Plaxgen Working to Expand Sales of Statin Test, Explore Lipid Morphology Data

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https://www.360dx.com/cardiovascular-disease/plaxgen-working-expand-sales-statin-test-explore-lipid-morphology-data

Plaxgen Working to Expand Sales of Statin Test, Explore Lipid Morphology Data

Nov 21, 2017 | Adam Bonislawski

NEW YORK (360Dx) – Diagnostics firm Plaxgen is looking to expand sales of its StatRes test for predicting patient response to statins.

The Fremont, California-based company has been offering the test on an early-access basis through an agreement it signed last year with St. Joseph Health, a regional hospital system with five hospitals throughout Northern California and is now working to expand its reach through similar agreements with additional hospitals, said Shanmugavel Madasamy, Plaxgen’s founder and CEO.

The company is also investigating whether data on the morphology of cholesterol particles could help identify patients at risk of cardiac events and guide statin therapy. In September, company researchers and their collaborators published a study in the Journal of Visualized Experiments in which they found links between particle morphology and abnormal lipid levels, and observed changes in patient particle morphology following treatment with various statins.

Launched by Madasamy in 2007, Plaxgen uses a system that combines the capture of target biomarkers on plaque arrays with the isolation and analysis of those markers by techniques including flow cytometry and MALDI mass spectrometry.

The company’s plaque array system works essentially as an enrichment step, allowing researchers to investigate only plaque-related serum proteins, as opposed to the full serum proteome. The arrays are composed of soluble plaque-forming constituents that are then incubated with serum from test subjects. These plaque-forming constituents work as substrates for the plaque-related serum analytes, allowing for their pull-down and subsequent analysis.

Last year, the company published a paper on the StatRes test in the American Journal of Cardiology looking at 30 serum samples from patients with high cholesterol who went on to receive treatment with statins. It found that it was able to predict response in 13 of 15 patients receiving simvastatin and 12 of 15 patients on atorvastatin.

The company is now putting together a larger clinical validation trial in which it plans to follow thousands of patients over the course of four years. Madasamy said it hopes with that data to take the test through the US Food and Drug Administration regulatory process. Plaxgen currently offers the StatRes test as a laboratory-developed test through its CLIA lab.

In the JoVE study, the company paired its plaque capture system with analysis by imaging flow cytometry, which allowed it to study the shape of circulating cholesterol particles.

ESPN Deportes — ESPN’s 24-hour, Spanish-language sports network http://www.devensec.com/devserv.html viagra prescription in the U.S. will carry the NASCAR Nationwide Series race telecast and the Daytona 500 with NASCAR-related programming and coverage. You need to see that you taking the medicine in proper discount levitra purchase way. Glutathione’s role in liver detoxification is devensec.com super cheap viagra paramount. The major ones are loss of vision hearing and erection longer than 4 cheapest viagra tablets hours. “In general, it’s understood that in atherosclerosis, not only the number of particles, but also the morphology and size of the particles, plays an important role [in the condition],” Madasamy said. However, he noted, the role of morphology has seen relatively little study compared to work focused on quantification of lipids involved in atherosclerosis.

The researchers used Plaxgen’s technology coupled to imaging flow cytometry to compare the morphology of cholesterol particles in 50 patients with plaque disease and age-matched healthy controls, and found that the subjects with plaque disease had higher levels of linear-shaped particles (mean of 18.3 percent) compared to healthy controls (mean of 11.1 percent).

They also used the platform to look at the changes in morphology of cholesterol particles in response to treatment with various lipid-lowering agents, incubating isolated particles with lovastatin, simvastatin, atorvastatin, rosuvastatin, fluvastatin, ezetimibe, fibrate, niacin, and omega-3 fatty acid. They analyzed drug-induced morphology changes and found that lovastatin, simvastatin, atorvastatin, and ezetimibe induced the formation of both linear and globular morphologies, while rosuvastatin, fluvastatin, fibrate, niacin, and omega-3 fatty acid induced formation of only globular particles.

The results, Madasamy said, suggest both the role of morphology in plaque disease and that different lipid-lowering drugs may have different effects on this morphology.

“We believe that in specific populations, the morphology data could be a biomarker to complement [existing] diagnostics to improve accuracy,” he said. “Because, yes, a patient’s lipid levels can look fine, but they can still have a heart attack or stroke.”

Madasamy said Plaxgen is now applying its morphology analysis to the amyloid-beta plaques characteristic of Alzheimer’s disease, another area of focus for the company.

“We are expanding to that and have data that we hope to publish next year,” he said.

 

 

 

 

 

Dx Firm Plaxgen Moving Plaque-based Alzheimer’s, Atherosclerosis Tests toward Commercialization

genomewebClick here to read full article…

NEW YORK (GenomeWeb) – Having spent the last seven years prepping its technology, proteomic diagnostics firm Plaxgen is now moving tests for Alzheimer’s disease and atherosclerosis towards commercialization.

