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News page readership 18 April - 1 October 2004: 2965


12 November 2005

Lipids play important role in nervous system development
Medical College of Georgia (26 October 2005)
[FullText] [AlzClub.org Record] [Author contact]

Leading text: "Blocking a signaling lipid can keep nerves from developing the arm-like extensions they need to wire the body and may even cause neurons to die, researchers have found. The researchers hope this piece of the puzzle of how the central nervous system develops in the first place will one day help them repair loss from injury or disease. It’s already helped them understand the ailments of a spontaneous mouse mutant that has about 20 percent function of the protein that helps the lipid get to the cell surface so it can help axons grow, says Dr. Wen-Cheng Xiong, developmental neurobiologist and corresponding author on the study published in the November issue of Nature Cell Biology.

The mutant mouse is small and has motor neuron degeneration, with tremors, short limbs and a short life, she says. Before this new work, what the blocked lipid transfer protein regulated was still a mystery. The lipids in question aren’t those measured during an annual physical exam, rather those that help give shape and function to units within cells such as the nucleus and cell powerhouse, or mitochondria, she says. “Traditionally people didn’t think these lipids were regulated. They thought they were just there,” says Dr. Xiong. “But what we found is this particular lipid is regulated; it’s like a signaling molecule. Especially during axon growth, the dynamic regulation is more dramatic.”

She and her colleagues found the lipid is transferred to the cell surface at just the right time and place by phosphatidylinositol transfer protein-a, which humans also have. It’s been known that many proteins can be regulated, especially signaling proteins that enable intracellular chatter. “Now we have found this protein regulates lipids and lipids also travel,” Dr. Xiong says. The mouse mutant is a clear example of what can happen when the lipids don’t travel. The researchers also studied a similar mutant chick embryo that had reduced axon growth. For this paper, they added the zebrafish embryo, which forms most of its major organs within the first 24 hours and remains transparent for the first few days of life, to further document the role of these regulated lipids and their transfer protein.

When they injected an agent that blocks expression of a related lipid transport protein, the next they could see the impact on axon growth and neuron survival, says Dr. David J. Kozlowski, developmental geneticist and director of the MCG Transgenic Zebrafish Core Laboratory. They looked at different levels of suppression, finding the greater the suppression, the greater the resulting defect. “It shows this protein is critical for development,” Dr. Xiong says of repeated findings. Next they’ll use a version of the transgenic zebrafish that will enable them to watch axon development ­ or lack of it ­ in live embryos and in real time, Dr. Kozlowski says. They also want to look at what happens to the lipid activity in an injury model. They already know some signaling proteins are disturbed.

MCG contributors included the laboratories of Drs. Xiong and Kozlowski as well as Dr. Lin Mei, program chief in Developmental Neurobiology and Georgia Research Alliance Eminent Scholar in Neuroscience. Collaborating institutions include the University of Alabama at Birmingham; the Institute of Neuroscience and Key Laboratory of Neurobiology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences; Howard Hughes Medical Institute; and the Jackson Laboratory in Bar Harbor, Maine. The work was supported by the National Institutes of Health."

contributed by Alexei Koudinov  | This item permanent URL


3 November 2005

European researchers, publishing in a leading scientific journal, show a biological link between cholesterol and Alzheimer’s disease. Authors of the paper acknowledge the EU’s contribution to their work through the Lipidiet project, which investigated the role of lipids in neurodegeneration
Europa.eu.int (28 October 2005)
[FullText] [Lay News on earlier related studies: 1 | 2 | 3 | 4 ] [Author contact]

Leading text: "Alzheimer's, or the 'memory disease', as it is sometimes called, is a fatal condition affecting higher brain function. Around one-third of the EU population develops it during their lifetime. It generally affects the elderly but early onset is known. Its prevalence in older people has led to the misconception that “losing your mind” is just part of ageing. Scientists are keen to dispel this, showing that Alzheimer’s is a disease and not a process of normal ageing. On average, it progresses from the first clinically apparent symptoms to death in about nine years. But this can vary.

The disease starts with minor memory problems and ends with patients completely forgetting even friends and family and becoming dependent on full-time care. Until now, the only treatments have been for the symptoms. More active treatments and possibly a cure will take the burden of Alzheimer’s off healthcare systems and families who have to watch this tragic degradation of the mind.

