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News Release says: "The Company also disclosed its dermatological development program in which dermal formulations of its lead compound are being developed for common chronic skin disorders such as psoriasis, eczema (e.g., atopic dermatitis) and rare or orphan skin disorders. Patients and key opinion leaders agree there are unmet medical needs requiring new, safe and effective first-line treatments for dermatological diseases, and the Company believes the novel anti-inflammatory mechanism of action of its lead compound is well suited to meet these needs. The Company is directing its strategy to gain regulatory approval accordingly."
My comments: Keyword is 'orphan'. This may be the cheapest and quickest way for RCPI to get Anatabloc approved by the FDA and start generating revenues. From approval as a 'orphan drug', it can use this platform to enter the broader (and more rewarding) areas of anti-inflammatory issues and diseases.
Wikipedia excerpt about orphan drugs:
"An orphan drug is a pharmaceutical agent that has been developed specifically to treat a rare medical condition, the condition itself being referred to as an orphan disease.
In the US and EU it is easier to gain marketing approval for an orphan drug, and there may be other financial incentives, such as extended exclusivity periods, all intended to encourage the development of drugs which might otherwise lack a sufficient profit motive.[1][2] The assignment of orphan status to a disease and to any drugs developed to treat it, is a matter of public policy in many countries, and has resulted in medical breakthroughs that may not have otherwise been achieved due to the economics of drug research and development.[3]
According to Thomson Reuters in their 2012 publication "The Economic Power of Orphan Drugs", there has been increased investing in orphan drug Research and Development partly due to the U. S. Orphan Drug Act (ODA) 1983 and similar Acts in other regions of the world and also driven by "high-profile philanthropic funding."[4][5] The period between 2001 to 2011 was the "most productive period in the history of orphan drug development, in terms of average annual orphan drug designations and orphan drug approvals."[5]:660 For the same decade the compound annual growth rate (CAGR) of the orphan drugs was an "impressive 25.8 percent, compared to only 20.1 percent for a matched control group of non-orphan drugs."[4]:6 By 2012 the market for orphan drugs was worth USD$637 million compared to the USD$638 million matched control group of non-orphan drugs, Thomson Reuters.[4]
Wikipedia article at:
https://en.wikipedia.org/wiki/Orphan_drug
Study: If You Want To Reach 100, Keep Your Inflammation Levels Low in 'Forbes', David DiSalvo, 8/09/2015
Excerpts:
"In a new study on aging, researchers have identified which health markers play crucial roles in people reaching 100 and beyond. More than any other, chronic inflammation surfaced as the most important changeable factor for both reaching the century mark and enjoying better physical and mental health on the way.
The study included more than 1,500 people, with ages ranging from 50 to 110. About 680 of the participants were centenarians, and 167 others were pairs of offspring from that group. The researchers measured several health markers known to contribute to aging, including metabolic rate, inflammation levels, liver and kidney function, and telomere length (telomeres are the protective “caps” at the end of a chromosome that are linked to aging and susceptibility to disease).
The researchers found that offspring of centenarians have the best chance of keeping telomere length “youthful,” which seems to give them a better-than-average chance of hitting 100. But telomere length isn’t a malleable factor for most of the population. If one of your parents lived to 100 or beyond, it’s good news for you, but less so for anyone else.
Inflammation, on the other hand, is malleable, and it’s the factor this study identified as playing the biggest role in how long people live and their mental sharpness as they get there.
“It has long been known that chronic inflammation is associated with the ageing process in younger, more ‘normal’ populations, but it’s only very recently we could mechanistically prove that inflammation actually causes accelerated ageing in mice,” according to study co-author Professor Thomas von Zglinicki, from Newcastle University’s Institute for Ageing. “This study, showing for the first time that inflammation levels predict successful ageing even in the extreme old, makes a strong case to assume that chronic inflammation drives human ageing too.”
Inflammation levels increased with age for everyone in the study, but participants with the lowest levels had the best chance of growing older while staying sharper mentally and living independently."
"The study results make perfect sense in light of what we’ve learned about the role chronic inflammation plays in diseases ranging from diabetes to heart disease to depression to Alzheimer’s to some forms of cancer. We’re not talking about the sort of inflammation that hurts when you get a cut or burn, but the kind that exists below the perception of pain. The inflammation implicated in chronic disease is cellular inflammation, and it’s damaging your cells typically without any overt symptoms. That’s why it’s so insidious – the diseases that result from cellular inflammation manifest once the damage has reached a threshold level, at which point we’re facing serious symptoms. It logically follows that consistently lower inflammation levels would underpin longer, healthier lives."
Article at:
http://www.forbes.com/sites/daviddisalvo/2015/08/09/study-if-you-want-to-reach-100-keep-your-inflammation-levels-low/
Controlling inflammation to reduce chronic disease risk in 'Medical News Today', 7 August 2015
Excerpts:
"An unresolved inflammatory response is likely to be involved from the early stages of disease development. Controlling inflammation is crucial to human health and a key future preventative and therapeutic target. In a recent ILSI Europe's article published in the British Journal of Nutrition, a coalition of experts explain how nutrition influences inflammatory processes and help reduce chronic diseases risk.
Inflammation is a normal component of host defence, but elevated unresolved chronic inflammation is a core perturbation in a range of chronic diseases. Prevention or control of low-grade inflammation therefore seems to be an attractive target effect for healthy food or food ingredients. In a recent article commissioned by the ILSI Europe Obesity and Diabetes Task Force, experts present new approaches to capture inflammatory status in humans and to help quantify how much diet can positively modulate inflammation."
