TSX: AMF
TORONTO, Nov. 27 /CNW/ - Amorfix Life Sciences (TSX: AMF), a company
focused on treatments and diagnostics for brain-wasting diseases, today
announced the discovery of misfolded superoxide dismutase 1 (SOD1) protein in
the brains of people with Alzheimer's Disease. This breakthrough result
suggests that SOD1 is a common link between the two brain-wasting diseases,
Alzheimer's and ALS, also known as Lou Gehrig's Disease. SOD1 has a
"Jekyll-and-Hyde" nature as it normally plays an important protective role in
detoxifying free radicals in the body, but when misfolded can create lethal
oxidative free radicals.
"Amorfix previously reported results from pilot studies showing our
proprietary antibodies and vaccines targeting misfolded SOD1 showed life
extension in a mouse model of ALS. Amorfix will now investigate the use of
these same or similar agents to treat Alzheimer's disease," said Dr. Neil
Cashman, Chief Scientific Officer of Amorfix. "Evidence of free radical
toxicity has been observed in Alzheimer's disease for many years and the
discovery of the presence of misfolded SOD1 strongly suggests this toxicity is
associated with SOD1."
click here for the full story
Tuesday, November 27, 2007
Sunday, November 25, 2007
Getting out of the loop of Alzheimer's disease
Scientists from UCLA recently pinpointed a possible physical origin of Alzheimer's disease. The amyloid-beta protein has long been known to clump in the brain and be involved in the progression of the disease. The UCLA team identified a loop in the protein that is likely to enable amyloid-beta's adhesion process. This discovery sAlzheimer's disease (AD) is the most common cause of late-life dementia. It is estimated to affect 24 million people worldwide, and half of the people over 85 may suffer from it. This fatal disorder is characterized by a decline in the individuals' memory and in their ability to think and function independently. Current drugs treat the symptoms of Alzheimer's but not the underlying cause of the disease.
A protein called the amyloid-beta protein (A-beta) is thought to be a key cause of AD. A-beta proteins apparently stick together to form toxic deposits in the brain. Self-associations of A-beta can form various clump structures called "amyloid plaques". Recent studies suggest that these plaques have potent neurotoxic activities that may kill brain cells.
UCLA scientists, headed by David Teplow, Professor of Neurology at the David Geffen School of Medicine at UCLA, have recently identified a loop in the A-beta protein that is likely to be responsible for the adhesion process. The UCLA team employed an interdisciplinary research strategy. Among other methods, they have revealed morphologic, conformational, and aggregation features of synthetic A-beta in a tube ('in vitro'), examined the effects of various A-beta assemblies on the physiology of cultured neuronal cell lines ('in vivo') and used computerized methods ('in silico') to produce models of A-beta structures and to study its conformational dynamics and assembly. The researchers thus discovered that gene mutations in A-beta increase the flexibility of the protein's loop, enabling it to join easily with loops of other A-beta proteins to form clumps. The loop is also located in the region of the protein that regulates the formation of A-beta and its amount.
uggests new ways to treat the disorder's cause, rather than just the symptoms
click here to read the full story
A protein called the amyloid-beta protein (A-beta) is thought to be a key cause of AD. A-beta proteins apparently stick together to form toxic deposits in the brain. Self-associations of A-beta can form various clump structures called "amyloid plaques". Recent studies suggest that these plaques have potent neurotoxic activities that may kill brain cells.
UCLA scientists, headed by David Teplow, Professor of Neurology at the David Geffen School of Medicine at UCLA, have recently identified a loop in the A-beta protein that is likely to be responsible for the adhesion process. The UCLA team employed an interdisciplinary research strategy. Among other methods, they have revealed morphologic, conformational, and aggregation features of synthetic A-beta in a tube ('in vitro'), examined the effects of various A-beta assemblies on the physiology of cultured neuronal cell lines ('in vivo') and used computerized methods ('in silico') to produce models of A-beta structures and to study its conformational dynamics and assembly. The researchers thus discovered that gene mutations in A-beta increase the flexibility of the protein's loop, enabling it to join easily with loops of other A-beta proteins to form clumps. The loop is also located in the region of the protein that regulates the formation of A-beta and its amount.
uggests new ways to treat the disorder's cause, rather than just the symptoms
click here to read the full story
Thursday, November 22, 2007
Promising Blood Test for Alzheimer's
The online edition of the British journal Nature Medicine has a study of a blood test for Alzheimer's disease, developed at Stanford. The test lights up if 18 specific molecules are present in a blood sample. Using samples of stored blood, the test proved 90% accurate in identifying people who had been diagnosed with the disease by other methods. It was also 87% accurate in distinguishing samples from people who do not have Alzheimer's but exhibit some other form of dementia. The numbers of samples involved were small — SFGate's writeup has some details. The Mercury News's article says the test's developers want to begin selling it to laboratories in 2008, for which FDA approval would not be required. They hope to get FDA approval for general use by 2009.