While the cause of Alzheimer’s is still not fully understood, science is well on the way to providing some answers. It is already known that, in most cases, the disease is not inherited but may depend on environmental and genetic factors ­ in around 5% of cases, it is inherited through mutations in three different genes. These cases have revealed much about the disease, according to the Lipidiet project team.

Lipidiet ­ which stands for 'Role of Lipids in Neurodegeneration and their Preventive Potential in Diet' ­ was funded by the EU’s Fifth Framework Programme (FP5). The project’s coordinator, Tobias Hartmann of Heidelberg University, Germany, is the senior author of a recent publication in Nature Cell Biology which shows that regulation of cholesterol and another fat called ‘sphingomyelin’ (SM) involves a protein ­ called amyloid precursor protein (APP) ­ which is found in the brain, but also other organs like the heart, kidneys and lungs.

Lipidiet sought to better understand the basic cellular principles at work in the disease. The seven partners in the project cover an array of specialties, including molecular biology, neurobiology, lipid metabolism, physiology and medicine, and behavioural sciences, as well as a private firm specialising in health-targeted food.

What’s cholesterol got to do with it?
APP contains a small region ­ the amyloid beta domain. This domain is cut off from APP by certain enzymes, known as secretases. Accumulation of amyloid beta forms, over time, a hard plaque in the human brain which is difficult to break down. Everyone produces this but the quantity and its effects are not all the same. This is an area that has traditionally stumped scientists. But using mouse models to firm up the relationship between this accumulation and the onset of Alzheimer’s, the European team is now closer to understanding the sequence of events.

The team's newly-published findings show that amyloid beta, while toxic and disease causing when over produced, has a normal and non-toxic function. And this normal function is to regulate cellular lipid levels. Their function results in regulatory cycles in which the amyloid beta reduces cholesterol synthesis and sphingomyelin levels, the team writes in a recent statement.

The very same lipids control the activity of the enzyme which produces amyloid beta, resulting in altered amyloid-beta levels, leading to the troubling plaque. Altering these regulatory cycles ­ with drugs, genetics, or even diet ­ changes amyloid-beta production and thus the risk for Alzheimer’s, say the researchers.

"Knowledge of the natural amyloid-beta peptide function allows us to re-evaluate therapeutic and preventive approaches to Alzheimer’s disease and to generate more effective and safer novel therapies," notes the team. What’s more it explains the link between Alzheimer's and cholesterol, and how statins (cholesterol-lowering drugs) work to prevent it.

How does this relate to food and the Lipidiet project? Well, Lipids are an insoluble fat found in the blood and organs, including the brain. We eat foods with varying fat content and types. A strong case had already been presented for the use of lipid- and cholesterol-lowering drugs to either prevent or slow down Alzheimer’s. But non-drug approaches are equally promising.

A ‘designer diet’ that can delay the onset of Alzheimer's had earlier been devised by Lipidiet, according to a CORDIS News story. The consortium is testing it in clinical trials to validate its effectiveness and provide a more convincing case for diet’s potential to prevent, delay or slow down Alzheimer’s disease."

contributed by Alexei Koudinov | This item permanent URL


26 August 2005

Clinical & Research News: Cholesterol-Alzheimer's Link Backed by New Data
Joan Arehart-Treichel
Psychiatric News (19 August 2005) Vol. 40 (16) p.17
[FullText] [AlzClub.org Record] [Related stories] [Author contact]

Leading text: "Several cholesterol-related genes, not just the APOE one, have been implicated in Alzheimer's disease and may eventually be used to predict who is going to develop the illness. The e4 variant of the APOE gene has been strongly linked with susceptibility to Alzheimer's disease. Indeed, one-fourth of the population is estimated to carry this variant. What fewer people are aware of, however, is that the APOE gene is also known to be the major transporter of cholesterol in the blood and central nervous system and a risk factor for coronary disease.

Now a number of other genes involved in cholesterol metabolism appear to be involved in Alzheimer's susceptibility as well, a new study suggests. However, the APOE gene still seems to be the biggest culprit. The study was led by Andreas Papassotiropoulos, M.D., a psychiatrist and research professor at the University of Zurich in Switzerland. Results appeared in the July Journal of Clinical Psychiatry.

Papassotiropoulos and his colleagues enrolled more than 500 older persons from Switzerland and Greece. Half had been diagnosed with Alzheimer's disease; the other half did not have the illness. The researchers then analyzed DNA samples from these subjects to assess 12 single nucleotide polymorphisms—that is, variants in genetic material—from 11 genes related to cholesterol metabolism and previously linked to Alzheimer's disease. One of the single nucleotide polymorphisms was the APOE e4 variant. The scientists also examined the DNA samples to see whether they contained 48 single nucleotide polymorphisms that had never been linked with either cholesterol or Alzheimer's. Finally, they looked for links between any of the single nucleotide polymorphisms and the presence of Alzheimer's.

