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Praise the Lord!!!
Hope Ombow is hangin in there on the Cape...
Curry Spice Turmeric Could Help Treat Alzheimer's Disease, Study Finds
PA/ The Huffington Post UK
Posted: 26/09/2014 09:25 BST Updated: 26/09/2014 09:59 BST
http://www.huffingtonpost.co.uk/2014/09/26/turmeric-curry-alzheimers-brain-cell-treatment_n_5886296.html?utm_hp_ref=uk&ir=UK
There's good news for curry fans - your favourite meal could also be beneficial to your health.
An ingredient in the yellow curry spice turmeric may hold the key to repairing the brains of people with neurodegenerative diseases such as Alzheimer's, research suggests.
In laboratory tests, aromatic turmerone promoted the proliferation of brain stem cells and their development into neurons.
curry tumeric
The bio-active compound could help scientists develop treatments for conditions in which brain cells are lost, including Alzheimer's and stroke, it is claimed.
Lead researcher Dr Adele Rueger, from the Institute of Neuroscience and Medicine in Julich, Germany, said: "While several substances have been described to promote stem cell proliferation in the brain, fewer drugs additionally promote the differentiation of stem cells into neurons, which constitutes a major goal in regenerative medicine.
"Our findings on aromatic turmerone take us one step closer to achieving this goal."
The scientists examined the effect of aromatic turmerone on endogenous neutral stem cells (NSCs) found within adult brains.
NSCs go on to develop into neurons, and play an important role in recovery from neurodegenerative diseases.
At certain concentrations, the turmeric compound boosted the proliferation of rat foetal NSCs by up to 80%, and increased the speed at which they matured.
In living rats, injections of aromatic turmerone led to the expansion of two key brain regions, the subventricular zone (SVZ) and hippocampus.
Both are sites in adult mammalian brains where neurogenisis - the growth of new neurons - is known to occur.
The findings are published in the online journal Stem Cell Research & Therapy.
Aromatic turmerone is the lesser-studied of two major bio-active compounds in turmeric. The second, curcumin, is a well known anti-inflammatory agent and reputed to have anti-cancer properties.
Commenting on the study, Dr Laura Phipps, from Alzheimer's Research UK, said: "This early-stage study highlights the effects of aromatic turmerone in rat brains, but the findings are a long way from determining whether this compound could help fight diseases like Alzheimer's.
"It's not clear whether the results of this research would translate to people, or whether the ability to generate new brain cells in this way would benefit people with Alzheimer's disease.
We'd need to see further studies to fully understand this compound's effects in the context of a complex disease like Alzheimer's, and until then people shouldn't take this as a sign to stock up on supplies of turmeric for the spice rack.
"The death of brain cells is a key feature of Alzheimer's, and investment in research is crucial to understand how this cell death occurs and how to intervene.
"It takes many years for fundamental research such as this to be translated into new treatments, and for the best chance of success we need to see a range of approaches being taken."
The world will soon know (lol) what we the world should already know: There is no magic-silver-miracle bullet treatment:
Memory loss associated with Alzheimer's reversed: Small trial succeeds using systems approach to memory disorders
Date:
September 30, 2014
Source:
University of California, Los Angeles (UCLA), Health Sciences
http://www.sciencedaily.com/releases/2014/09/140930143446.htm
Summary:
In the first, small study of a novel, personalized and comprehensive program to reverse memory loss, nine of 10 participants displayed subjective or objective improvement in their memories beginning within three to six months after the program’s start.
Patient one had two years of progressive memory loss. She was considering quitting her job, which involved analyzing data and writing reports, she got disoriented driving, and mixed up the names of her pets. Patient two kept forgetting once familiar faces at work, forgot his gym locker combination, and had to have his assistants constantly remind him of his work schedule. Patient three's memory was so bad she used an iPad to record everything, then forgot her password. Her children noticed she commonly lost her train of thought in mid-sentence, and often asked them if they had carried out the tasks that she mistakenly thought she had asked them to do.
Since its first description over 100 years ago, Alzheimer's disease has been without effective treatment. That may finally be about to change: in the first, small study of a novel, personalized and comprehensive program to reverse memory loss, nine of 10 participants, including the ones above, displayed subjective or objective improvement in their memories beginning within three to six months after the program's start. Of the six patients who had to discontinue working or were struggling with their jobs at the time they joined the study, all were able to return to work or continue working with improved performance. Improvements have been sustained, and as of this writing the longest patient follow-up is two and one-half years from initial treatment. These first ten included patients with memory loss associated with Alzheimer's disease (AD), amnestic mild cognitive impairment (aMCI), or subjective cognitive impairment (SCI; when a patient reports cognitive problems). One patient, diagnosed with late stage Alzheimer's, did not improve.
The study, which comes jointly from the UCLA Mary S. Easton Center for Alzheimer's Disease Research and the Buck Institute for Research on Aging, is the first to suggest that memory loss in patients may be reversed, and improvement sustained, using a complex, 36-point therapeutic program that involves comprehensive changes in diet, brain stimulation, exercise, optimization of sleep, specific pharmaceuticals and vitamins, and multiple additional steps that affect brain chemistry.