Wednesday, November 14, 2007
Beta Carotene May Hold Dementia at Bay
Ivanhoe Newswire) -- Could a beta carotene supplement taken every other day keep your brain in good working order as you get older?
Boston researchers who followed a large group of men for about 18 years believe the answer may be yes. Their study shows men who took the supplements scored better on tests to measure cognitive functioning than men who received a placebo pill for comparison purposes.
While the differences in scores between the two groups were small, the researchers emphasize small changes can lead to a big difference in dementia risk down the road.
“Studies have established that very modest differences in cognition, especially verbal memory, predict substantial differences in eventual risk of dementia,” write the authors.
Beta carotene is thought to protect the brain by reducing oxidative stress that can lead to cognitive decline.
The researchers believe these results have important implications for public health policy and deserve further investigation. In an accompanying editorial, however, fellow investigators issue a word of caution. Specifically, they note other studies have associated high dose antioxidant use with adverse health consequences and even a greater risk of death.
Beta carotene, for example, has been linked to a increase risk of lung cancer in smokers.
This article was reported by Ivanhoe.com, which offers Medical Alerts by e-mail every day of the week. To subscribe, click on: http://www.ivanhoe.com/newsalert/.
SOURCE: Archives of Internal Medicine, 2007;167:2184-2190
Boston researchers who followed a large group of men for about 18 years believe the answer may be yes. Their study shows men who took the supplements scored better on tests to measure cognitive functioning than men who received a placebo pill for comparison purposes.
While the differences in scores between the two groups were small, the researchers emphasize small changes can lead to a big difference in dementia risk down the road.
“Studies have established that very modest differences in cognition, especially verbal memory, predict substantial differences in eventual risk of dementia,” write the authors.
Beta carotene is thought to protect the brain by reducing oxidative stress that can lead to cognitive decline.
The researchers believe these results have important implications for public health policy and deserve further investigation. In an accompanying editorial, however, fellow investigators issue a word of caution. Specifically, they note other studies have associated high dose antioxidant use with adverse health consequences and even a greater risk of death.
Beta carotene, for example, has been linked to a increase risk of lung cancer in smokers.
This article was reported by Ivanhoe.com, which offers Medical Alerts by e-mail every day of the week. To subscribe, click on: http://www.ivanhoe.com/newsalert/.
SOURCE: Archives of Internal Medicine, 2007;167:2184-2190
Tuesday, November 13, 2007
Drug May Restore Memory With Alzheimer's Disease
Drug May Restore Memory With Alzheimer's Disease
Tuesday, November 13, 2007 9:06 AM
A 2006 study by MetLife found that adults over age 55 fear Alzheimer’s disease more than cancer, and with good reason. Alzheimer’s creeps up on patients and their families, robbing more than half of all Americans over age 85 of their memory and ability to care for themselves. But what is perhaps most frightening is that available treatments for the disease are by and large ineffective.
Research from Georgetown University several years ago suggested that a new class of anti-Alzheimer’s molecule, spirostenols, might undo some of the characteristic pathophysiology of Alzheimer-affected brains. Further testing showed that one such molecule, Caprospinol, actually reversed the course of an Alzheimer-like condition induced in rats. Today, Samaritan Pharmaceuticals (Las Vegas, NV), is gearing up for human clinical studies with this compound, also known as SP-233.
Buildup of beta-amyloid plaque in the brain has been recognized as a hallmark sign of Alzheimer’s for close to a century. Significant research points to this buildup as a causative factor in the development and progression of the disease. Until recently this hypothesis could not be tested definitively because of a lack of treatments that eliminate beta-amyloid plaques.
Samaritan Pharmaceutical scientists, working with leading researchers from Georgetown and McGill Universities, have demonstrated in a rat animal model, used to test new innovative drugs for Alzheimer’s disease, that Caprospinol clears amyloid plaque from the brain and restored memory. More impressively, treated rats perform as well or better in standardized behavioral tests than healthy control animals. In addition to eliminating plaque, Caprospinol appears to reverse the damage to memory and cognition that amyloid plaque causes.
Dr. Vassilios Papadopoulos, of McGill University Health Center, an adviser to Samaritan, and the discoverer of anti-Alzheimer’s spirostenols recently published a paper reviewing current development-stage approaches to treating Alzheimer’s disease (Recent Patents on CNS Drug Discovery, 2007, 2, 113-123). In this article, he identified amyloid plaque as a key target for therapy. The paper also summarized the research on acetylcholinesterase inhibitors as well as beta-amyloid aggregation inhibitors, of which Caprospinol is an example.
The rat studies were conducted by treating rats with a method of inducing an Alzheimer’s-like condition in test animals within four weeks. Rats treated in this fashion gradually lose cognitive skills, as well exhibiting a host of pathophysiologic brain changes indicative of Alzheimer’s. Then treatment of sick rats with Caprospinol brought about significant positive changes in brain pathology. Neuritic plaques, neurofibrillary tangles, astrogliosis, microgliosis, neuronal death, and tissue shrinking were all either reversed or markedly improved.
Why another Alzheimer’s drug?