"The nutrition status of the individual with for example a deficiency or excess of certain micronutrients (e.g. folate, vitamin B12, vitamin B6, vitamin B1, vitamin E, zinc) may lead to an ineffective or excessive inflammatory response. Studies have showed that high consumption of fat and glucose may induce post-prandial inflammation (manifesting itself after the consumption of a meal), which may have consequences for the development of diabetes and cardiovascular diseases. The Western-style diet, rich in fat and simple sugars but often poor in specific micronutrients, is linked to the increased prevalence of diseases with strong immunogical and autoimmune components, including allergies, food allergies, atopic dermatitis and obesity."
Article at:
http://www.medicalnewstoday.com/releases/297915.php?tw
This might help understand what the FDA THINKS IS INTERSTATE COMMERCE:
Excerpt:
What the FD&C Act Means by "Interstate Commerce"
Section 201(b) of the FD&C Act [21 U.S.C. 321(b)] tells what circumstances place a product in interstate commerce:
"(1) commerce between any State or Territory and any place outside thereof, and
(2) commerce within the District of Columbia or within any other Territory not organized with a legislative body."
"Interstate commerce" applies to all steps in a product's manufacture, packaging, and distribution. It is very rare that a cosmetic product on the market is not in "interstate commerce" under the law. For example, at least some of your ingredients or packaging most likely originate from out of state, or even out of the country. Likewise, it is foreseeable that your products will leave the state. Although there are certain exemptions [21 CFR 701.9], factors such as these generally cause the requirements of the FD&C Act to apply to your products.
My comments: We don't know where Anatabloc is manufactured, it may not be Florida. Where is the box and bottles made? Seems to me the FDA has a monopoly on guidance, almost god-like.
FDA Statement at:
http://www.fda.gov/Cosmetics/GuidanceRegulation/LawsRegulations/ucm074248.htm
Excellent, objective article. Wish they had commented more on their pipeline and near-term milestones.
Scientists May Have Isolated The Secret To Staying Healthy Past Age 100 in Huffington Post, Carolyn Gregoire, 8/6/15
Excerpts:
"What's the secret of people who live vibrant, healthy lives well beyond the age of 100?
Low levels of inflammation -- the long-term overactivation of the immune response -- may be the answer, suggests a new study of centenarians from researchers in England and Japan. People with lower markers of chronic inflammation also tend to be less likely to develop diseases, meaning suppressing inflammation could be the No. 1 key to not only living longer but to staying healthy longer.
"Centenarians and supercentenarians are different -- put simply, they age slower," Dr. Thomas von Zglinicki, a cellular gerontologist at Newcastle University and the study's lead author, said in a written statement. "They can ward off diseases for much longer than the general population.""
""Control inflammatory status regularly and keep it down," von Zglinicki advised. "This should slow down the aging process and thus might postpone onset of multiple age-related diseases, potentially including dementia."
While current anti-inflammatory drugs are not safe for long-term use because of their side effects, the findings may open up avenues for research devising safer anti-inflammatory drugs to improve quality of life among older people. "
Article at:
http://www.huffingtonpost.com/entry/staying-healthy-after-100_55c249e0e4b0138b0bf4bf18
Scientists Turn Skin Cells Into Brain Cells, Using Alzheimers Patients in 'Gizmodo', Annalee Newitz, Aug 7, 2015
Excerpts:
"Using a special mix of small molecules, two groups of scientists in China have successfully turned human skin cells into neurons. They hope that their technique could one day help rejuvenate failing tissues in the brains of Alzheimers patients.
The two teams in China focused on strategies for converting skin cells to neurons, with one group focusing on skin cells from mice and the other on humans. Results of their work are published in two papers today from the journal Cell Stem Cell. The team working on human cells drew their samples from Alzheimers patients, because one possible end goal of this research would be to produce working brain cells that could supplement failing tissues in the brains of people with dementia."
"Even more exciting is the possibility that the small molecule mixture could be tweaked to induce skin cells to turn into very specific kinds of neurons.
Shanghai Institutes for Biological Sciences researcher Jian Zhao worked on the human study. She said:
It should be possible to generate different subtypes of neurons with a similar chemical approach but using slightly modified chemical cocktails. It also needs to be explored whether functional neurons could be induced by chemical cocktails in living organisms with neurological diseases or injury.
Her final comment is the most intriguing yet. She's hinting at the idea that we might be able to use these small molecules - which she calls "chemical cocktails" - in a living person to convert their cells into fresh neurons on the spot. Imagine growing neurons right on your arm, then transplanting them into your brain or spinal cord to heal an injury.
Medicine of the future might help us heal ourselves, by giving us new ways to control how our cells grow."
Article at:
http://www.gizmodo.in/science/Scientists-Turn-Skin-Cells-into-Brain-Cells-Using-Alzheimers-Patients/articleshow/48383449.cms
Soldiers show prolonged elevations in protein linked to Alzheimer's disease, CTE in 'Medpage Today', Kay Jackson
Excerpts:
"Military personnel who reported three or more traumatic brain injuries (TBIs) showed high total tau protein concentrations in plasma, in some cases long after the injuries had occurred, an observational study indicated."
"The post-concussive disorder (PCD) symptoms correlating to tau concentrations may be early signs of ongoing neurodegeneration that may benefit from early intervention," said Gill. "These findings require follow-up to determine temporal relationships related to total tau, TBIs and chronic symptoms."
Total tau concentration appears to relate to chronic symptoms of PCD that are present for months or years after injury. This suggests there may be a cumulative effect of multiple TBIs on recovery processes, the researchers indicated. Additionally, deposits of hyperphosphorylated tau are well-known features of Alzheimer's disease and have also been found in the condition known as chronic traumatic encephalopathy or CTE."