The findings, published in the current online edition of the journal Aging, "are very encouraging. However, at the current time the results are anecdotal, and therefore a more extensive, controlled clinical trial is warranted," said Dale Bredesen, the Augustus Rose Professor of Neurology and Director of the Easton Center at UCLA, a professor at the Buck Institute, and the author of the paper.
In the case of Alzheimer's disease, Bredesen notes, there is not one drug that has been developed that stops or even slows the disease's progression, and drugs have only had modest effects on symptoms. "In the past decade alone, hundreds of clinical trials have been conducted for Alzheimer's at an aggregate cost of over a billion dollars, without success," he said.
Other chronic illnesses such as cardiovascular disease, cancer, and HIV, have been improved through the use of combination therapies, he noted. Yet in the case of Alzheimer's and other memory disorders, comprehensive combination therapies have not been explored. Yet over the past few decades, genetic and biochemical research has revealed an extensive network of molecular interactions involved in AD pathogenesis. "That suggested that a broader-based therapeutics approach, rather than a single drug that aims at a single target, may be feasible and potentially more effective for the treatment of cognitive decline due to Alzheimer's," said Bredesen.
While extensive preclinical studies from numerous laboratories have identified single pathogenetic targets for potential intervention, in human studies, such single target therapeutic approaches have not borne out. But, said Bredesen, it's possible addressing multiple targets within the network underlying AD may be successful even when each target is affected in a relatively modest way. "In other words," he said, "the effects of the various targets may be additive, or even synergistic."
The uniform failure of drug trials in Alzheimer's influenced Bredesen's research to get a better understanding of the fundamental nature of the disease. His laboratory has found evidence that Alzheimer's disease stems from an imbalance in nerve cell signaling: in the normal brain, specific signals foster nerve connections and memory making, while balancing signals support memory loss, allowing irrelevant information to be forgotten. But in Alzheimer's disease, the balance of these opposing signals is disturbed, nerve connections are suppressed, and memories are lost.
The model of multiple targets and an imbalance in signaling runs contrary to the popular dogma that Alzheimer's is a disease of toxicity, caused by the accumulation of sticky plaques in the brain. Bredesen believes the amyloid beta peptide, the source of the plaques, has a normal function in the brain -- as part of a larger set of molecules that promotes signals that cause nerve connections to lapse. Thus the increase in the peptide that occurs in Alzheimer's disease shifts the memory-making vs. memory-breaking balance in favor of memory loss.
Given all this, Bredesen thought that rather than a single targeted agent, the solution might be a systems type approach, the kind that is in line with the approach taken with other chronic illnesses -- a multiple-component system.
"The existing Alzheimer's drugs affect a single target, but Alzheimer's disease is more complex. Imagine having a roof with 36 holes in it, and your drug patched one hole very well -- the drug may have worked, a single "hole" may have been fixed, but you still have 35 other leaks, and so the underlying process may not be affected much."
Bredesen's approach is personalized to the patient, based on extensive testing to determine what is affecting the plasticity signaling network of the brain. As one example, in the case of the patient with the demanding job who was forgetting her way home, her therapeutic program consisted of some, but not all of the components involved with Bredesen's therapeutic program, and included:
(1) eliminating all simple carbohydrates, leading to a weight loss of 20 pounds;
(2) eliminating gluten and processed food from her diet, with increased vegetables, fruits, and non-farmed fish;
(3) to reduce stress, she began yoga;
(4) as a second measure to reduce the stress of her job, she began to meditate for 20 minutes twice per day;
(5) she took melatonin each night;
(6) she increased her sleep from 4-5 hours per night to 7-8 hours per night;
(7) she took methylcobalamin each day;
(8) she took vitamin D3 each day;
(9) fish oil each day;
(10) CoQ10 each day;
(11) she optimized her oral hygiene using an electric flosser and electric toothbrush;
(12) following discussion with her primary care provider, she reinstated hormone replacement therapy that had been discontinued;
(13) she fasted for a minimum of 12 hours between dinner and breakfast, and for a minimum of three hours between dinner and bedtime;
(14) she exercised for a minimum of 30 minutes, 4-6 days per week.
The results for nine of the 10 patients reported in the paper suggest that memory loss may be reversed, and improvement sustained with this therapeutic program, said Bredesen. "This is the first successful demonstration," he noted, but he cautioned that the results are anecdotal, and therefore a more extensive, controlled clinical trial is needed.
The downside to this program is its complexity. It is not easy to follow, with the burden falling on the patients and caregivers, and none of the patients were able to stick to the entire protocol. The significant diet and lifestyle changes, and multiple pills required each day, were the two most common complaints. The good news, though, said Bredesen, are the side effects: "It is noteworthy that the major side effect of this therapeutic system is improved health and an optimal body mass index, a stark contrast to the side effects of many drugs."
The results for nine of the 10 patients reported in the paper suggest that memory loss may be reversed, and improvement sustained with this therapeutic program, said Bredesen. "This is the first successful demonstration," he noted, but he cautioned that the results need to be replicated. "The current, anecdotal results require a larger trial, not only to confirm or refute the results reported here, but also to address key questions raised, such as the degree of improvement that can be achieved routinely, how late in the course of cognitive decline reversal can be effected, whether such an approach may be effective in patients with familial Alzheimer's disease, and last, how long improvement can be sustained," he said.