The FDA purchase cheap cialis ensures that the drug is completely safe for use as it is approved by FDA. There are multiple issues that produce impaired hearing sensitivity. viagra rx For example, if someone isn’t managing their stress, the blood pressure medication becomes an “enabler,” – merely allowing deeper prescription canada de cialis stress issues to compound. In this case a preferably discount viagra cialis higher dosage is to be avoided at all costs. First in line is the company’s Alzheimer’s diagnostic, named Amyload, for which it is currently planning a validation study expected to begin in June 2015 and run through approximately January 2016, Plaxgen Founder and CEO Shanmugavel Madasamy told GenomeWeb.

The company plans to offer the test initially out of its Fremont, Calif.-based CLIA facility while simultaneously filing for US Food and Drug Administration 510(k) clearance, he said, noting that it plans to target the test to pharma firms that would use it for selecting patients for clinical trials and measuring response to treatment.

UM researcher uses stem cells to fight Alzheimer’s

The Detroit News

UM researcher uses stem cells to fight Alzheimer’s

http://www.detroitnews.com/story/news/local/michigan/2014/11/11/um-researcher-uses-stem-cells-fight-alzheimers/18895621/

Kim Kozlowski, The Detroit News 11:38 p.m. EST November 11, 2014

Ann Arbor — Inside a laboratory at the University of Michigan, researchers have been injecting stem cells into the brains of mice engineered to have Alzheimer’s disease, and making remarkable discoveries.

The experiments are among the first in the nation to examine how stem cell therapies might alter the course of Alzeheimer’s, a fatal disease that afflicts more than 5 million people in the U.S. and is widely regarded as an epidemic predicted to explode as the nation’s population ages.

The research is being overseen by UM’s Dr. Eva Feldman, who pioneered the nation’s first clinical trial using stem cells in patients with amyotrophic lateral sclerosis — a disease that received global awareness last summer thanks to the ALS ice bucket challenge.

Dr. Feldman

While Feldman’s ALS trial is not complete, it is showing promise. That’s why she began an experiment to see how stem cells might fare in treating Alzheimer’s disease, another neurodegenerative disorder.

Although it’s very early in the research, the Alzheimer’s experiment with mice showed that stem cells made a mouse with Alzheimer’s disease indistinguishable in behavior and memory from a mouse that didn’t have the disease.

“When you work in science, you do as many experiments that don’t work that do,” Feldman said. “When you get something that works so beautifully (like this experiment), you can quickly see its translational potential. I am looking at a mouse but some day I could be looking at a man. As a clinician scientist, those are the moments you live for.”

The findings from Feldman’s preclinical trial were presented last month in Boston at the Congress of Neurological Surgeons annual meeting.

While some experts are cautiously optimistic, others hailed Feldman’s work.

“The special design of the present study sets new standards for further clinical translation in regenerative medicine for neurological diseases,” Tamir Ben-Hur, a Jerusalem-based neurology professor, wrote earlier this year in the Annals of Neurology. “This study design represents the best moral solution for the difficult task of testing risky procedures in a deadly disease with no alternative therapy or hope.”

Feldman, a UM professor and neurologist, began testing stem cells years ago. Her research began with rats and pigs with ALS — also known as Lou Gehrig’s disease — before she launched a clinical trial in humans with the disease five years ago.

Last year, some participants in the human study either improved or stabilized in the closely watched clinical trial.

Soon after, the Alzheimer’s study was launched. That study used fetal stem cells provided by Neuralstem Inc., a Maryland company. It used mice that had been engineered with the inherited gene of Alzheimer’s but had not yet displayed symptoms.
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With one group of the mice, UM researchers injected the stem cells into the hippocampus, the area of the brain that controls learning and memory. Another group of mice were injected with saline solution. The mice that got the stem cells were evaluated with several behavioral and memory tests — and looked the same as mice without Alzheimer’s disease.

“Those animals retained their ability to think, as a mouse does, to recognize objects so they looked just like an animal that doesn’t have Alzheimer’s disease,” Feldman said. “It’s really remarkable.”

Feldman is still deciding which larger animal model to use for further research, but her associates say it likely will be rhesus monkeys.

“She’s doing stuff that needs to be done,” said Robert Karbel, manager of the Sinai Medical Staff Foundation in Southfield, a group of physicians that has supported Feldman’s research with $500,000. “She has the courage to do it … and she seems to be making progress. There are no cures yet, but she’s working at it.”

Feldman’s latest study is generating excitement because if successful, it has the potential to impact millions of lives. About 5,600 people are diagnosed with the disease each year, according to the ALS Association, but Alzheimer’s afflicts 100 times more people, not counting their family caregivers.

Alzheimer’s is a fatal disease with no cure and no meaningful agents to delay its course. The disorder slowly robs people of their ability to remember and perform daily tasks, which is why so many end up in long-term care facilities.