They found that nine of the 12 single nucleotide polymorphisms previously implicated in cholesterol metabolism and Alzheimer's were also significantly associated with Alzheimer's in their study. In contrast, they were not able to find any association between Alzheimer's and the 48 single nucleotide polymorphisms not previously tied to cholesterol and Alzheimer's. Moreover, they found that some of the nine single nucleotide polymorphisms were more strongly associated with Alzheimer's than the others were. The APOE e4 gene variant headed the list. Then came material from a gene called SOAT1. Then came material from the APOE promoter. "This study is potentially important for several reasons," Eric Reiman, M.D., a professor of psychiatry at the University of Arizona and deputy editor of the Journal of Clinical Psychiatry, asserted in an editorial accompanying the report. For example, "It implicates a cluster of genes, including, but not limited to, the APOE e4 allele, in the susceptibility to late-onset Alzheimer's disease."

Also, he added, "It provides further support for the role of higher cholesterol levels in the pathogenesis of Alzheimer's disease and the potential role of cholesterol-lowering strategies in the treatment and prevention of this disorder." However, as Reiman cautioned in an interview with Psychiatric News, the findings will not be used clinically any time soon to predict Alzheimer's for several reasons—they have not yet been replicated, "they do not predict with sufficient certainty whether or when a person might develop symptoms," and "they don't yet tell the person what he or she might be able to do to prevent the disorder." In fact, he said, testing for the APOE e4 variant alone to predict Alzheimer's risk is not recommended for clinical use at this point because of the danger of triggering false alarms or creating false reassurances, and because no preventive measures are available.

Josepha Cheong, M.D., an associate professor of psychiatry at the University of Florida and chair of the APA Council on Aging, told Psychiatric News that the study impressed her for several reasons. For one, the researchers attempted to identify the interplay of a cluster of genes that may be involved in the etiology and clinical presentation of Alzheimer's disease instead of looking for the effect of a single gene at a time, which is more common. For another, she believes that the study "represents a continuation in the discovery of genes involved in the pathogenesis of Alzheimer's disease." And finally, whereas the "research results may not be acutely clinically relevant, they portend significant possibilities for diagnosis and treatment."

Meanwhile, Papassotiropoulos said, "I anticipate that several genetics groups will attempt to replicate the findings, among others Dr. Jonathan Prince from the Karolinska Institute in Sweden. There are [also] several [other] lipid-related genes to be looked at. In addition, it will be important to combine this genetic information with data on brain activation patterns by means of PET or fMRI."

The study was funded by the Swiss National Science Foundation, the Early Diagnosis of Alzheimer's Disease and Related Dementia Program in Switzerland, and the National Center for Competence in Research in Switzerland.

"A Cluster of Cholesterol-Related Genes Confers Susceptibility for Alzheimer's Disease" can be accessed online at www.psychiatrist.com/toc.htm by searching on the article title in the July issue."

contributed by Ilya Reznik | This item permanent URL


15 July 2005

Statins Fail to Hold off Alzheimer's in Study
Kathleen Fackelmann
USA Today (11 July 2005)
[FullText] [AlzClub.org Record] [Related stories] [Author contact]

Leading text: "Popular cholesterol-lowering drugs called statins did not protect elderly people from Alzheimer's or other kinds of dementia, a study reports today. Statins are a group of drugs widely prescribed to reduce the risk of heart disease. Recent scientific evidence suggested these drugs also might protect the brain from Alzheimer's. The new findings don't support that hope as yet, but Sam Gandy, an Alzheimer's researcher at Thomas Jefferson University in Philadelphia, says they represent just one piece of evidence in a line of studies that suggested a role for statins in the prevention or treatment of Alzheimer's.

Statins might work as a shield only if given early in life, before the disease has a chance to take hold in the brain, says Gandy, who is also a spokesman for the Chicago-based Alzheimer's Association. The people in the study averaged 75 years old and had been taking statins for an average of five years, says lead researcher Thomas Rea of the University of Washington in Seattle. Their age could explain the negative findings, he says.