Cognitive decline is a major concern of the aging population. Already, Alzheimer's disease affects approximately 5.4 million Americans and 30 million people globally. Without effective prevention and treatment, the prospects for the future are bleak. By 2050, it's estimated that 160 million people globally will have the disease, including 13 million Americans, leading to potential bankruptcy of the Medicare system. Unlike several other chronic illnesses, Alzheimer's disease is on the rise--recent estimates suggest that AD has become the third leading cause of death in the United States behind cardiovascular disease and cancer.
Story Source:
The above story is based on materials provided by University of California, Los Angeles (UCLA), Health Sciences. Note: Materials may be edited for content and length.
Journal Reference:
Dale E. Bredesen. Reversal of cognitive decline: A novel therapeutic program. Aging, September 2014
We all screw up...I do it all the time. Most of the time I correct before submitting, or edit in the allotted time after. Sometimes I miss it or don't know of the error. But this was never about me, it was about perceptions by regulators and experts when dealing with important issues.
There is too much defensiveness here...
A) A doctor is smart enough to have someone edit an official comment or opinion; and B) A doctor has a title that supercede any doubts that may arise due to sloppy english.
It's simply a credibility issue. I'm not saying that is necessarily my opinion or how I feel about it...it is just the way it is in the real world.
Inaccurate statements, misspellings, and grammatical errors will not help the cause.
What a conundrum. If one must wait to ingest anatabine citrate (the 'drug') via a synthetic pill, I agree, we are looking at 5-10 years, if ever. It is a little crazy to me, and lacking common sense, that a mimicked extract from a vegetable, which has shown decent anti-inflammatory action (and no serious side effects), is being labeled a drug that needs an expensive, rigorous, and drawn-out series of clinical trials. If the company wanted to develop a pharmaceutical version, fine: make it more powerful, combine it with other compounds and look for synergies, etc. But to force this backwards, bureaucratic, biased restart of this product/compound, seems to contradict reasoned and compassionate judgement. From the standpoint of the current consumers, and potential consumers later: as more clinical confirmation of the benefits of anatabine come to pass (assuming it does), is the FDA protecting us? Or are they preserving a very broken and flawed medical system?
Was this not just a technical misstep...not applying for an NDIN before marketing? Why punish the beneficiaries of a supplement because of a technicality? Seems short-sighted to me. I feel like there can be a solution to get it back on the market with intelligent and reasonable discourse between the FDA and the company. Laws clearly can be confusing, misinterpreted, suffocating, biased, or just flat out stupid. If you like the decision, however, you can always 'hide' behind the 'law' (Who Am I? lol).
Another issue is 'filing an IND on a marketed supplement'. Another non-drug related technicality? Once again, if a product/supplement demonstrates a reasonable benefit from user accounts and human studies, and the manufacturer decides, as more evidence of efficacy comes to light, to pursue a pharmaceutical version, why should they (and consumers) be punished for that? Maybe there is a logical explanation, or maybe the law in this case is too restrictive or counterintuitive.
Finally, on the FDA written 'response', is there seriously an issue with the company referring to the product as "providing anti-inflammatory support"? If the FDA thinks they are protecting anyone from this language, it must only be complete morons, or those with serious mental disabilities. The language on the bottle couldn't be any more accurate, subtle, and to the point. Suffocating...
Rock Creek/Mullan must be very careful here. Cooler heads and careful dialogue must prevail, but so must not giving up on the supplement, which is helping people. Clearly Mullan sees the benefit of anatabine, and it would send a mixed message if he is not determined to restart supplement sales. Is there a solution to get the supplement version back on the shelves? What if they extract anatabine from the plant (which plant has the highest concentration of anatabine, and will cost the least to grow and extract?). Could they dry the selected plant, grind it, and form a pill that way (pepper pill?)? Obviously these are just cursory angles, and only intended to suggest that a way can be found to make everyone happy (and healthy). Where there's a will...
It would be frustrating to think that a very simple, chronically used, heavily ingested molecule, needs a prescription and a bevy of more time-consuming trials just to be vetted in a way that does not break the 'law'.
Idiotic indeed!
Fred Couples to Host New Show on SiriusXM PGA TOUR Radio
World Golf Hall of Fame member and 1992 Masters Champion debuts Sep. 25
"The Fred Couples Show" will cover the world of golf and showcase his passion for all sports
http://finance.yahoo.com/news/fred-couples-host-show-siriusxm-140000884.html
NEW YORK, Sept. 11, 2014 /PRNewswire/ -- SiriusXM announced today that World Golf Hall of Fame member, 1992 Masters Champion and two-time PLAYERS Championship winner Fred Couples has joined SiriusXM PGA TOUR Radio (XM channel 93, Sirius channel 208).
He will host The Fred Couples Show monthly starting Thursday, September 25 at 7:00 pm ET, the night before the Ryder Cup.