""Ultimately," said Gill, "studies that provide a direct mechanistic relationship between TBIs and tau aggregation could support the use of therapeutics such as direct delivery of proteasomes for reducing tau aggregates. This would be invaluable considering the dearth of treatments for TBIs and chronic PCD symptoms.""
Article at:
http://www.medpagetoday.com/Neurology/HeadTrauma/52944
Anatabine Attenuates Tau Phosphorylation and Oligomerization in P301S Tau Transgenic Mice in 'Brain Disorders & Therapy'
Daniel Paris1*, David Beaulieu-Abdelahad1, Ghania Ait-Ghezala1, Venkat Mathura1, Megha Verma1, Alex E Roher3, Jon Reed1,Fiona Crawford1 and Michael Mullan1,2
Abstract:
We have previously shown that the natural alkaloid anatabine displays some anti-inflammatory and Alzheimer amyloid (Aß) lowering properties in the central nervous system associated with reduced STAT3 and NFkB activation. We investigated here the impact of a chronic oral treatment with anatabine in a model of tauopathy. We found that anatabine reduces the incidence of paralysis and abnormal hind limb extension reflex while improving rotarod performances in P301S mutant human Tau transgenic mice (Tg Tau P301S) suggesting that anatabine delays the disease progression in this model of tauopathy. Analyzes of brain and spinal cord homogenates reveal that anatabine reduces tau phosphorylation at multiple pertinent Alzheimer’s disease (AD) epitopes and decreases the levels of pathological tau conformers/oligomers in both detergent soluble and insoluble fractions. Pathological tau species reduction induced by anatabine was accompanied by decreased Iba1 expression suggesting a diminution of microgliosis in the brain and spinal cord of Tg Tau P301S mice. In addition, we found that anatabine administration increases phosphorylation of the inhibitory residue (Ser9) of glycogen synthase kinase-3ß, a primary tau kinase, associated with AD pathology, providing a possible mechanism for the observed reduction of tau phosphorylation. These data support further exploration of anatabine as a possible disease modifying agent for neurodegenerative tauopathies and, in particular AD, since anatabine also displays Aß lowering properties."
Article at:
http://www.omicsgroup.org/journals/anatabine-attenuates-tau-phosphorylation-and-oligomerization-in-ps-tau-transgenic-mice-2168-975X.1000126.php?aid=26406
Traumatic Brain Injury Research Program at 'Roskamp Institute'
Excerpt:
"Each year 1.4 million people in the United States sustain a traumatic brain injury (TBI), contributing to 30% of injury-related fatalities in the US. TBI consists of both an initial primary injury to the brain caused by the mechanical and sheering forces of impact and a delayed secondary injury driven by downstream events in the hours and days thereafter. The delayed nature of secondary brain injury means that there may be a window of opportunity for therapeutic intervention to prevent neurodegeneration, but at the moment there are no approved drugs available for reducing secondary injury after TBI.
The majority of traumatic brain injuries that occur are mild in nature, but recent studies by our research team and others have shown an association of increased and progressive long-term damage associated with repetitive mild injuries. At the Roskamp Institute we are developing, characterizing and applying models of repetitive mild TBI in order to target molecular pathways involved in the secondary injury processes and find potential treatments to ameliorate the detrimental long term consequences of injury. Recently we have begun applying our model of repetitive mild traumatic brain injury to examine progressive intraneuronal Tau alterations which correlate with behavioral dysfunctions after TBI. Understanding the molecular consequences of injury may lead to novel therapeutic approaches. We have also evaluated potential therapeutic compounds targeting neuroinflammation after TBI, including the dietary supplement anatabine. Anatabine shows great promise at rescuing memory in animals, even when taken at long term time points after the initial insult."
Article at:
http://www.rfdn.org/tbi.html#page=team
Inflammation, not telomere length, predicts healthy longevity of centenarians in 'Medical Press', August 5, 2015
Excerpts:
"Scientists have cracked the secret of why some people live a healthy and physically independent life over the age of 100.
For the first time, a team of experts from Newcastle University's Institute for Ageing and Keio University School of Medicine, Tokyo, explored which biological and pathological processes may be the most important for successful ageing after 100 years of age.
They identified that to live past the age of 100 you must keep inflammation down in the body and telomeres long – which are the part of human cells that affect how our cells age.
Severe inflammation is part of many diseases in the old, such as diabetes or diseases attacking the bones or the body's joints, and chronic inflammation can develop from any of them."
"Centenarian offspring maintained lower levels of markers for chronic inflammation. These levels increased in everybody with age including centenarians and older, but those who were successful in keeping them low had the best chance to maintain good cognition, independence and stay alive for longer."
""Accordingly, designing novel, safe anti-inflammatory or immune-modulating medication has major potential to improve healthy lifespan.""
Article at:
http://medicalxpress.com/news/2015-08-inflammation-telomere-length-healthy-longevity.html
The Intriguing Link Between Spicy Food and a Longer Life in 'Time',
Mandy Oaklander, Aug. 4, 2015
Excerpts:
"“We know something about the beneficial effects of spicy foods basically from animal studies and very small-sized human studies,” says study author Lu Qi, associate professor at the Harvard School of Public Health. Some of those preliminary studies have found that spicy food and their active components—like capsaicin, the compound found in chili peppers—might lower inflammation, improve metabolic status and have a positive effect on gut bacteria and weight, he says."