Rea and his colleagues studied 2,798 older people who had no sign of cognitive problems at the study's start. The team also kept track of those who developed dementia, including Alzheimer's, over a six-year period. They also noted whether participants were taking statin drugs such as Lipitor or Zocor. Participants took cognitive and memory tests throughout the study. The researchers found that those who took statins developed dementia or Alzheimer's at about the same rate as those who were not taking the drugs. The findings are reported in the Archives of Neurology.

Despite the results, Rea and other experts aren't ready to give up on statins. "We did not find any evidence of protection, but our study is not definitive," Rea says. To get more proof, researchers will have to give a large number of middle-aged people either statins or placebo pills and then check to see whether the people getting the statins are shielded from the disease years later. "Maybe if you start giving these drugs when people are 50 instead of 75, you'll get a better effect," says Larry Sparks, an Alzheimer's researcher at Sun Health Research Institute in Sun City, Ariz.

Sparks has evidence suggesting that statins can help people who already have developed Alzheimer's. His small study published in May shows that atorvastatin (Lipitor) helps boost memory and cognitive ability in people with mild to moderate Alzheimer's. Ongoing studies could help clear up some of the confusion about whether statins can help protect the brain, Gandy says: "We may have some answers later this year."""

contributed by Alexei Koudinov


24 November 2004

Alzheimer's at 30-something. Five percent of cases are early forms, devastating young lives and families
Jamie Talan
Newsday (19 October 2004)
[Free FullText] [Author contact]

Leading text: "Three years ago, Michael Henley began keeping a diary so that he could chronicle a mind that would one day be lost to Alzheimer's. He was 36 years old, and the first hints of the disease came crashing down on his family during a vacation when he forgot that his teenage daughter had gone off with a relative. A year later, he wrote in his journal: "Today was a bad day. I couldn't complete a full sentence." Things have progressed rapidly for Henley, who is now 39 and in the full-blown stages of Alzheimer's dementia. While he still knows his wife and two children, he is not able to hold a meaningful conversation. He loves to walk, but is now timid on his feet. When outside, he has to be led by the hand or he'll wander into traffic. His eyes still sparkle when his wife tells him how much he is loved, but the intimate connection between husband and wife is gone. Only three years ago the main provider for the family, Henley now needs round-the-clock care..."

contributed by Alexei Koudinov


15 November 2004

Pesticides may promote Parkinson's disease and exercise may offer protection, according to new reports
The Society for Neuroscience 34th Annual Meeting News Release (24 October 2004)
[Free FullText] [Author contact]

Leading text: "New research into Parkinson's disease is helping scientists better understand some of the mechanisms of this serious and disabling brain disorder, which affects about 1 million people in the United States. Knowledge of the environmental factors and genetics of this illness has allowed investigators to create models of disease that are being used to examine potential causes of neuron disease and to test experimental therapeutics in animals. Some of the research will eventually lead to the development of more effective treatments of this human illness. The second most common neurodegenerative disease (after Alzheimer's disease), Parkinson's occurs when certain groups of nerve cells are damaged and destroyed. For example, neurons in the substantia nigra, an area of the brain that is important for normal voluntary movements, are invariably damaged. These abnormalities result in a variety of signs, including tremor, muscle stiffness, and slowness of movement. People with Parkinson's may also experience depression, anxiety, dementia, constipation, urinary difficulties, and sleep disturbances. Symptoms tend to worsen over time..."

contributed by Alexei Koudinov


1 November 2004

Promise of stem cells amplified; new evidence shows cells may help treat many disorders including paralysis and brain cancer
The Society for Neuroscience 34th Annual Meeting News Release (24 October 2004)
[Free FullText] [Author contact]

Leading text: "Continuing to counter the dogma that once brain cells give out, they're gone forever, new evidence shows that newly created neurons may provide hope for treating a wide variety of disorders. Embryonic stem cells have been shown to restore movement after paralysis. And with genetic engineering, stem cells can act as sophisticated protein delivery systems. Scientists have used them to deliver GDNF, a factor to aid in the survival of neurons targeted by Parkinson's and Huntington's diseases. Another team has used them to seek and destroy brain tumor cells. And a Norwegian group has proved that even in adults, neural stem cells have the power to become functioning neurons. Scientists at the University of California , Irvine , have reversed spinal cord damage in paralyzed adult rats, allowing them to walk again..."

contributed by Alexei Koudinov


24 October 2004

New way of controlling cholesterol may help treat Alzheimer's
Sue McGreevey
Innovations-report.com (14 October 2004)  Source: EurekAlert
[Free FullText] [ARF News] [Author contact]

