Large epidemiologic study supports brain power of fish in older people

Experts estimate that over 24 million people worldwide suffer from dementia, and many of these people live in low- and middle-income countries. Recently, there has been growing interest in whether dietary factors, particularly oily fish and meat, might influence the onset and/or severity of dementia. Oily fish are rich in omega-3 long-chain polyunsaturated fatty acids, which some studies suggest are positively related to cognitive function in later life. Conversely, there is a suggestion from some studies that increased meat consumption may be related to cognitive decline. To examine this, a group of international researchers studied older people in 7 middle- to low-income countries. You can read the results of their study in the August 2009 issue of the American Journal of Clinical Nutrition.

Data from 14,960 participants (≥65 y of age) living in China, India, Cuba, the Dominican Republic, Venezuela, Mexico, and Peru were analyzed. Dietary habits were assessed by using standard, culturally appropriate face-to-face interviews, and dementia was diagnosed by using validated culturally and educationally fair criteria.

In each of the study countries, except India, there was an inverse association between fish consumption and dementia prevalence. These data extend to low- and middle-income countries previous conclusions from industrialized countries that increased fish consumption is associated with lower dementia prevalence in later life. The authors propose that this relation is not due to poor overall nutritional status in those with dementia, because meat consumption tended to be higher in this group. The relation between meat consumption and dementia remains unclear.


To access full text of the study visit: http://www.nutrition.org/media/publications/ajcnAug709.pdf

Evidence for a New Genetic Link to Therapeutic Efficacy for Alzheimer's Disease

Tue Jul 14, 2009 7:08am EDT

Study to be presented at the 2009 International Conference on Alzheimer's
Disease

BROOMFIELD, Colo., July 14 /PRNewswire/ -- Accera, Inc., a biotechnology
company delivering breakthrough therapies in central nervous system diseases,
today announced further evidence for genetic interactions impacting the
efficacy of the ketogenic compound AC-1202 (Axona(TM)) in Alzheimer's disease.
New data from the company's previously completed double-blind,
placebo-controlled trial in patients with mild-to-moderate Alzheimer's disease
demonstrates an interaction between two genetic markers that strongly
influence the therapeutic response in patients. Dr. Samuel Henderson,
Executive Director of Research, will present these results at the 2009
International Conference on Alzheimer's Disease (ICAD) sponsored by the
Alzheimer's Association.

During this study, patients received daily administration of either AC-1202 or
placebo for 90 days, with efficacy assessments performed at Baseline (Day 0),
Day 45, Day 90 and after a two week washout from their assigned product on Day
104. In addition, analyses of a number of genotypic markers judged to be
relevant to the physiological background of Alzheimer's disease were also
performed.

Previous analysis of the study revealed that patients administered AC-1202 who
lacked the epsilon 4 variant of the APOE gene (E4(-)), demonstrated
significant improvement from baseline values in the Alzheimer's Disease
Assessment Scale-Cognitive (ADAS-Cog) and improvement compared to placebo of
4.77 at Day 45 and 3.36 at Day 90 (p <0.05). ADAS-Cog, a neuropsychometric
battery of tests that measures short-term memory and cognition, is probably
the most widely used cognitive instrument used in clinical trials of
anti-dementia drugs within the United States and Europe. Numerous clinical
studies have demonstrated that modest improvements in ADAS-cog scores - on the
order of 2 to 3 points over the course of a year - have been associated with
significant cost reductions in overall managed care expenditures.

To further investigate pharmacogenomic responses of AC-1202 in AD, the effects
of APOE4 carriage status and a polymorphism (IDE_7) in the insulin degrading
enzyme gene (IDE) on ADAS-Cog scores were evaluated over the study course. In
addition to degrading insulin, the Ide protein also degrades amyloid beta
peptide and has been implicated in playing a role in Alzheimer's disease.

In the population of patients who were both APOE4(-) and lacked the C/C
polymorphism in IDE 7, more pronounced improvements in ADAS-cog scores than
those previously reported were observed at each assessment time point (Day 45,
90 and 104). At Day 45 the improvement in ADAS-cog score was 4.18 (p=0.0004),
while at Day 90 the difference was 4.73 (p=0.001). Of interest, a significant
difference in cognitive test scores of 3.27 was observed two weeks after
termination of AC-1202 treatment (p=0.034). This finding suggests that daily
administration of AC-1202 may produce lasting effects in those patients with
this combination of genotypic markers.