Article at:
http://time.com/3984274/spicy-food-chili-peppers/?xid=newsletter-brief
Lack of vitamin B-1 may lead to Alzheimer's(5:08) video at 'Market Watch
Commentary:
"New research in a clinical trial by NIH shows a link between vitamin B-1 and Alzheimer’s or other forms of dementia. Burke Medical Research Institute’s Dr. Gary Gibson joins Lunch Break With Tanya Rivero. Photo: Getty"
Video at:
http://www.marketwatch.com/story/video-lack-of-vitamin-b-1-may-lead-to-alzheimers-2015-08-04
Discovery about brain protein causes rethink on development of Alzheimer's disease in'Medical News Today, 31 July 2015
Excerpts:
"An international team of researchers, led by Dr Simon Drew at the University of Melbourne and Prof Wojciech Bal at the Polish Academy of Sciences, has revealed that a shorter form of a protein called beta amyloid, may act as a sponge that safely binds a metal that can damage brain tissue when it's in excess."
"In the late 1990s, high levels of copper were discovered within these clumps. Copper is essential to health, but too much can produce harmful free radicals. Many scientists began to suspect that this copper might be contributing to the disease. They found that beta-amyloid can bind to copper indiscriminately and allow it to produce these damaging free radicals.
Closer analysis of beta amyloid protein has revealed different sizes. A good proportion of beta amyloid is missing the first three links at the start of the protein's chain-like structure.
"This short form has been overlooked by most researchers since the composition of beta amyloid was first identified 30 years ago," Dr Simon Drew explains.
"We know that the shorter form of beta amyloid is present in the diseased brain, but we now know that it is abundant in healthy brains as well.
"The small change in length makes a huge difference to its copper binding properties. We found that the short form of the protein is capable of binding copper at least 1000 times stronger than the longer forms. It also wraps around the metal in a way that prevents it from producing free radicals.
"Given these properties and its relative abundance, we can speculate this type of beta amyloid is protective. It's very different from the current view of how beta amyloid interacts with biological copper.""
""As the amount of beta amyloid in the brain increases during Alzheimer's disease, the shorter form can also clump together and this may interfere with its normal function. Higher levels of the short form may further enable it to soak up copper from other places where it is needed. It could be a Jekyll and Hyde scenario.""
Article at:
http://www.medicalnewstoday.com/releases/297615.php?tw
High Blood Sugar May Up Alzheimer’s Disease Risk, New Iowa State University Study Finds in'Biospace.com, 7/28/2015
Excerpts:
"The study, published in the Journal of the American Medical Association Neurology, found a strong association between insulin resistance and memory function decline, increasing the risk for Alzheimer’s disease. Auriel Willette, a research scientist in the Department of Food Science and Human Nutrition at Iowa State, says insulin resistance is common in people who are obese, pre-diabetic or have Type 2 diabetes. "
"This is the first study to look at insulin resistance in late middle-aged people (average age was 60), identify a pattern of decreased blood sugar use related to Alzheimer’s and link that to memory decline, Willette said. Participants were recruited through the University of Wisconsin-Madison and Wisconsin Registry for Alzheimer’s Prevention study, an ongoing study that examines genetic, biological and lifestyle factors that contribute to dementia.
The link between insulin resistance and Alzheimer’s disease is important for prevention, but the risk is much more immediate, Willette said. Problems regulating blood sugar may impact cognitive function at any age. Testing for insulin resistance in obese patients and taking corrective action, through improved nutrition and moderate exercise, is a crucial first step, he said. "
Article at:
http://www.biospace.com/News/high-blood-sugar-may-up-alzheimers-disease-risk/385788
Turn Off Your Body's Aging "Switch" in 'Pro Health', Morris Eagleton • www.ProHealth.com • July 29, 2015
Excerpts:
"How HMGB1 Triggers Inflammation
The molecule HMGB1 is responsible for initiating acute inflammation, which is a helpful reaction when your body is under attack by germs, or following an injury.5,6 Unfortunately, when a cell is damaged, its contents of HMGB1 leak out, leading to chronic inflammation.5,6
When HMGB1 leaks out, it acts as a "danger signal" that triggers the release of chemical signaling molecules (called cytokines) that call in more white blood cells, which release still more cytokines, in a vicious cycle."
"Laboratory experiments have demonstrated that putting the brakes on HMGB1 is a powerful means of slowing and reversing the processes involved in inflammation.3,4 In fact, scientists are examining the role of HMGB1 in the body and are using experimental models to begin making strides in the fight against inflammation in asthma, rheumatoid arthritis, diabetes, multiple sclerosis, and inflammatory bowel diseases.12-20
Big Pharma is frantically working to create treatments that target HMGB1, but at this point no anti-HMGB1 drug is anywhere near market-ready."
"Summary
Chronic inflammation accelerates aging and is an underlying factor in many of the diseases associated with aging.1,2,34 Scientists have discovered a way to inhibit HMGB1, the molecule that "turns on" the release of inflammatory cytokines.3-6,24
Mung beans and green tea have been in use for thousands of years in traditional Chinese medicine.3,4 They both contain powerful substances that inhibit HMGB1. Lab studies have proven that these substances are highly effective at "turning off" the HMGB1 switch that induces chronic inflammation.3,4,24
Mung bean seed coat extract and EGCG are available in oral form, making their combined HMGB1-blocking effect convenient to take by mouth."
Article at:
http://www.prohealth.com/library/showarticle.cfm?libid=20896
Link between inflammation and cancer in'Genetic Literacy Project',
Ben Locwin, July 29, 2015
Excerpts:
"New research from MIT gives further evidence that inflammation is related to cancerous processes. But that alone isn’t the whole story – the study authors found reason why inflammatory processes drive the development of cancer, and how the effect seems to also relate to the timing of exposure. The senior researcher in the finding observed, “…you do get synergy between cell division and inflammation-induced DNA damage, but in these studies there was only a mutation risk if there is chronic or repeated inflammatory responses.”