One might ask why the world needs another Alzheimer’s disease drug. The answer lies in the relatively poor performance by existing Alzheimer’s medications.
Of the five Alzheimer’s disease drugs approved in the U.S., four (Razadyne®, Exelon®, Aricept®, and Cognex®) are inhibitors of cholinesterase, an enzyme that shuts down the activity of the neurotransmitter choline. Cholinesterase inhibitors are approved for mild to moderate Alzheimer’s. The fifth medication, Namenda®, is an antagonist of the N-methyl D-aspartate receptor which regulates glutamate, another neurotransmitter. None of these agents cure Alzheimer’s disease or significantly change the course of the disease. The best that some patients can expect is a delay in symptom progression and/or improvements in some memory and behavioral functions.
Enhancement of neurotransmitter activity is a logical approach to treating AD. However, there are problems with cholinesterase and glutamate-acting agents. The first is that they do not address the underlying pathology of Alzheimer’s, treating only the symptoms and not the disease. The second, related shortcoming is that the most responsive patients get worse. The positive benefits of drug treatment are, disappointingly, measured in weeks or at best, months. Alzheimer’s drugs also tend to be quite expensive, and organ toxicities are not uncommon.
Click here for the whole story
Tuesday, November 13, 2007 9:06 AM
A 2006 study by MetLife found that adults over age 55 fear Alzheimer’s disease more than cancer, and with good reason. Alzheimer’s creeps up on patients and their families, robbing more than half of all Americans over age 85 of their memory and ability to care for themselves. But what is perhaps most frightening is that available treatments for the disease are by and large ineffective.
Research from Georgetown University several years ago suggested that a new class of anti-Alzheimer’s molecule, spirostenols, might undo some of the characteristic pathophysiology of Alzheimer-affected brains. Further testing showed that one such molecule, Caprospinol, actually reversed the course of an Alzheimer-like condition induced in rats. Today, Samaritan Pharmaceuticals (Las Vegas, NV), is gearing up for human clinical studies with this compound, also known as SP-233.
Buildup of beta-amyloid plaque in the brain has been recognized as a hallmark sign of Alzheimer’s for close to a century. Significant research points to this buildup as a causative factor in the development and progression of the disease. Until recently this hypothesis could not be tested definitively because of a lack of treatments that eliminate beta-amyloid plaques.
Samaritan Pharmaceutical scientists, working with leading researchers from Georgetown and McGill Universities, have demonstrated in a rat animal model, used to test new innovative drugs for Alzheimer’s disease, that Caprospinol clears amyloid plaque from the brain and restored memory. More impressively, treated rats perform as well or better in standardized behavioral tests than healthy control animals. In addition to eliminating plaque, Caprospinol appears to reverse the damage to memory and cognition that amyloid plaque causes.
Dr. Vassilios Papadopoulos, of McGill University Health Center, an adviser to Samaritan, and the discoverer of anti-Alzheimer’s spirostenols recently published a paper reviewing current development-stage approaches to treating Alzheimer’s disease (Recent Patents on CNS Drug Discovery, 2007, 2, 113-123). In this article, he identified amyloid plaque as a key target for therapy. The paper also summarized the research on acetylcholinesterase inhibitors as well as beta-amyloid aggregation inhibitors, of which Caprospinol is an example.
The rat studies were conducted by treating rats with a method of inducing an Alzheimer’s-like condition in test animals within four weeks. Rats treated in this fashion gradually lose cognitive skills, as well exhibiting a host of pathophysiologic brain changes indicative of Alzheimer’s. Then treatment of sick rats with Caprospinol brought about significant positive changes in brain pathology. Neuritic plaques, neurofibrillary tangles, astrogliosis, microgliosis, neuronal death, and tissue shrinking were all either reversed or markedly improved.
Why another Alzheimer’s drug?
One might ask why the world needs another Alzheimer’s disease drug. The answer lies in the relatively poor performance by existing Alzheimer’s medications.
Of the five Alzheimer’s disease drugs approved in the U.S., four (Razadyne®, Exelon®, Aricept®, and Cognex®) are inhibitors of cholinesterase, an enzyme that shuts down the activity of the neurotransmitter choline. Cholinesterase inhibitors are approved for mild to moderate Alzheimer’s. The fifth medication, Namenda®, is an antagonist of the N-methyl D-aspartate receptor which regulates glutamate, another neurotransmitter. None of these agents cure Alzheimer’s disease or significantly change the course of the disease. The best that some patients can expect is a delay in symptom progression and/or improvements in some memory and behavioral functions.
Enhancement of neurotransmitter activity is a logical approach to treating AD. However, there are problems with cholinesterase and glutamate-acting agents. The first is that they do not address the underlying pathology of Alzheimer’s, treating only the symptoms and not the disease. The second, related shortcoming is that the most responsive patients get worse. The positive benefits of drug treatment are, disappointingly, measured in weeks or at best, months. Alzheimer’s drugs also tend to be quite expensive, and organ toxicities are not uncommon.
Click here for the whole story
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