The combination of the E4(-); IDE_7(C/C)(-) genotype is prevalent in
approximately 40% of the AD population, so the number of potential responder
patients is substantial.

"This pharmacogenomic finding provides both insight into the mechanism of
ketone-based therapies for Alzheimer's disease, and also allows for the
identification of patients who may respond best to therapy, " said Dr. Samuel
Henderson, Research Director at Accera. "This is the first scientific report
of the role of IDE and its interaction with APOE on therapeutic efficacy in
Alzheimer's disease patients."

The study results will be presented on Wednesday, July 15 under the title,
"Evidence of an Interaction Between APOE and IDE in Ketone Body Therapies in
Mild to Moderate Alzheimer's Disease." The conference is being held in
Vienna, Austria at the Messe Wien Exhibition and Congress Center.


About Axona(TM)
Axona is a first-in-class medical food for the clinical dietary management of
the metabolic processes associated with mild-to-moderate Alzheimer's disease.
Dispensed by prescription, Axona targets the metabolic deficiencies and
imbalances associated with Alzheimer's disease by providing an alternative
energy source for brain cells. With simple administration and once-a-day
convenience, Axona is complementary to current Alzheimer's disease therapies.
For more information about Axona, please visit www.about-axona.com or ask your
physician.

About Alzheimer's Disease
Alzheimer's disease, the most common form of dementia, is a progressive and
fatal disease for which there is no cure. In the United States, 5.2 million
people are living with AD, and it has become the sixth leading cause of death.
The disease attacks the brain's cells, resulting in loss of memory, executive
function and language skills.

AD significantly impacts millions of family members and other caregivers -
mentally, physically and financially. The national Family Caregiver Alliance
estimates that approximately 80 percent of caregivers provide unpaid
assistance seven days a week. With the lack of innovative new medications for
AD, both patients and caregivers are seeking alternatives to improve quality
of life.

About Accera, Inc.
Accera, Inc. is a privately held commercial-stage biotechnology company that
developed and now markets Axona in the US. Axona is a prescription-only
medical food intended for the clinical dietary management of the metabolic
processes associated with mild-to-moderate Alzheimer's disease. In clinical
trials, Axona has been shown to safely improve cognitive function and memory
in AD patients. Axona addresses the hypometabolism or defective metabolism of
glucose that occurs in those areas of the brain that are involved in
Alzheimer's disease. Accera engages in research, development and
commercialization of other clinical applications for Axona.

For more information about Accera, please visit www.accerapharma.com.

Contacts:
Accera, Inc.
Steve Orndorff, Ph.D.
President and CEO
sorndorff@accerapharma.com

Richard Lewis Communications, Inc.
(212) 827-0020
Andrew Mielach, Media
amielach@rlcinc.com
Cecelia Heer, Investors
cheer@rlcinc.com




SOURCE Accera, Inc.

Steve Orndorff, Ph.D., President and CEO of Accera, Inc. ,
sorndorff@accerapharma.com; or Media, Andrew Mielach, amielach@rlcinc.com, or
Investors, Cecelia Heer, cheer@rlcinc.com, both of Richard Lewis
Communications, Inc. , +1-212-827-0020, for Accera, Inc.
© Thomson Reuters 2009 All rights reserved

Scientists aim to create robot-insects

The Northern Star | July 14, 2009

Japanese scientists are hoping to rebuild the brain of an insect to create a robo-bug.

POLICE release a swarm of robot-moths to sniff out a distant drug stash. Rescue robot-bees dodge through earthquake rubble to find survivors.

These may sound like science-fiction scenarios, but they are the visions of Japanese scientists who hope to understand and then rebuild the brains of insects and program them for specific tasks.

Ryohei Kanzaki, a professor at Tokyo University's Research Centre for Advanced Science and Technology, has studied insect brains for three decades and is a pioneer in the field of insect-machine hybrids.