What this means is that inflammatory processes will often be accompanied by DNA damage; Now if the body has sufficient time between inflammatory bouts, it can most often repair the damaged DNA without mutations and abnormal cell growth occurring, which precedes cancerous proliferation. But if the periods are more chronic or with less time in-between, the proliferating cells, which are more susceptible to DNA damage, can be adversely affected. Another major factor the researchers looked at was the presence of DNA-alkylating agents during cell division. Alkylating agents are used in a variety of products that we are frequently exposed to.
As above, in small doses periodically spaced, the body’s DNA repair mechanisms are able to efficiently contend with the damage. However, in inflamed tissues exposed to alkylating agents, the alkylated DNA bases became too overwhelming, and cell mutations were detected that could cause cells to become cancerous. Extending this logic as the authors did would mean that individuals who were experiencing inflammation of some sort, or with a chronic inflammatory condition, would be more susceptible to DNA-induced cell mutations contributed by carcinogenic cofactors."
Article at:
http://www.geneticliteracyproject.org/2015/07/29/link-between-inflammation-and-cancer/
Naturally occurring protein fragment found in brain inhibits key enzyme implicated in Alzheimer's in 'Medical News Today, 29 July 2015
Excerpts:
"For the first time, UCLA researchers have shown that a natural protein fragment produced in the brain can act as an inhibitor of a key enzyme implicated in the onset of Alzheimer's disease, a finding that could lead to the development of new drugs to treat the disease.
The study found that the protein fragment, sAPPa, inhibits the proteolytic enzyme BACE1. Increased BACE1 activity contributes to production of the amyloid beta aggregates and plaques that are the hallmark of Alzheimer's.
"Because sAPPa inhibits the BACE1 enzyme, it may be possible that it can be used to help prevent potentially dangerous increases in BACE1 activity, and thus prevent the onset of Alzheimer's disease," said senior study author Varghese John associate professor of neurology and principle investigator of the Drug Discovery Lab in the Mary S. Easton Center for Alzheimer's Disease Research at UCLA.
The findings appear July 28, 2015 in the peer-reviewed Journal of Alzheimer's Disease."
Article at:
http://www.medicalnewstoday.com/releases/297477.php?tw
Reference to Anatabine Citrate in PubMed:
"we show that anatabine lowers NF?B activation at doses that inhibit Aß production in vitro. Since NF?B is known to regulate BACE-1 expression (the rate limiting enzyme responsible for Aß production), we determined the impact of anatabine on BACE-1 transcription. We show that anatabine inhibits BACE-1 transcription and reduces BACE-1 protein levels in human neuronal like SHSY-5Y cells suggesting that the Aß lowering properties of anatabine are mediated via a regulation of BACE-1 expression. In vivo, we show that an acute treatment with anatabine for four days significantly lowers brain soluble Aß1?40 and Aß1?42 levels in a transgenic mouse model of Alzheimer's disease. Altogether our data suggest that anatabine may represent an interesting compound for regulating brain Aß accumulation."
PubMed article at:
http://www.ncbi.nlm.nih.gov/pubmed/21958873
Neuroinflammation in Alzheimer's disease in 'PubMed', 14 April 2015
Heneka MT1, Carson MJ2, El Khoury J3, Landreth GE4, Brosseron F5, Feinstein DL6, Jacobs AH7, Wyss-Coray T8, Vitorica J9, Ransohoff RM10, Herrup K11, Frautschy SA12, Finsen B13, Brown GC14, Verkhratsky A15, Yamanaka K16, Koistinaho J17, Latz E18, Halle A19, Petzold GC20, Town T21, Morgan D22, Shinohara ML23, Perry VH24, Holmes C25, Bazan NG26, Brooks DJ27, Hunot S28, Joseph B29, Deigendesch N30, Garaschuk O31, Boddeke E32, Dinarello CA33, Breitner JC34, Cole GM12, Golenbock DT35, Kummer MP36.
Excerpts:
"External factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain and further promote disease progression. Modulation of risk factors and targeting of these immune mechanisms could lead to future therapeutic or preventive strategies for Alzheimer's disease."
Article at:
http://www.ncbi.nlm.nih.gov/pubmed/25792098
Alzheimers Clinical trials---Excellent resource at:
https://clinicaltrials.gov/search/open/condition=%22Alzheimer+Disease%22
The Role of Tau Protein Aggregates in Alzheimer's Disease, Robert Doerksen , April 21, 2015
My comments: Short 5 minute video---Mullan knows!
Video at:
And don't forget: Anatabine Attenuates Tau Phosphorylation and Oligomerization in P301S Tau Transgenic Mice in 'Brain Disorders & Therapy', Daniel Paris1*, David Beaulieu-Abdelahad1, Ghania Ait-Ghezala1, Venkat Mathura1, Megha Verma1, Alex E Roher3, Jon Reed1,Fiona Crawford1 and Michael Mullan1,2
1Roskamp Institute, Sarasota, Florida, USA
2Rock Creek Pharmaceuticals
Abstract:
We have previously shown that the natural alkaloid anatabine displays some anti-inflammatory and Alzheimer amyloid (Aß) lowering properties in the central nervous system associated with reduced STAT3 and NFkB activation. We investigated here the impact of a chronic oral treatment with anatabine in a model of tauopathy. We found that anatabine reduces the incidence of paralysis and abnormal hind limb extension reflex while improving rotarod performances in P301S mutant human Tau transgenic mice (Tg Tau P301S) suggesting that anatabine delays the disease progression in this model of tauopathy. Analyzes of brain and spinal cord homogenates reveal that anatabine reduces tau phosphorylation at multiple pertinent Alzheimer’s disease (AD) epitopes and decreases the levels of pathological tau conformers/oligomers in both detergent soluble and insoluble fractions. Pathological tau species reduction induced by anatabine was accompanied by decreased Iba1 expression suggesting a diminution of microgliosis in the brain and spinal cord of Tg Tau P301S mice. In addition, we found that anatabine administration increases phosphorylation of the inhibitory residue (Ser9) of glycogen synthase kinase-3ß, a primary tau kinase, associated with AD pathology, providing a possible mechanism for the observed reduction of tau phosphorylation. These data support further exploration of anatabine as a possible disease modifying agent for neurodegenerative tauopathies and, in particular AD, since anatabine also displays Aß lowering properties.