Leading text: "A new approach to controlling blood cholesterol levels that is already being investigated to prevent cardiovascular disease also may be a potential treatment for Alzheimer's disease. In their report in the October 14 issue of Neuron, researchers from Massachusetts General Hospital (MGH) show that blocking a pathway that controls the distribution of cholesterol in cells dramatically reduces the number of amyloid plaques in the brains of transgenic mice. Some of the treated mice were much better at learning their way through a maze than were untreated mice. "We found that this way of reducing cholesterol levels in the brains of living animals both decreased amyloid deposition and improved learning," says the study leader Dora Kovacs, PhD, director of the Neurobiology of Disease Laboratory in the Genetics and Aging Research Unit of MassGeneral Institute for Neurodegenerative Disorders. "As far as we know, this is the first study of cholesterol metabolism's impact on amyloid levels that included cognitive testing..."

contributed by Alexei Koudinov


6 October 2004

SfN Member Linda Buck Awarded Nobel Prize
The Society for Neuroscience News Release (4 October 2004)
[Free FullText] [Author contact]

Abstract: "Society for Neuroscience member Linda Buck, PhD, of the Fred Hutchinson Cancer Research Center in Seattle and the Howard Hughes Medical Institute, and Richard Axel, MD, also of the Howard Hughes Medical Institute and Columbia University, were awarded this year's Nobel Prize in Physiology or Medicine. The prize, “for discoveries of odorant receptors and the organization of the olfactory system,” was announced October 4 by the Nobel Assembly at The Karolinska Institute in Stockholm, Sweden. Smell has long been considered the most enigmatic of senses because the principles and mechanisms involved in identifying and remembering thousands of different odors were largely unknown. Axel and Buck discovered a large gene family-comprised of 1,000 genes-responsible for an equal number of olfactory receptor sites that occupy the upper nasal epithelium and detect inhaled molecules. Each of these receptors is specialized and can detect a limited number of related odors, the researchers found independently. Axel’s team used mice to demonstrate the role the receptors played, while Buck’s group further researched the sensitivity of the olfactory cells by examining the contents of each cell to discover which odorant receptor gene was expressed. It was then possible to demonstrate which cells were activated by a certain smell."

contributed by Alexei Koudinov


6 August 2004

Fevered Debate Over Alzheimer's Origins Causes Deep Divisions
Begley, Sharon.
The Wall Street Journal (6 August 2004) p.B.1
[FullText at WSJ] [Free FullText at SFChronicle] [Author contact]

Abstract: "AS I WROTE last April, there are growing doubts that amyloid is guilty as charged. Autopsies of people with early-stage Alzheimer's show that the tangles form first, before plaques, in brain regions initially affected by the disease. "If you look at the evidence, it's the tangles that cause neuronal degeneration, and they come first, before the amyloid," says neurologist Patrick McGeer of the University of British Columbia, Vancouver, who was awarded one of the Alzheimer's Association's top scientific prizes at the meeting.

Another problem for the amyloid dogma is that "almost all aged brains have extensive amyloid deposition, even in people who die with no symptoms of Alzheimer's," says neurologist Peter Davies of the Albert Einstein College of Medicine in the Bronx. Worse, adds neurobiologist Nikolaos Robakis of Mount Sinai School of Medicine, New York City, autopsies of the brains of Alzheimer's victims show that "plaques don't correlate with neuronal death. The amyloid is here and the dead neurons are somewhere else."

No existing drug stops, let alone reverses, the inexorable cognitive and memory decline of Alzheimer's. The one thing baptists, tauists and apostates agree on is that drugs that prevent the disease will not cure it, and drugs effective against early Alzheimer's won't be the same as those that work against late Alzheimer's. We'll need a whole armamentarium."

Do not miss other WSJ Science J articles and letters on Alzheimer's: 16 April 2004 | 9 April 2004 | 27 April 2004

contributed by Alexei Koudinov (Related articles by contributor: 1 | 2 ) | Related NoL Subject collection


1 August 2004

Assessing Amyloid b. Research suggests a physiological role for the presumed villain
Adams, Jill U
The Scientist (29 March 2004) 18(6): p. 25
[FullText] [Author contact]

Leading text: "Recent work has revealed a potential physiological role for amyloid b, often considered a major culprit in Alzheimer disease (AD) pathology. This suggests that Ab, an ordinarily upstanding protein, turns bad as the result of a mob-type effect, when the physical buildup into plaques promotes neuronal damage and loss. "There's been a growing awareness over the last three or four years that it's not just a toxic peptide," says Hugh Pearson from the University of Leeds, UK."

contributed by Alexei Koudinov | Related NoL Subject collection


1 August 2004

Pressure rises on Elan over Alzheimer's drug brain shrinkage
Crowley, Des
The Sunday Times (1 August 2004)
[FullText] [FullText at Yahoo!ELN] [Author contact]

Leading text: "Elan Corporation, the Athlone-based biotechnology firm, is under pressure to abandon further development of its treatment for Alzheimer’s.