His original and ultimate goal is to understand human brains and restore connections damaged by diseases and accidents - but to get there he has taken a very close look at insects' "micro-brains".

The human brain has about 100 billion neurons, or nerve cells, that transmit signals and prompt the body to react to stimuli.

Insects have far fewer - about 100,000 inside the two-millimetre-wide brain of a silk moth.

But size isn't everything, as Kanzaki points out.

Insects' tiny brains can control complex aerobatics such as catching another bug while flying, proof that they are "an excellent bundle of software" finely honed by hundreds of millions of years of evolution, he says.

For example, male silk moths can track down females from more than a kilometre away by sensing their odour, or pheromone.

Kanzaki hopes to artificially recreate insect brains.

"Supposing a brain is a jigsaw-puzzle picture, we would be able to reproduce the whole picture if we knew how each piece is shaped and where it should go," he told AFP.

"It will be possible to recreate an insect brain with electronic circuits in the future. This would lead to controlling a real brain by modifying its circuits," he said.

Kanzaki's team has already made some progress.

In an example of 'rewriting' insect brain circuits, Kanzaki's team has succeeded in genetically modifying a male silk moth so that it reacts to light instead of odour, or to the odour of a different kind of moth.

Such modifications could pave the way to creating a robo-bug which could in future sense illegal drugs several kilometres away, as well as landmines, people buried under rubble, or toxic gas, the professor said.

Scientists Zero In on Elusive 'Allergy Gene'

THURSDAY, July 9 (HealthDay News) -- A defective gene significantly increases the likelihood of developing such allergic disorders as eczema and asthma, Scottish researchers report.


Reviewing the findings of 24 studies, researchers from the University of Edinburgh concluded that mutations of the filaggrin gene -- which is thought to help maintain an effective skin barrier against the environment -- significantly increase the risk for developing allergic sensitization, atopic eczema, allergic rhinitis and asthma in people with eczema.


The link between atopic eczema and filaggrin gene mutations appeared to be particularly strong, the study found.


"These findings provide strong supporting evidence that, at least in a subset of those with allergic problems, the filaggrin gene defect may be the fundamental predisposing factor not only for the development of eczema but also for initial sensitization and progression of allergic disease," the study authors wrote. "Our findings suggest that filaggrin is a robust biomarker for allergic conditions."


They called for further research to investigate whether filaggrin can be used to identify people at high risk for allergic conditions. Restoring skin barrier function early in life in people with filaggrin defects might help prevent the development of allergic sensitization and stop the development and progression of allergic disorders, the researchers suggested.


The study was to be published online July 10 in BMJ.


In an accompanying editorial, Hugo Van Bever, a professor of pediatric allergy and immunology at National University Singapore, and his colleagues described the finding as an important advance in understanding the genetic basis of allergic disease.


The next step is to determine whether it's possible to distinguish different genotypes of allergy, which could provide a breakthrough in the prevention, diagnosis and treatment of allergies in children, they said.

Genes Linked to Cholesterol in Cells Are Identified

07.07.09, 12:00 PM EDT

Discovery could lead to new treatment targets, researchers say


TUESDAY, July 7 (HealthDay News) -- Twenty genes that play major roles in controlling cholesterol within cells have been identified by German researchers, who said that some of the genes may play a role in heart disease risk and offer new targets for drug treatment.

The 20 genes are likely to be "immediately relevant" for maintaining cholesterol levels in the cell, as well as controlling the uptake of low-density lipoprotein (LDL) cholesterol, the researchers explained in the July 8 issue of Cell Metabolism.

"High cholesterol in the blood is considered to be responsible for excess cardiovascular morbidity and mortality," Dr. Heiko Runz, of the University of Heidelberg, said in a news release from the journal's publisher. "Blood cholesterol levels are controlled by cholesterol in cells. Therefore, some of the genes identified by us as regulators of cellular cholesterol in future studies might turn out to be disease genes that contribute to hypercholesterolemia [high cholesterol] in some cases."

The genes identified in the study may also have potential as targets for new cholesterol-lowering drugs, the researchers say. And the new methods used in the study could help identify many more cholesterol genes.

"Until now, disease-associated genes affecting blood cholesterol levels have successfully been identified in single families and, more recently, genomic studies involving large number of patients," Runz and colleagues wrote.