Daily Value for Added Sugars Coming to Food Labels in'Web MD', Brenda Goodman, MA, Reviewed by Brunilda Nazario, MD on July 24, 2015
Excerpts:
"Food manufacturers will be required to tell consumers how much sugar is added to their products and show how the amount compares to recommended daily limits under new changes to nutrition labels proposed by the FDA on Friday.
Many nutritionists and public health experts blame rising amounts of added sugars in processed foods for contributing to rising rates of diabetes, obesity, and heart disease.
But it can be tough to tell how much of the sweet stuff is in processed foods. Nutrition labels only tally total sugars, a measure that includes both those naturally present in foods like fruits and vegetables and those that are added during manufacturing."
"Specifically, regulators are proposing that people limit the added sugar they eat to no more than 10% of their total daily calories. For a person who eats 2,000 calories a day, that’s about 12 teaspoons of sugar a day. A teaspoon of sugar is about 16 calories.
Studies show that the average American now takes in almost twice that much sugar -- 22 teaspoons -- each day, which amounts to an extra 350 calories."
"The food industry has lobbied hard to keep added sugars off food labels. Public policy experts say they expect significant pushback on the changes.
“I expect the food industry -- led by the Grocery Manufacturers Association -- to go berserk over this one,” says Marion Nestle, PhD, in an email to WebMD. Nestle is a professor of nutrition, food studies, and public health at New York University. She predicts food makers will go to Congress to try to block the changes."
Article at:
http://www.webmd.com/diet/20150724/daily-added-sugars-labels?page=2
Encouraging Results Of AXON's Tau Vaccine Advance Alzheimer's Therapy in 'Biospace.com', BUSINESS WIRE, 7/23/2015
Excerpts:
"Biotech firm AXON Neuroscience has presented encouraging results from a Phase 1 study with a vaccine designed to target diseased tau proteins in Alzheimer’s patients. AXON is not only the first company to successfully complete a Phase 1 study with an active tau vaccine, but the first to show excellent safety profile with an active treatment in Alzheimer’s research.
This Smart News Release features multimedia. View the full release here: http://www.businesswire.com/news/home/20150723005117/en/
"According to coordinating investigator Professor Reinhold Schmidt from Medical University Graz, who presented the results at the at the Alzheimer’s Association International Conference 2015 (AAIC) in Washington D.C., the vaccine is safe and well tolerated in all assessed parameters. Additionally, the treatment induced robust immune response in vast majority of the study participants and the average cognition of patients remained stable over 6 months. These promising results lead to big expectations in the upcoming Phase II study.
TAU AS A DRIVING FORCE IN ALZHEIMER’S
The researchers at AXON Neuroscience have extensively worked on tau hypothesis for more than 25 years. Through the years, they have proven in various experiments that tau is the driving force in Alzheimer’s disease. This was also recently confirmed by the researchers at Mayo Clinic, USA, who have found by examining more than 3,600 postmortem brains that the progression of dysfunctional tau protein drives the cognitive decline and memory loss seen in Alzheimer's disease."
News Release at:
http://www.biospace.com/News/encouraging-results-of-axons-tau-vaccine-advance/385338
Method to Halt the Advance of Liver Cancer Study suggests that drugs targeting the lymphotoxin-beta receptor may improve liver cancer treatment in 'Newswise', Sanford Burnham Prebys Medical Discovery Institute, 23-Jul-2015
Excerpts:
"For some time we have known about the interconnection between the receptor, inflammation—including inflammation caused by hepatitis—and liver cancer. Now, we have demonstrated how the receptor’s signals create an environment that accelerates oncogenic activity and tumor growth,”"
"The LTßR, originally discovered by Ware, is best known for controlling the development of lymphoid organs, supporting the body’s immune response to pathogens, and regulating inflammation. His work has led to the understanding that blocking the activity of the receptor inhibits inflammation. This approach is currently studied as a treatment for chronic inflammatory diseases, including Sjögren’s syndrome."
"Importantly, the research team found that LTßR levels were elevated in human liver cancer cell lines, reflecting the need for enhanced receptor activity to maintain oncogene activity. Similarly, higher levels of the receptor correlated with poor survival in patients with intrahepatic cholangiocarcinoma, the second most common type of liver tumor."
Article at:
http://www.newswise.com/articles/researchers-find-new-method-to-halt-the-advance-of-liver-cancer
In Alzheimer's, hope, hype and disappointment as biopharma goes all in on amyloid in 'Fierce biotech', Damian Garde, July 23, 2015
My comments: Has anyone looked at chronic inflammation as a prelude to Alzheimers? ie is CRP an pre-Alzheimers biomarker also?
Excerpts:
"By 2050, all living baby boomers will be over 85, and half of them will have Alzheimer's, according to a new report from the Lewin Center for Aging and Disability Policy. That phenomenon will come to account for nearly 25% of all Medicare spending, the group figures, up from an estimated 2% in 2020.
Dr. Dean Hartley
"It's a tsunami that's going to break the healthcare system," said Dr. Dean Hartley, director of science initiatives for the Alzheimer's Association.