This follows negative findings from a leading scientist that showed the brains of patients who were being treated for the disease shrank when they were expected to expand."

contributed by Alexei Koudinov (Related articles by contributor: 1 | 2 ) | Related NoL Subject collection


31 July 2004

Mixed results after trials for Alzheimer's vaccine
Dembner, Alice, Globe Staff
Boston Globe (22 July 2004)
[FullText] [Author contact]

Leading text: "The first test in people of a vaccine to treat Alzheimer's disease produced mixed results, but it showed enough promise that companies are pressing ahead with other vaccines, researchers reported yesterday at the ninth International Conference on Alzheimer's Disease in Philadelphia.

Tests of the vaccine, made by Elan Corp. of Ireland and Wyeth of New Jersey, were halted in January 2002 when 18 of the 300 people in the trial developed a potentially fatal brain inflammation."

contributed by Alexei Koudinov | Related NoL Subject collection


31 July 2004

New Hope Seen For Vaccine For Alzheimer's
Hensley, Scott
The Wall Street Journal (22 July 2004) p.B.1
[WSJ Online] [Related News at Alz.Org] [Author contact]

Article summary: "The vaccine, known as AN-1792 and co-developed by Wyeth of Madison, N.J., and Elan Corp. of Dublin, Ireland, seeks to halt or reverse Alzheimer's by stimulating antibodies that attack protein clumps called amyloid plaques found in victims' brains. A clinical test was cut short when the vaccine caused some patients' immune systems to attack healthy brain tissue as well, causing life-threatening side effects.

To be sure, none of the patients was cured of Alzheimer's, and improvement in the patients' mental function was modest. On some standard tests of memory and alertness, the vaccinated patients did no better than the placebo group. And the risks in the vaccine are clear: Eventually, 18 of the 300 elderly Alzheimer's patients getting the injection came down with brain inflammation, or encephalitis, and the experiment was halted. Most recovered and none died, but the companies aborted the trial.

Some say the risks from vaccines against Alzheimer's are too great to continue testing such treatments. The encephalitis cases were a "catastrophe" says Peter Davies, an Alzheimer's researcher at the Albert Einstein College of Medicine, New York. A skeptic of the amyloid hypothesis, Dr. Davies nonetheless supports the testing of drugs against amyloid to help settle the debate about the root cause of Alzheimer's. But he remains steadfast against vaccines."

Do not miss two other WSJ articles on Alzheimer's: 16 April 2004 | 9 April 2004

contributed by Alexei Koudinov | Related NoL Subject collection


25 July 2004

Cholesterol drug maker disputes complaints
By Lauran Neergaard, AP Medical Writer
Boston Globe (22 July 2004)
[FullText] [Author contact]

Leading text: "WASHINGTON -- A drug company urged the government Wednesday to dismiss a petition to ban the new anti-cholesterol drug Crestor, arguing there's no evidence it is riskier than its competitors.

AstraZeneca said initial reports that a 39-year-old woman died of a muscle-destroying side effect of Crestor were false. A later autopsy instead declared her death a heart attack due to long-standing cardiovascular disease.

"The safety and efficacy of Crestor are well-documented," AstraZeneca said in documents filed with the Food and Drug Administration.

The company insisted there's no evidence that Crestor users are at higher risk of the rare but life-threatening muscle condition rhabdomyolysis than users of other cholesterol-lowering statin drugs -- a risk it put at one in 10,000 patients..."

contributed by Alexei Koudinov | Related NoL Subject collection


25 July 2004

FDA approves cholesterol drug Vytorin
Unsigned note
Boston Globe (23 July 2004)
[FullText] [Author contact]

Leading text: "WASHINGTON -- The Food and Drug Administration has approved a new cholesterol-lowering drug called Vytorin, the agency said Friday.

The pill, manufactured and marketed by a joint venture between Merck & Co. Inc. and Schering-Plough Corp., is a combination of two other cholesterol drugs, Zetia and Zocor..."

