswamy said.

The bad news came on the heels of what researchers see as a resurgence of hope in this challenging field. With new cooperation in research they have made advances in diagnosing Alzheimer’s, a disease that used to be uncertain until autopsy.

And those new diagnostic tests are still exciting, researchers said.

PET scans of amyloid plaques in the brain and tests of cerebrospinal fluid can show amyloid accumulation long before people have symptoms of Alzheimer’s disease and, as was recently reported, appear to identify people at high risk of developing the disease. Researchers believe the best time to try to alter the course of the disease is before memory loss — by that time, brain cells are dead or dying and are unlikely to be restored.

At this point, though, when there is no treatment, those tests are primarily a benefit for companies testing new therapies and researchers trying to understand the disease’s progress.

The long journey of semagacestat began more than a decade ago, when Lilly scientists discovered it could block gamma secretase in laboratory experiments. Years of work followed, showing it appeared safe, that it got into the brains of people, that it reduced the production of amyloid in the brain.

Finally, in 2008, Lilly began two large studies of semagacestat, enrolling more than 2,600 people with Alzheimer’s disease. The company did not expect its drug to reverse the disease — patients’ brains were too ravaged for that, said Richard Mohs, Lilly’s team leader in Alzheimer’s research. But it did hope to slow the disease’s progression.

Now, with the abrupt end of the studies, patients will continue to be followed but no one will be taking any more of the drug.

“The fact that people got worse means there is biology we don’t understand,” Dr. Mohs said.

There are several possible explanations.

page 2

One is that the drug altered the functioning of other proteins in the brain and body — it now appears that gamma secretase is involved in the production of about 20 proteins in addition to beta amyloid. Companies, including Lilly, are developing drugs that block gamma secretase from making amyloid but do not have much of an effect on the other proteins.

One company, Bristol-Myers Squibb, says that is what its drug does. Its drug is now being tested in two clinical trials. In one, the participants have Alzheimer’s. In the other, they have memory impairment that falls short of Alzheimer’s dementia and have brain amyloid PET scans and tests of cerebrospinal fluid showing amyloid is accumulating in their brains, indicating that they are likely to go on to develop Alzheimer’s.

“We still like the amyloid hypothesis,” said Charlie Albright, a Bristol-Myers group director in neuroscience biology. The Lilly drug failure “doesn’t affect our enthusiasm about going forward.”

Another possibility is that the enzyme is decreasing production not just of a dangerous form of amyloid, known as a beta 42, but also of another form, a beta 40, that may protect the brain. Companies are developing so-called selective gamma secretase inhibitors, Dr. Paul said, which only block the production of a beta 42.

Companies are also pursuing other ways of reducing amyloid levels in the brain. One, a Lilly drug that uses a monoclonal antibody to block amyloid, is being tested in a large clinical trial.

And companies are pursuing a more difficult target — blocking a protein, tau, that accumulates in dead and dying nerve cells after the disease is under way.

But Alzheimer’s experts worry about the future. The research is extremely expensive — Lilly spent hundreds of millions of dollars on its failed drug — and it can take a decade or more to know if a drug works. It can take even longer if drugs are tested in people with mild symptoms of Alzheimer’s disease or in people who are at high risk but have no symptoms yet — a direction many think is necessary to really make a difference.

“I am certainly concerned that if we see some more failures it will be a harder to convince companies to invest that much money in testing these hypotheses,” Dr. Paul said.

Dr. Samuel Gandy, an Alzheimer’s researcher at Mount Sinai Medical Center, shares that concern.

“Failures certainly don’t build energy and enthusiasm,” he said. “The market is still there, but failures do take their toll.”

Eli Lilly halted development of anti-amyloid Alzheimer's drug

The question: Why Eli Lilly stopped developing Alzheimer's drug?

The answer by Alexei Koudinov: "Because contemporary mainstream Alzheimer's disease science is bullshit! Read on for details"

Reprinted for educational Alzheimer's scholar information, and enhanced with Dr. Koudinov comment, original publication and comment are available

*****

Eli Lilly halts development of Alzheimer's drug
By TOM MURPHY (AP)

INDIANAPOLIS — Eli Lilly and Co. has stopped developing a potential Alzheimer's disease treatment at a time when the drugmaker is searching wide and far for new drugs to fill a large revenue hole that will form starting next year.
The Indianapolis company said Tuesday preliminary results from late-stage studies of semagacestat showed it did not slow the progression of Alzheimer's, and patients taking the drug actually fared worse than those on a placebo.

Despite the setback, Lilly Chairman and CEO John Lechleiter said the company remains committed to developing new drugs while competitors make large-scale acquisitions. The industry is racing to compensate for patent expirations that will hit in the next few years and expose many key drugs to generic competition.

"In a risky business like ours, these things do happen," he said. "One failure of this sort does not undermine our strategy."

Lilly has eight drugs in late-stage testing, the last step before a company seeks regulatory approval. That includes potential cancer and diabetes treatments and another Alzheimer's drug. The company also touts a pipeline of nearly 70 drugs that are in some form of human testing.