And the prognosis has been similarly grim on the research side. Reviewing clinical trial data from 2002 to 2012, Cleveland Clinic researchers calculated a 99.6% failure rate for all would-be Alzheimer's treatments, including promising early technologies that proved toxic and high-profile breakthroughs that ultimately fizzled in the final stages of testing."
"With all that prologue, the eventual letdown was that much more dramatic. On Wednesday morning, Biogen revealed that not only did the 6 mg injection fail to come through as the "Goldilocks dose" it had hoped for, but it failed to measure up to even the 3 mg group. Aducanumab at 6 mg per kilogram didn't lead to a statistically significant improvement over placebo on two measures of cognition and function, effectively poking a hole in that dose-dependent efficacy response that stirred up excitement in March."
"But if the scientists are going to finally clear that hurdle, it's going to take more than a handful of candidates targeting amyloid, Hartley said. The field needs more clinical endeavors, more exploration of potential targets and more funding for basic research in order to build on the past decade's breakthroughs in the disease, he said.
"We now know the disease may start some 15 to 20 years prior to clinical symptoms," Hartley said. "That set us along the pathway of thinking of Alzheimer's as a continuum. … Now we need more shots on goal, in other words more drugs coming into those clinical trials.""
Article at:
http://www.fiercebiotech.com/story/alzheimers-hope-hype-and-disappointment-biopharma-goes-all-amyloid/2015-07-23
Positive initial phase 2a study data with ANAVEX 2-73 showing early evidence of improving cognition in patients with Alzheimer's disease in Medical News Today, 24 July 2015
Excerpts:
"Anavex Life Sciences Corp. has announced initial positive cognitive data for ANAVEX 2-73, the Company's lead investigational oral treatment for Alzheimer's targeting sigma-1 and muscarinic receptors, which is believed to reduce protein misfolding including reduction of beta amyloid, tau and inflammation. Cognitive EEG/ERP P300 data, a real-time physiological measure of cognitive processes with demonstrated sensitivity to Alzheimer's disease, is being presented today for the first 12 of 32 mild-to-moderate Alzheimer's patients in the ongoing ANAVEX 2-73 Phase 2a clinical trial at AAIC 2015 in Washington, DC.
ANAVEX 2-73 showed in 83 percent (10/12) of patients positive cognitive effects during PART A of the study, which consists of a 36-day on-off-on not-yet-optimized dosing regimen to assess bioavailability. At day 36, the amplitude of the cognitive EEG/ERP biomarker P300 increased 38 percent from baseline. Published data suggests that a 38 percent increase is approximately 4 times higher than donepezil (Aricept®), the current standard of care, in the same timeframe."
Article at:
http://www.medicalnewstoday.com/releases/297272.php?tw
Sounds creepy. Wish they would say more about the New Zealand trials and why/what they plan to do because of it. OTC supplement? Also anxious to hear any update on their European trials. I wonder if the 'creep' you see is real maybe because of their inside knowledge of the data they have from these two trials so far? I can't believe they just blindly test anatabine on 'healthy' individuals without regard to issues they may have that could be affected by these dosages. Well, more to come---in slow motion. Worried also about their last private offering that seems to hit a wall. How does this impact their future plans? Based on what I've seen so far re licensing, joint-ventures, and buy-outs, the big pharmas seem to wait until they get some positive data from the clinical trials, ie phase 2 or phase 3 before making offers. Can they make it? Also wondering what data they got when they were doing the Anatabloc trials on Alzheimers? Good, bad, or nada???
Keep watching. Though the stock is creeping down, there is someone who seems to buy thousand share blocks of stock while shorts or others sell in 100 share blocks? Hey Johnny what'cha doing?
Alzheimer's Data Diverge in 'Investor.com', 07/22/2015
News Brief:
"Biogen (NASDAQ:BIIB) stock sank 4.3% as ambiguous clinical trial results for its Alzheimer's drug candidate, aducanumab, prompted chatter and a downgrade.Eli Lilly (NYSE:LLY) released follow-up data on a phase-three trial of its own Alzheimer's drug, solanezumab. Evercore ISI said it was "incrementally positive but not thesis- or stock-changing." Lilly rallied to close up 1%."
Brief at:
http://news.investors.com/072215-762947-alzheimers-data-diverge.htm
Women Descend Into Alzheimer's at Twice the Speed of Men: Study in 'Drugs.com', July 21, 2015
Excerpts:
"Women with mild thinking and memory problems -- known as mild cognitive impairment -- deteriorate twice as fast mentally as men with the same condition, according to new research.
Mild cognitive impairment isn't severe enough to interfere with daily life, but it is linked to higher odds of developing Alzheimer's disease or another type of dementia, the researchers said."
"Several factors may account for this increased vulnerability among women, Lin added. Women may be genetically predisposed to developing more plaque in the brain, which is a hallmark of Alzheimer's, or perhaps there is an as-yet-unknown genetic cause, she said."
Article at:
http://www.drugs.com/news/women-descend-into-alzheimer-s-twice-speed-men-study-57614.html?utm_source=ddc&utm_medium=email&utm_campaign=Today%27s+news+summary+-+July+21%2C+2015&utm_content=Women+Descend+Into+Alzheimer%27s++at+Twice+the+Speed+of+Men%3A+Study
Early signs drug delays Alzheimer's in BBC News, James Gallagher
Health editor, BBC News website, July 22, 2015
Excerpts:
"Data from pharmaceutical company Eli Lilly suggests its solanezumab drug can cut the rate of the dementia's progression by about a third."
"A new trial is due to report next year and should provide definitive evidence.
The death of brain cells in Alzheimer's is currently unstoppable. Solanezumab may be able to keep them alive."