Beware about "statins' mind boggling effects"!

contributed by Alexei Koudinov | Related NoL Subject collection


22 July 2004

Seeking a Fuller Picture of Statins
David Tuller
The New York Times (20 July 2004)
[FullText: Part 1 | Part 2] [NYTimes on statins][Author contact]

contributed by Alexei Koudinov | Related NoL Subject collection


20 June 2004

Goodbye came early
Ryan, Jennifer
East Valley Tribune Online (20 June 2004)
[FullText] [Alternate FullText URL] [Author contact]

Leading text: "When Scott Phelps visits his mother, she calls him Bobby. Pauline Phelps gives her son a hug, sits on the couch next to him and forgets he’s there. The 84-year-old prefers to talk to her brother, Paul, or Aunt Shorty, both of whom died decades ago.

"We’re ready to go home," Pauline says to the air in front of her. "We are home," Scott, 52, of Ahwatukee Foothills tells her. Not really. Pauline, who is cared for in an Ahwatukee Foothills group home, lost the life she once knew and the mind she once had after participating in a clinical drug trial for Alzheimer’s disease.

The drug being studied, AN-1792, held the promise of becoming a vaccine that could prevent or slow the decline of Alzheimer’s — a disease that afflicts an estimated 4 million people nationwide, including 85,000 in Arizona, yet has few effective treatment options. Instead, the experimental drug made about a half dozen people like Pauline worse..."

contributed by Alexei Koudinov | Related NoL Subject collection


15 June 2004

Reagan's Experience Alters Outlook for Alzheimer's Patients
By Shankar Vedantam, Washington Post Staff Writer
Washington Post (14 June 2003) Page A01
[FullText] [Author contact]

Leading paragraph: "An Alzheimer's diagnosis means something very different today than when former president Ronald Reagan announced 10 years ago that he had the illness: More than any other Alzheimer's patient in history, Reagan -- with his fame and sunny personality -- dramatically reduced the stigma attached to the deadly degenerative disease, advocates say.

Nancy Reagan, furthermore, has championed the cause of Alzheimer's patients with the kind of clout that few other caregivers could wield, and the Reagan name has helped raise millions for research. Nancy Reagan has also led the fight against federal restrictions on embryonic stem cell research -- discreetly challenging President Reagan's most prominent admirer, President Bush, who imposed the restrictive policy..."

contributed by Alexei Koudinov | Related NoL Subject collection


15 June 2004

Cholesterol skeptics and the bad news about statin drugs
Napoli, Maryann
MedicalConsumers.org (June 2003)
[FullText] [FullText and the followup] [Author contact]

Leading paragraph: "The cholesterol skeptics were there. So were the physicians who challenge the safety and necessity of cholesterol-lowering drugs. And then there were the lipid researchers whose findings totally contradict the prevailing dietary advice to the public: Avoid saturated fats, limit cholesterol, and use more polyunsaturated oils..."

contributed by Alexei Koudinov | Related NoL Subject collection


14 June 2004

The soft science of dietary fat
Taubes, Gary
Science Magazine (30 March 2001) 291, 2536-2545.
[PubMed] [FullText] [Letter to the Editor: PubMed | FullText] [Author contact]

Leading paragraph: "Mainstream nutritional science has demonized dietary fat, yet 50 years and hundreds of millions of dollars of research have failed to prove that eating a low-fat diet will help you live longer..."

contributed by Alexei Koudinov


14 June 2004

Statins' Mind-Boggling Effects
CBS Evening News (24 May 2004)
[FullText] [Related article] [Author contact]

Leading paragraph: "When Jim Matthews needed to slash his cholesterol and heart attack risk, he joined the millions taking the world's top-selling drug, Lipitor. After five weeks, he was struck by cognitive chaos and confusion..."