Couples became one of the game's most prominent and beloved players while rising to #1 in the Official World Golf Ranking in the 1990s and remains as popular as ever today. On his new show he will take calls and interact with golf fans around the country, discuss the latest news from around the game, and offer instructional tips for players of all different skill levels.
The program will also regularly venture beyond the world of golf. Couples is a fervent sports fan and examples of his involvement with other sports and athletes are plentiful. The Seattle native was given the honor of raising the "12th man" flag at a Seahawks game late last season during Seattle's run to the Super Bowl. In 2009 he famously invited NBA legend Michael Jordan to be one of his assistant coaches for the U.S. Presidents Cup team, and he can regularly be seen sitting courtside at basketball games. Couples will invite his listeners to call in and talk about the NFL, NBA, major league baseball, college sports and more.
"Hosting this show is going be a lot of fun for a sports nut like me, and SiriusXM is the perfect place to do it," said Couples. "We'll cover anything and everything in golf with the freedom to dive into many other sports and topics as well. It's a great time of year to be a fan. I'm excited to get on the air to share my thoughts and hear what people across the country are thinking."
"Fred, in addition to being one of the game's greatest players, has the kind of engaging personality that is made for radio," said Scott Greenstein, SiriusXM's President and Chief Content Officer. "We're thrilled to have him on SiriusXM PGA TOUR Radio to share stories and insight from his illustrious career, especially on the eve of the Ryder Cup, a competition that he knows as well as anybody. With Fred's wide-ranging interests, he is as comfortable talking about football, basketball and baseball as he is talking golf, which will make this an entertaining show for any sports fan."
Couples turned professional in 1980 and rose to #1 in the Official World Golf Ranking in 1992. His resume includes 15 PGA TOUR wins, including memorable victories in the 1992 Masters Tournament and the PLAYERS Championships in 1984 and 1996. He won both PGA TOUR Player of the Year and the Vardon Trophy, awarded for lowest scoring average, in 1991 and 1992. A fixture for the United States in international team competitions, Couples played on five Ryder Cup teams and four Presidents Cup teams, and he captained the winning Presidents Cup teams in 2009, 2011 and 2013. He has 11 victories on the Champions Tour since joining that circuit in 2010, and he was inducted into the World Golf Hall of Fame in 2013.
SiriusXM PGA TOUR Radio offers live golf play-by-play of PGA TOUR events and major championships. This year the channel unveiled an expanded programming lineup that offers the best daily golf talk, news, analysis and instruction on radio. Hosts on the channel include World Golf Hall of Fame members Ben Crenshaw and Hubert Green, Henrik Stenson, Ian Poulter, Annika Sorenstam, Chris DiMarco, Rich Beem, Hank Haney, David Leadbetter, Jim McLean, Mark Carnevale, John Maginnes, Carl Paulson, Dennis Paulson, Matt Adams, Brian Katrek, Sandy McIlree, Larry Rinker, Lorne Rubenstein, Ben Shear, John Swantek, Jeff Warne, Greg Warmoth and Taylor Zarzour. Listeners can also hear Golf Channel programming.
Maybe someone should tell him about anatabine (what an impressive unpaid/unofficial sponsor he could be!). Of course, if you like this style of eating, even better:
http://finance.yahoo.com/news/heres-lebron-james-eating-lose-201318444.html
Here's What LeBron James Is Eating To Lose Weight This Summer
Business Insider By Tony Manfred
LeBron James is losing a bunch of weight this summer. He lost a reported 10 pounds in the first few weeks of the summer, and shocked the NBA world when he posted of photo on Instagram looking downright skinny.
View gallery
A key part of LeBron's weight-loss plan is cutting carbohydrates. Miami Heat teammate Ray Allen came into camp in the best shape of anyone on the team last fall, Windhorst reports, and that influenced LeBron this summer.
Some are referring to it as a Paleo diet, although it's unclear if LeBron is calling it that.
Ken Berger of CBS Sports did a long article on the rising popularity of Paleo diets among NBA players in December. Here's his definition of Paleo:
"The Paleolithic diet -- Paleo, for short -- involves eating like our caveman ancestors did: lean meats, wild-caught fish, vegetables, nuts and seeds, some fruit, little starch and no sugar or processed foods. Its proponents call it the 'anti-inflammatory diet' on the theory that avoiding processed carbs and sugars decreases inflammation in the body -- the kind that causes joint pain and the kind that a growing number of medical authorities believe contributes to heart disease, obesity and diabetes."
So what's LeBron eating?
His Instagram holds some clues.
For one lunch he had "arugula salad with chicken, strawberries, mango, cashews and olive oil/lemon vinaigrette dressing" with a bowl of squash and zucchini.
This meal is full of "powerhouse" foods. Arugula is the 18th most nutritious food in the world, strawberry is 30th, and winter squash is 32nd.
Another particularly delicious-looking dinner was lobster salad with asparagus and mango chutney:
As with any diet, the key here is sticking to it. While he was in Greece, a restaurant made LeBron a personalized cake, and he didn't eat it.
"To dang on bad I can't eat it! Grrrrrrrrrr!! Smh." he said on Instagram.