It also is awaiting a Food and Drug Administration decision on its antidepressant Cymbalta as a possible chronic pain treatment and a longer-acting version of Byetta, a diabetes drug on which it partners with Amylin Pharmaceuticals Inc.
Lilly, which supplements its pipeline with several smaller-scale acquisitions, faces one of the worst "patent cliffs" in the industry. It loses protection for its top seller, the anti-psychotic Zyprexa, next year and its second-best seller, Cymbalta, in 2013.

In addition, a U.S. District Court judge has ruled invalid a patent protecting the attention deficit hyperactivity drug Strattera. Lilly expects generic competition to enter the market soon.

To counter all this, Lilly aims to launch two new drugs a year by 2013.
"We think we're plenty big enough to continue to innovate and to bring new medicines forward that will help Lilly resume a growth trajectory following the expiration of these various patents," Lechleiter said.

However, analysts covering the company have doubts. Bernstein analyst Dr. Tim Anderson said in a research note Lilly's lineup of drugs in late-stage development "looks relatively thin."

"The company has disavowed doing bigger deals which implies it is counting on its pipeline to deliver," Anderson wrote. "Today's setback would seem to make this more difficult to achieve."

Lilly said Tuesday patients taking semagacestat [Alexei Koudinov in-text note: Semagacestat blocks the enzyme γ-secretase, which (along with β-secretase) is responsible for APP proteolysis, to be explained at Alzheimer's Amyloid beta course] saw their cognition, or memory and reasoning skills, and their ability to complete daily living activities like getting dressed worsen "to a statistically significantly greater degree" than patients taking a placebo.

The drug also was tied to an increased risk of skin cancer. Lilly said the decision to halt semagacestat's development will not affect its other potential Alzheimer's treatment, solanezumab [Alexei Koudinov in-text note: humanized monoclonal antibody against Amyloid beta, this Alzheiemr's therapy trial to fail in due course].

There is no known cure for Alzheimer's disease. Drugs on the market that treat it only temporarily alleviate symptoms. Scientists aren't even sure what causes Alzheimer's.

Earlier this year, Pfizer Inc. and partner Medivation Inc. said the promising Alzheimer's treatment Dimebon failed to work in a late-stage study, but the companies are continuing another study of the drug as an add-on treatment for Alzheimer's.
Johnson & Johnson also is developing the potential treatment bapineuzumab, and there are several other drugs in late-stage testing.

The Alzheimer's Association counts about 75 potential treatments in some form of human testing. But most drugs do not make it beyond initial clinical trials.
Shares of Lilly slipped 2.3 percent, or 81 cents, to $34.76 in Tuesday afternoon trading.

Also on Tuesday, the FDA posted a review Lilly's application to market Cymbalta for pain and raised questions about whether the drug is safe and effective enough to be approved. The FDA will ask a panel of outside experts on Thursday to consider the additional use.

AP Medical Writer Marilynn Marchione in Milwaukee contributed to this report.
Copyright © 2010 The Associated Press. Repinted for educational purpose

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AlzClub News by Alexei Koudinov, MD, PhD, DrSci

There is a kind of magic in my awaking at 5AM this Sunday, 15 August 2010. After having morning physical excersises and breakfast and logged in to make a new life of my http://www.alzclub.org web site. Previously (since 2004 I beleive), it look as this archieved copy at my koudinov.info/alzclub web folder.

For years I was (and still I am) confident, that Alzheiemr's is such a corrupted research field, that you one can take an academic leave for three, five, or even ten years, and then come back exactly to the date he or she left. Those bastards and mafia-like strucrure of academic science and hidden big pharmaceutical bucks behind them leaves no space for an open minded innovative ideas. Don't ask how it is possible, it is the way Alzheimer's research exists.

So, I decided to remove digital dyst out of my advocacy, scientific and lay language writings and make it public here, so, you, dear reader, while have original content from the author, directly and with no "dealers", like poor and often corrupted academic journals.

It was no surprise that three days later Eli Lilly announced the halt of Alheimer's therapy trial, as patients worsen on a chemical called secretase inhibitor, which is an anti-amyloid beta therapy based on ill-fated and poor-minded (yet commercially, not public succesful) amyloid hypothesis (read dogma) of Alzheimer's disease.

Today, by the end of the day August 19, I decided to start another theme web site, devoted exclusively to reprinting Alzheimer's news and press releases from different sources. I thus would like to separate my original content from content by others. I will still announce interesting news at major AlzClub.org web site while providing brief summary. All other web sites, including Alzheimer's History, Alzheimer's Amyloid beta courses for Public and Professionals, Alzheimer's Code and other emerging projects will syndicating the content of each other, so, every new material will be visible, and just click away.

Surely, all the projects are non-profit, public and ad supported: while I do not expect to make revenue, it will be nice to have advertisement support cover my publishing and associated expenses.

Remaining independent and truly yours,

Alexei Koudinov, MD, PhD, DrSci

neuroscientist, Alzheimer's researcher

a man of 44 who loves this world

P.S. First annotated by me news item to follow in just 10 minutes or so, with Press release of Alzheimer's Association on Eli Lilly Alzheimer's clinical trial termination