Includes free video "Dangers of Statin drugs"

contributed by Alexei Koudinov | Related NoL Subject collection


10 June 2004

You're my wife?
Pagan, Sylvia
New Scientist (6 December 2003)
[FullText at: Eurekalert | AlzheimerSupport] [Related article] [Author contact]

Leading paragraph: "One day former astronaut Duane Graveline came back from a walk and failed to recognise his wife. He blamed this temporary bout of amnesia on the drug Lipitor, which he had been taking for several weeks. Doctors dismissed his fears, but six weeks after he started taking the drug again he suffered another bout of amnesia. This time he could not remember anything after high school, not even his children..."

contributed by Alexei Koudinov | Related NoL Subject collection


10 June 2004

Companies race for Alzheimer's drug. Disease that afflicted Reagan for a decade has no cure
Lisa Sanders
CBS Market Watch (10 June 2004)
[FullText] [More news stories at Alz.org] [Author contact]

Leading paragraph: "With millions of lives and billions of dollars at stake, companies are in fierce competition to cure the disease that killed former President Ronald Reagan..."

contributed by Alexei Koudinov | Related NoL Subject collection


10 June 2004

Reagan's death renews Alzheimer's interest?
Amanda Gardner
Forbes.com (10 June 2004)
[FullText] [Author contact]

Leading paragraph: "While the elaborate rituals of national respect for former President Ronald Reagan will come to a close tomorrow, the Reagan family's dedication to raising awareness about Alzheimer's disease shows no signs of ending..."

contributed by Alexei Koudinov | Related NoL Subject collection


10 June 2004

Lifestyle changes may be key to stop Alzheimer's. Youth could set stage for dementia?
Kotulak, Ronald
Chicago Tribune (9 June 2004)
[FullText at Houston Chronicle] [Related News: 1 | 2 | 3] [Author contact]

Leading paragraph: "Ronald Reagan's death, caused primarily by Alzheimer's disease, comes as researchers are beginning to discover that the illness likely has its start long before old age, possibly even in childhood..."

contributed by Alexei Koudinov | Related NoL Subject collection


28 April 2004

Does Bias Confound Alzheimer's Research?
Mahley, Robert W; Goldberg, Sheldon; Hodes, Richard J.
The Wall Street Journal (27 April 2004) p.A.19
[WSJ Online] [Letters at alternative URLs: 1 | 2 | UCDavis ADRC ] [Authors' contact: 1 | 2 | 3 ]

Do not miss other Wall Street Journal articles on Alzheimer's: 9 April 2004 | 16 April 2004 | 6 August 2004

contributed by Alexei Koudinov (Related articles by contributor: 1 | 2 ) | Related NoL Subject collection


28 April 2004

Statins for Blindness? Anticholesterol drugs may protect the retina.
Gupta, Sanjay.
Time (26 April 2004)
[FullText] [Editor contact]

contributed by Alexei Koudinov


24 April 2004

Nominal Benefits Seen in Drugs for Alzheimer's
Grady, Denise
New York Times (7 April 2004)
[FullText at NYTimes, requires free registration] [Author contact]

contributed by Alexei Koudinov | Related NoL Subject collection


18 April 2004

Scientists World-Wide Battle a Narrow View Of Alzheimer's Cause
Begley, Sharon.
The Wall Street Journal (16 April 2004) p.A.9
[FullText at WSJ][Free FullText at SFChronicle][Letters to the editor: 1 | 2 ][Abstract at SFC WSJ Digest] [Author contact]

Do not miss other Wall Street Journal articles on Alzheimer's: 9 April 2004 | 27 April 2004 | 6 August 2004

contributed by Alexei Koudinov (Related articles by contributor: 1 | 2 ) | Related NoL Subject collection


18 April 2004

Is Alzheimer's Field Blocking Research Into Other Causes?
Begley, Sharon.
The Wall Street Journal (9 April 2004) p.B.1
[FullText at WSJ][Free FullText at SFChronicle][Letters to the editor: 1 | 2 ][Derivative stories: 1 | 2 ][Author contact]

Do not miss other Wall Street Journal articles on Alzheimer's: 16 April 2004 | 27 April 2004 | 6 August 2004

contributed by Alexei Koudinov (Related articles by contributor: 1 | 2 ) | Related NoL Subject collection


18 April 2004

Anti-stroke drug eases Alzheimer's symptoms: Atorvastatin unclogs arteries and may help memory too.
Check, Erika
Nature News (16 March 2004)
[FullText] [Related story at: PRNewswire ][Authors contact]

contributed by Alexei Koudinov | Related NoL Subject collection


18 April 2004

Maverick Scientist Is Winning Converts On Alzheimer's
Wysocki, Bernard
The Wall Street Journal (26 Dec 2003)
[FullText Acrobat .PDF] [Author contact]

Beware that this article has communication arising matter published as letter to the editor, search WSJ to find it:

Letters to the Editor: Alzheimer's Research Funds
Rieder, Corinne H.
The Wall Street Journal (26 Dec 2003) p.A.19

contributed by Alexei Koudinov


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