As you can see above, all of LeBron's meals feature lean meats and vegetables.
LeBron's wife, Savannah Brinson, is also into eating healthy. She opened a shop called The Juice Spot in Miami last year that calls itself "Miami's first Wifi bar fully equipped with organic cold pressed juices, superfood smoothies, Acai and Oatmeal bowls."
Last December, LeBron was eating Acai bowls and drinking beet juice from the juice bar, so he has a history with these sorts of food:
Kobe Bryant was the first NBA superstar to recognize the importance of dieting and losing weight once you enter the back half of your career. Now Carmelo Anthony, Dwyane Wade, LeBron and others are following suit.
The result is a leaner, more energetic LeBron James, which is terrifying for the rest of the league.
It seems that new mgmnt has developed a prioritized interest in the ampakine platform, ie, respiratory depression. I didn't recognize any prominent interest in past communications. If RD is as novel and reliable as studies have shown, then good management could finally take us to another level, notwithstanding an existing handicap courtesy of the prior pathetic team of Stoll/Varney. They were awful leaders, without question.
Choroid Plexus May Hold a Key To Aging Brain
http://www.alzforum.org/news/research-news/choroid-plexus-may-hold-key-aging-brain
23 Aug 2014
In the August 21 Science, researchers led by Michal Schwartz and Ido Amit, Weizmann Institute of Science, Rehovot, Israel, report that the choroid plexus, the barrier separating the blood and the cerebrospinal fluid, plays a key role in brain aging. They found that as wild-type mice got older, the balance between immune signals in the tissue shifted. They found similar changes in human postmortem brains. By restoring immune signaling in old animals to that of young whippersnappers, the researchers quelled inflammation and reversed age-related deficits in neurogenesis and memory. “The study opens a new window to the process of brain aging and suggests a completely new age-modulating function for the choroid plexus,” said Costantino Iadecola, Weill Cornell Medical College, New York. “It could be just the tip of the iceberg,” he said, speculating that other points of contact between the blood and brain could contribute a similar function.
Astrocytes (red) flare up in the hippocampus of older mice, but cool off when mice are treated with an antibody that curbs IFN-I responses. (Neuronal nuclei in blue.) [Image courtesy of Science/AAAS.]
The choroid plexus lines portions of the brain’s ventricles and forms a rare interface between the blood and the cerebrospinal fluid (CSF). It is responsible for producing the latter, pumping out about 500 ml per day. It also supplies nutrients and hormones to the brain while clearing waste. Since the CSF changes with age, Schwartz and colleagues wondered if the choroid plexus might also, and if it could be manipulated to slow age-associated cognitive decline.
To find out, first authors Kuti Baruch and Aleksandra Deczkowska compared mRNA profiles among 11 tissues from 3-month-old and 22-month-old wild-type mice. The choroid plexus alone demonstrated significant changes in interferon signaling. Interferons are cytokines released when a virus invades. Most cell types secrete type I interferons, which make recipient cells resistant to viruses. The type II variety comes from natural killer cells and T lymphocytes and serves as an alert to the immune system. Typical genes that depend on type I interferons include interferon regulatory factor 7, interferon-ß 1, and interferon-induced protein with tetratricopeptide repeats 1, according to the Interferome Database hosted by Monash University in Melbourne, Australia. Baruch and colleagues found that transcript levels of all three were higher in aged choroid plexus. At the same time, mRNA typical of an IFN-II response—such as intercellular adhesion molecule 1, interferon ?-induced protein 10, and chemokine (C-C motif) ligand 17, were less abundant. The same signature prevailed in aged wild-type mice from three other institutions. Postmortem brain tissue from healthy older people also demonstrated an uptick in IFN-I-related gene expression.
To figure out whether the signals that brought about these changes came from blood or cerebrospinal fluid, the researchers conducted two sets of experiments. Collaborating with Tony Wyss-Coray at Stanford University, California, they first tested blood by joining the vascular systems of young mice to old via parabiosis (see May 2014 news story). The blood of young mice raised expression of IFN-II related genes in the choroid plexus of older animals. In contrast, the blood of the older mice caused the choroid plexus of the younger mice to express fewer IFN-II-related transcripts. Next, the authors tested the effect of the CSF by bathing primary cultures of young choroid plexus epithelial cells in the fluid. CSF from aged animals caused IFN-I related transcripts to rise. They did not expose epithelial cells from old mice to the CSF of young animals. Together, the parabiosis and cell culture experiments suggest that IFN-II-related signals come from the periphery, while factors inducing the IFN-I genes originate in the brain, Schwartz said.
Could these signals be manipulated to reverse signs of aging? To find out, Baruch and Deczkowska injected antibodies into the CSF to block IFN-I type receptors in old wild-type C57BL/6 mice. They chose mice that fared particularly poorly on object-recognition tasks compared with cognitively intact animals of the same age. The antibodies not only improved memory but reduced inflammation in the brain (see image above) and restored neurogenesis to levels seen in mice that were the same age, yet had preserved cognition. “This study suggests a new approach to treat aging,” said Schwartz. In addition, since IFN-I and IFN-II seem to have a reciprocal relationship, it might be possible to boost IFN-II in the periphery to affect IFN-I signals coming from the brain, she suggested. Schwartz emphasized that this requires further investigation.