"Most of what we know about the molecular machinery that keeps cholesterol levels balanced, however, comes from using cultured cell models," they said. "A functional analysis of many genes at once by the integrated functional genomics technology applied here now harbors potential not only to ease identification, but also to better describe the molecular roles of cholesterol regulators in health and disease."

Rules Will Allow Financing for Old Stem Cell Lines

By GARDINER HARRIS
Published: July 6, 2009


WASHINGTON — The Obama administration released final rules governing stem cell research on Monday that will allow many older stem cell lines to be eligible for federally financed research.

The changes came in response to criticism from scientists that the rules that the administration proposed in April — requiring that donors of fertilized eggs sign extensive consent forms — would have made even some of the stem cell lines approved by the Bush administration ineligible for further money.

Dr. Raynard S. Kington, acting director of the National Institutes of Health, said in a news conference that his agency would insist that any scientists creating stem cell lines after Tuesday follow the new rules to the letter for their work to be eligible.

Scientists using stem cell lines created before Tuesday may seek review by a group of the Advisory Committee to the Director. If the lines were created under conditions that met the spirit but not the letter of the new rules, they will be approved, Dr. Kington said.

“Many of the lines already in existence may have met very rigorous standards of informed consent but may have been implemented in ways not consistent with the present guidelines,” Dr. Kington said. “It’s unreasonable to retroactively apply procedures intended for future use.”

The crucial test is whether the embryos used to create the stem cell lines were created for reproductive purposes, and whether donors freely consented for their use in research procedures, Dr. Kington said. Some researchers had used videos in addition to written forms, and such a minor difference in process should not render the work ineligible for financing, Dr. Kington said.

Some older stem cell lines will be eligible, but he refused to speculate which of the older lines would be approved. The committee will also review the eligibility of stem cell lines created in other countries, where different rules may apply.

“I’m very pleased they have taken feedback of an overwhelming majority of the scientific community and responded with a science-friendly proposal,” said Dr. George Q. Daley, director of the stem cell transplantation program at Children’s Hospital Boston.

Dr. Daley also praised the agency for creating a registry of stem cell lines that meet the agency’s approval.

“Every institution shouldn’t have to rediscover which cell lines are eligible for N.I.H. funding, so having a registry is very practical,” Dr. Daley said.

The rules still forbid financing of research using stem cell lines from embryos created solely for research.

With more than $10 billion in stimulus money, health institute officials have been eager to expand stem cell research. Just 21 stem cell lines have been eligible for federal financing under the old rules. But researchers using private money have created more than 700 stem cell lines.

Research Reveals Clues to Breast Cancer's Spread

07.06.09, 12:00 PM EDT
Interrupting key signals might prevent recurrence, investigators say


MONDAY, July 6 (HealthDay News) -- A U.S. research team says it has spotted key signals that help breast cancer cells survive in the bone marrow of patients who've undergone treatment.

The finding, reported in the July issue of the journal Cancer Cell, could lead to new treatments to prevent breast cancer's return, according to the researchers.

"We sought to identify signaling pathways that support the survival of metastasized breast cancer cells and thereby extend the period during which metastasis may emerge after the diagnosis and removal of a breast tumor," senior study author Dr. Joan Massague, of the cancer biology and genetics programs at Memorial Sloan-Kettering Cancer Center and the Howard Hughes Medical Institute, explained in a journal news release.

The researchers analyzed samples from more than 600 breast tumors and found that a cancer-related enzyme called Src was associated with late-onset bone metastasis. This link was independent of breast cancer subtype and was selective and specific for breast cancer cell survival in bone marrow.

Massague and colleagues then identified Src-regulated signaling molecules that were expressed in bone marrow and promoted survival of breast cancer cells. They also found that Src increased resistance to a key cell death-inducing signal.

The findings provides insights into breast cancer's spread, "and suggests strategies to hasten the attrition of disseminated breast cancer cells," the researchers concluded. They also noted that drugs designed to inhibit Src have recently been developed "that may be worthy of consideration" to help fight tumor recurrence.

More information

Breastcancer.org has more about recurrent and metastatic breast cancer.