As the baby boomer population ages, many regard Alzheimer’s as a tsunami that could swamp the nation’s health care system if a better intervention is not discovered, in part because of how costly it is to care for its victims.

In 2014, the direct costs to care for those with Alzheimer’s will total an estimated $214 billion, including $150 billion in Medicare and Medicaid costs, according to the Alzheimer’s Association.

By 2050, those costs are expected to soar to an estimated $1.2 trillion.

There are all kinds of studies — nearly 50 — in various stages of research to address the disease. But Feldman is among the first to examine stem cells, according to Dr. Keith Fargo, director of scientific programs and outreach at the Alzheimer’s Association.

Fargo said the research is very preliminary, and should be regarded cautiously. But he also said it is intriguing.

“We think all kind of research is needed,” Fargo said. “We support a full-court press in Alzheimer’s disease research.”

For people like Ted Harada, the research is more personal. Harada, 42, of McDonough, Ga., was in the first phase of Feldman’s ALS trials, shortly after he was diagnosed with ALS in 2011.

He received millions of stem cells in his spinal cord in two separate surgeries.

By his doctor’s predictions, he could have already lost his battle to the disease. Instead, he no longer uses a cane and has stabilized.

“We’ve all heard for years that stem cells could be the next big frontier in medicine,” Harada said.

“It’s great they are finally allowing these type of trials and I am so thankful researchers like Dr. Feldman are on the front lines pushing the envelopes and not accepting the status quo. Her research is giving hope to communities where hope was an absent commodity.”

 

Scientists slowly unravel Alzheimer’s mystery

Alzheimer’s disease appears to have multiple causes,
and scientists are slowly unraveling them

By Alice Dembner
GLOBE STAFF
A century after Alois Alzheimer identified the
debilitating dementia that carries his name, scientists
are still trying to determine what causes the
disease in old age. Their quest takes on increasing
urgency, with predictions that unless a cure is found,
the number of Americans with the disease will rise
from about 4.5 million now to 13 million in 2050.
Many scientists believe that Alzheimer’s results
from a complex interplay of environmental factors,
lifestyle choices, and genes and proteins gone haywire.
But the changes in the brain that characterize
the disease develop over decades and also occur in
some healthy seniors, making it diffi cult to sort out
the culprits from the bystanders.
Yet, tantalizing tidbits have surfaced in the last
few weeks, including discovery of a new genetic
mutation that appears to increase the risk of getting
Alzheimer’s and new evidence that insulin defi ciencies
may contribute to deterioration of the brain.
“The pieces are coming together. We’ve got the
outline of the puzzle in place, and we’re beginning to
see the form,” said Stephen Snyder, who oversees
research on the causes of Alzheimer’s for the National
Institute on Aging. “It’s probably fi ve or six genes and
a dozen proteins that get out of kilter,” said Snyder, and certainly not just the sticky clumps of
proteins called beta-amyloid plaques that
have received the most attention.
In the brain, the disease’s hallmarks
are those plaques, tangles of another protein
called tau, and the progressive death
of nerve cells, called neurons, that gradually
strip a victim of memory, language,
reasoning, and, finally, life.
Mutations in three genes cause earlyonset
Alzheimer’s, the rare form of the
disease that strikes people in their 30s,
40s, or 50s. Those altered genes trigger
production of too much beta-amyloid. But
none appears to be involved in the kind of
Alzheimer’s that strikes after age 60.
So far, researchers have linked two major
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and are on the trail of four or five more.
These mutations do not cause the disease,
but rather increase the risk of developing
it. One, ApoE4, increases the risk of getting
the disease three- to four-fold. A second
potential gene mutation, called
UBQLN-1, was identified this month by
Rudy Tanzi, a geneticist at Massachusetts
General Hospital. Tanzi, founder of TorreyPines
Therapeutics, which is working
on Alzheimer’s drugs, said he believes it
may increase the risk one- to two-fold, but
its specific role in the disease has not been
determined.
The lead suspect in the search for a
cause remains the protein beta-amyloid
because of its clear involvement in early
onset Alzheimer’s and its big presence in
Alzheimer’s brains.
Tests of an amyloid vaccine in people,
which might have proved amyloid’s leading
role, were halted in 2002 when 18 of
300 subjects developed a potentially fatal
brain inflammation. Nevertheless, some
participants showed inklings of a positive
effect, enough to keep researchers pursuing
similar experiments. In addition, antibodies
to amyloid reversed memory problems
in mice, and cleared out amyloid
deposits and then tau.
‘‘It’s my feeling that all the cases of Alzheimer’s
are caused by an imbalance in
the accumulation versus removal of the
beta-amyloid protein,’’ said Dr. Dennis
Selkoe, a leading amyloid researcher who
is codirector of the Center for Neurologic
Diseases at Brigham and Women’s Hospital,
and who is a director of Elan Corp.,
which is working on amyloid-based treatments.
Much of the amyloid research is shifting

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