Why does older choroid plexus produce inflammatory signals to begin with? Schwartz proposed that when the brain ages, dying cells and inflammatory factors cause a chronic distress signal that continuously elicits an IFN-I response. This could be an important risk factor in age-related neurodegenerative disease, she said. Her lab is now looking in mouse models of Alzheimer’s disease (AD) to determine the influence of type I and type II interferon signals.
Recent studies by Wyss-Coray and others have used parabiosis to seek out as-yet-unknown circulating factors in the blood that hasten or reverse signs of aging in the brain (see Nov 2009 news story). Some propose that the chemokine CCL11 could be one of them, while others contend it is the growth differentiation factor GDF11 (see Aug 2011 news story, May 2014 conference story on Katsimpardi et al., 2014). “The current study may help explain the age-defying effects of young blood and why aging contributes Alzheimer’s disease," Wyss-Coray told Alzforum. “Cognitive deficits that develop in AD may be influenced by the choroid plexus and through interferon responses,” he added. Age-related changes may also impair the choroid plexus' ability to generate CSF and to produce beneficial factors, he speculated.
Scientists need to next pinpoint the downstream effectors of interferon signaling responsible for these effects, said Iadecola. Richard Ransohoff of Cleveland Clinic added that researchers should seek the upstream factors responsible, too. He was intrigued that these experiments reveal age-related changes in the choroid plexus that are driven by signals from the brain. However, he cautioned that factors other than interferons could drive the gene alterations. “It is premature to tighten the focus to only two cytokines, type I and type II interferons, because other factors can regulate several of these genes,” he told Alzforum. “The most important thing is to gain a deeper understanding for the basis of these gene expression changes, and then focus on their physiologic significance.” He pointed out that improved cognition brought about by the IFN-I receptor antibody indicates a short-term effect of interferon signaling, but says little about long-term, age-related changes in cognition.—Gwyneth Dickey Zakaib
The obvious one. Eom
It is not an either/or scenario for the former, but is for the latter. Dangerous drugs get thru, and dangerous drugs are stopped. Therefore, the Fda kills and saves. As far as Anatabloc, it may or may not save, but it doesn't kill. That would be an 'or' for Anatabloc.
It can be argued that the FDA (and doctors) kill people. There is no such rational or valid argument that anatabine does the same. Your logic/analogy is irrelevant.
It is akin to someone referring to being 'raped', to add emphasis to being wronged (i.e, overcharged) in some relatively insignificant way.
What a coincidence...
Yes...useless; ineffectual. Anatabloc does not kill people, and supplements don't kill people (see #msg-105497821 for some history). Therefore your extrapolation is poor. Self-medication, as you call it (even though it may be nothing more than preventative nutrition/supplementation) can help/save people. On the other hand, the FDA's decisions and doctors decisions (or negligence) can kill people too. It helps to have a more reasoned perspective.
So, if I go to my doctor, and he/she tells me that I may have inflammation, and I decide not take the anti-inflammatory he prescribes, but instead, eat healthy foods or take supplements based on foods with known anti-inflammatory properties, am I putting myself at risk? If so, isn't that my right? Isn't there a risk with prescription medications which I might be wise to avoid? Have you seen the side effect profile for many medications?
Also, how do you differentiate self-medicating from other forms of health modification? If I feel a cold coming on and I take Emergen-C or Vitamin C pills, am I self-medicating? Am I putting myself at risk? If I made that choice, did I realize the risk and accept the risk? Is that my right?
Your blanket statements leave a lot to be desired.
That is a dumb analogy.
You are both right. The fact is...this is not a perfect world. The FDA and Congress are run by people. People have the vulnerability of being bought and influenced/pressured by others, ie., lobbyists, wealthy donors, schemers, etc. Most of the time, those in a position to influence have an agenda, and most agendas are not altruistic in nature. Thus, they are flawed. While the FDA are regulators in charge of maintaining the food and drug laws and protecting citizens, it is not uncommon for bias and temptation to interfere with their stated objective. The same holds true for Congress/politicians, if not much more so. To think that is not the case, is naive and unrealistic. Keep in mind that the pharmaceutical industry contributes handsomely to the FDA payroll (and also to Congress!), and the executives/scientists that the FDA deal with are more along the lines of peers than they are adversaries (ditto with politicians). Food for thought...
NSAIDs may lower breast cancer recurrence rate in overweight, obese women
Date:
August 14, 2014
Source:
American Association for Cancer Research
Summary:
Recurrence of hormone-related breast cancer was cut by half in overweight and obese women who regularly used aspirin or other nonsteroidal anti-inflammatory drugs, according to a study. The study found that women whose body mass index (BMI) was greater than 30 and had estrogen receptor alpha (ER-alpha)-positive breast cancer had a 52 percent lower rate of recurrence and a 28-month delay in time to recurrence if they were taking aspirin or other NSAIDs.
Recurrence of hormone-related breast cancer was cut by half in overweight and obese women who regularly used aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs), according to data published in Cancer Research, a journal of the American Association for Cancer Research.
"Our studies suggest that limiting inflammatory signaling may be an effective, less toxic approach to altering the cancer-promoting effects of obesity and improving patient response to hormone therapy," said Linda A. deGraffenried, PhD, associate professor of nutritional sciences at The University of Texas in Austin.
The study found that women whose body mass index (BMI) was greater than 30 and had estrogen receptor alpha (ERa)-positive breast cancer had a 52 percent lower rate of recurrence and a 28-month delay in time to recurrence if they were taking aspirin or other NSAIDs.
"These results suggest that NSAIDs may improve response to hormone therapy, thereby allowing more women to remain on hormone therapy rather than needing to change to chemotherapy and deal with the associated side effects and complications," said deGraffenried. "However, these results are preliminary and patients should never undertake any treatment without consulting with their physician."
Using blood from obese patients, deGraffenried and colleagues conducted experiments in the laboratory to recreate a tumor environment containing cancer cells, fat cells, and the immune cells that promote inflammation. They found that the factors associated with obesity initiate a network of signaling within the tumor environment to promote growth and resistance to therapy.
"These studies show that the greatest benefit from aspirin [and other NSAIDs] will be in those with a disease driven by inflammation, and not just obesity," explained DeGraffenried.
Researchers used data from 440 women diagnosed with invasive, ERa-positive breast cancer and treated at The University of Texas Health Science Center and the START Center for Cancer Care clinic, both in San Antonio, Texas, between 1987 and 2011.
Of the women studied, 58.5 percent were obese and 25.8 percent were overweight. About 81 percent took aspirin, and the rest took another NSAID. About 42 percent and 25 percent took statins and omega-3 fatty acid, respectively.
There was an indication of protection from aspirin and other NSAIDs even after controlling for statins and omega-3 fatty acid use, which also have anti-inflammatory effects.
Story Source:
The above story is based on materials provided by American Association for Cancer Research. Note: Materials may be edited for content and length.
Journal Reference:
L. W. Bowers, I. X. F. Maximo, A. J. Brenner, M. Beeram, S. D. Hursting, R. S. Price, R. R. Tekmal, C. A. Jolly, L. A. deGraffenried. NSAID Use Reduces Breast Cancer Recurrence in Overweight and Obese Women: Role of Prostaglandin-Aromatase Interactions. Cancer Research, 2014; 74 (16): 4446 DOI: 10.1158/0008-5472.CAN-13-3603
RIGL's profile confirms potential synergies. From Yahoo Finance:
Rigel Pharmaceuticals, Inc., a clinical-stage drug development company, discovers and develops novel, small-molecule drugs for the treatment of inflammatory and autoimmune diseases, as well as muscle disorders. Its product development programs include fostamatinib, an oral spleen tyrosine kinase (SYK) inhibitor that intends to enter Phase III clinical trials for immune thrombocytopenic purpura and a Phase II clinical trial for immunoglobulin A nephropathy; R348, a topical janus kinase/SYK inhibitor in Phase II clinical trials for the treatment of keratoconjunctivitis sicca or chronic dry eye; R118, an adenosine monophosphate-activated protein kinase activator that intends to enter Phase I clinical trial; and two oncology product candidates in Phase I development. It also has small molecule discovery programs in muscle wasting. Rigel Pharmaceuticals, Inc. has collaboration agreement Daiichi Sankyo to pursue research related to a specific target from a class of drug targets called ligases that control cancer cell proliferation through protein degradation; and a license agreement with BerGenBio AS for the development and commercialization of an oncology program. The company was founded in 1996 and is based in South San Francisco, California.
RIGL - Another candidate loaded with cash, but weighed down with a string of clinical failures, which could give RCPI what they need. Rigel Pharmaceuticals has over $170M in cash, and is reeling from a drug setback in dry eye disease ("The drug is aimed at reducing the underlying inflammation responsible for the symptoms of chronic dry eye syndrome"):
http://finance.yahoo.com/news/rigel-experimental-eye-drug-fails-121954918.html
Rigel eye drug fails mid-stage study, shares fall
Reuters
Aug 13 (Reuters) - Rigel Pharmaceuticals Inc said it would stop testing its drug for some patients with dry eye disease after the treatment failed a mid-stage study.
The study was evaluating the eye drop formulation of the drug, R348, against a placebo. The drug is aimed at reducing the underlying inflammation responsible for the symptoms of chronic dry eye syndrome.
R348's failure is the latest in a string of setbacks for Rigel. The company stopped developing its skin disorder and asthma drugs last year after the treatments failed mid-stage trials.
British drugmaker AstraZeneca Plc scrapped its licensing deal for Rigel's rheumatoid arthritis treatment in June 2013.
The only other drug left in Rigel's armory, fostamatinib, is being tested for use in Immune Thrombocytopenic Purpura, a blood disorder, and IgA Nephropathy, a chronic autoimmune disease.
Rigel said it planned to continue another mid-stage study of R348 in dry eye patients with graft versus host disease.
There "may be more scientific rationale" in developing the compound in this indication, Wells Fargo analyst Brian Abrahams said.
Chronic dry eye syndrome affects the eye's tear-producing glands. Patients suffer from blurred vision and also experience itching or a burning sensation in the eyes.
The disease affects more than 5 million Americans and many patients with chronic dry eye syndrome also suffer from autoimmune conditions, the company said.
Rigel also said it would stop testing another drug, codenamed R118, due to its side-effect profile in early-stage trials.
The San Francisco, California-based company's stock was down 10.5 pct at $2.77 on the Nasdaq on Tuesday. The stock recorded its biggest intra-day percentage fall in about a year.
(Reporting by Natalie Grover in Bangalore; Editing by Simon Jennings)
If people are honestly getting benefit from either Cigrx or Anatabloc for smoking cessation (or other real afflictions), this has got to be extremely disheartening. I am sympathetic to you. If Mullan & Co. don't do everything they can to correct it, this is a very bad precedent. If this is a company strategy -- to remove it permanently -- shame on them. Additionally, if this is the case, I must conclude the product does not work well, if at all. Finally, if it does work and they don't straighten this out with the FDA, wouldn't want to invest with them anyway. Can't trust 'em to do the right thing...
(Edit):
Dr. Mullan:
You need to hit this head on and in a linear fashion. Go after the primary target, inflammation.
You also need to get the supplement back on the market. Give the people what they want (as opposed to taking it away), and as the science progresses (favorably, hopefully), the revenue will flood in. It's been built, so let them come. Don't tear it down unnecessarily. There are thousands and thousands of supplements out there with much less corroborative evidence, don't get dragged down and out by a flawed FDA system. If it works, fight for its existence, period!
This was also discussed two months ago in #msg-103262093, and no reasonable explanation was provided. Do they think that parsing out the indications is a better way to leverage the assets? In a perfect world, or with a highly sought and valued asset, maybe. But there is too much risk at losing it all right now. They need to go after the primary benefit, anti-inflammation, and stop playing games by going after the byproducts of the disease. I would gather the anti-inflammatory market is a multibillion dollar business, so they should quit f#cking around with the fancy leverage game. Why? Because now, they have zero leverage. And without the supplement, less than zero.
Dr. Mullen:
You need to hit this head on and in a linear fashion. Go after the primary target, inflammation.
You also need to get the supplement back on the market. Give the people what they want (as opposed to taking it away), and as the science progresses (favorably, hopefully), the revenue will flood in. It's been built, so let them come. Don't tear it down unnecessarily. There are thousands and thousands of supplements out there with much less corroboratory evidence, don't get dragged down by a flawed FDA system. If it works, fight for its existence, period!
The concern regarding what is going on now was discussed (you were involved also) 4 months ago, starting about here: #msg-100362488
I think it is a little surprising...I've read you echoing my previously expressed thoughts in the past. But whatever...
So voluntarily taking a 'safe', revenue generating, relief-providing supplement off the market to pursue a pharmaceutical version, which will likely take 5-10 years to begin to produce any revenue, if ever, is suggestive that this is a non-profit? You need to get your logic straight on this one...
While the pharmaceutical route makes sense for another stronger/better version of anatabine, it is masochistic and cruel to keep the current version off the market indefinitely, and away from people who claim to derive a significant benefit. This is particularly the case if consumers don't have the luxury of alternative treatments (drugs included). So does the company believe that anatabine, 'the supplement', works effectively, or not?
If you say that it will impede their leverage in partnerships, then they are selling out the people for the partnership. Frankly, if something works, and clinical studies continue to show the benefit, the supplement would be a boon. The money would be so good, it would likely dwarf that of a partnership or two. Now, a couple partnerships within the next 5-10 years without supplement sales...that is all risk. Risk tied even more to a complex FDA, I may add. Do you think they are difficult now? Wait 'til the bar continues to rise.
The drug version cannot be the same as the supplement version, therefore it should not compete with the supplement. If it is, then it is generally recognized as safe now, and the justification for removing it at the expense of those benefiting is problematic on a basic ethical level, for both the FDA and the company. They both must consider the implication of this.
JW 'forgot' about appropriate means? I think you have to look at his earlier past -- pre-Star -- to realize how consistent he has been, as a silky-smooth southern salesman.
You are correct that JW is different from Clinton and Biden, but you are wrong about the difference and accountability. While Clinton and Biden have always been civil servants, JW has always been self-serving.
Accountability? Biden's plagairism cost him a few presidential runs, and Clinton's dirty laundry was thrown out there for the world to see closely, and thus judge accordingly. The JW scandal is small-time, comparatively, and a circus atmosphere, entirely.
Slick JWillie is much slicker and sleazier then Slick Willy himself, with one exception: At least, as far as we know, JW's scandal did not involve an extramarital affair. I give JW credit for that one, as it could have made the story much messier (lol).
This person does not belong hiding in a letter, at a desk, or in front of a computer. She belongs at the forefront of this crusade. She should be the poster child/lady for the benefits of Anatabine. She should be on 20/20, Dateline, the Doctors, Dr Oz...going through the whole circuit. That would make it more believable.
I don't want to take anything away from this person, or you, but seeing is believing.