"Solanezumab has long been the great hope of dementia research, yet an 18-month trial of the drug seemingly ended in failure in 2012.
But when Eli Lilly looked more closely at the data, there were hints it could be working for patients in the earliest stages of the disease.
So the company asked just over 1,000 of the patients in the original trial with mild Alzheimer's to take the drug for another two years."
"44 million globally have dementia
135 million will have the disease in 2050
By then 71% will be poor and middle income
$600bn global cost of dementia
In the UK, cancer research gets 8x as much funding as dementia
Source: Alzheimer's Society"
Article at:
http://www.bbc.com/news/health-33617141
New 8-K Filed:
"tem 3.01. Notice of Delisting or Failure to Satisfy a Continued Listing Rule or Standard; Transfer of Listing
As previously disclosed in a Form 8-K filed on June 19, 2015, Rock Creek Pharmaceuticals, Inc. (the “Company”) completed on that date a registered direct offering (the “Transaction”) with five institutional investors pursuant to which the Company issued 1,644,500 shares of common stock (the “Shares”) and warrants to purchase up to 1,233,375 shares of common stock (the “Warrants”). The Shares and Warrants were sold in units, each of which was comprised of one Share and 0.75 Warrants to acquire one share of common stock. The purchase price per unit in the offering was $2.25, and the exercise price of the Warrants was $2.83 per share.
On July 16, 2015, the Company received a letter from the Listing Qualifications Department of The Nasdaq Stock Market, LLC (“Nasdaq”), notifying the Company that the Transaction did not comply with Nasdaq’s shareholder approval rules. Under Nasdaq Listing Rule 5635(d)(2), a listed issuer is required to obtain prior stockholder approval for any “sale, issuance or potential issuance by the Company of common stock (or securities convertible into or exercisable common stock) equal to 20% or more of the common stock or 20% or more of the voting power outstanding before the issuance for less than the greater of book or market value of the stock.” The closing bid price of the Company’s common stock on June 16, 2015 (the date of the Securities Purchase Agreement for the Transaction) was $2.80 per share, and the Company had 8,482,358 shares of common stock outstanding as of May 31, 2015.
In connection with the Transaction, the Company intended to comply with Rule 5635(d)(2) by following a Nasdaq policy which provides that warrants issued in a transaction will not be aggregated with the common stock issued in the same transaction if the warrants are not exercisable for at least six months following the closing and are not exercisable for less than the greater of book or market value. Although the Warrants issued in the transaction have an initial exercise price of greater than book or market value (an exercise price of $2.83 compared to a deemed fair market value of $2.80 per share) and are not exercisable until after six months following issuance, Nasdaq has informed the Company that the inclusion in the Warrants of a price-protection provision requires aggregation of the Warrants with the Shares for purposes of Rule 5635(d)(2). The price-protection provision in the Warrants provides that, subject to certain exceptions, if the Company issues shares of its common stock at a price less than $2.83 per share during the six-month period following the closing of the Transaction, then the exercise price will be reduced to such lower price. As such, after giving effect to the aggregation of the Warrants, Nasdaq concluded the Transaction resulted in the potential issuance of 35% of the pre-Transaction shares outstanding at a price less than the greater of book or market value, and, as a result, the Company violated the shareholder approval requirement set forth in Rule 5635(d)(2).
Under applicable Nasdaq rules, the Company has 45 calendar days to submit a plan to regain compliance with all Nasdaq listing requirements. The Company is in the process of developing a plan to regain compliance, which it intends to submit to Nasdaq promptly. If the plan is accepted, Nasdaq can grant the Company an extension of up to 180 calendar days from July 16, 2015 to evidence compliance."
Posted at:
http://investors.rockcreekpharmaceuticals.com/investors-sec-filings
Novel monoclonal antibodies show promise for Alzheimer's disease treatment in 'Medical News Today', 21 July 2015
Excerpts;
"Scientists at NYU Langone Medical Center's Center for Cognitive Neurology have evidence that monoclonal antibodies they developed may provide the blueprint for effective treatments for Alzheimer's disease and other neurodegenerative diseases, such as Parkinson's disease.
A team led by Fernando Goni, PhD, an adjunct associate professor of Neurology, and Thomas Wisniewski MD, director of the Center for Cognitive Neurology at NYU Langone, showed that a novel class of monoclonal antibodies successfully targeted proteins that change shape and misfold, becoming toxic and triggering the hallmark beta-amyloid plaques and abnormal tau proteins that are known to accumulate in Alzheimer's and other neurodegenerative conditions. The monoclonal antibodies were also successful at targeting the proteins linked to Parkinson's development.
The research team's findings were released at the Alzheimer's Association International Conference 2015, July 19, 2015 in Washington, D.C."
""We have been developing this strategy for many years, and now we have results. Other labs are trying similar strategies", says Dr Wisniewski, the Lulu P. and David J. Levidow Professor of Neurology and a professor of Pathology and Psychiatry. "The importance of this concept is being increasingly recognized."
Researchers have plans for further animal tests of their monoclonal antibody regimen, on its own and in combination with other approaches, before proceeding to clinical trials."
Article at:
http://www.medicalnewstoday.com/releases/297061.php?tw
Gut worms protect babies' brains from inflammation in 'Medical News Today, 21 July 2015
Excerpts:
"A Duke University study in rats finds that gut worms can protect babies' brains from long-term learning and memory problems caused by newborn infections.
Baby rats with tapeworms avoided the brain inflammation that plagued worm-free rats after exposure to immune triggers in adulthood.
What's more, the benefits began early, while still in the womb. Expectant mother rats with tapeworms passed similar protection on to their worm-free pups, the researchers found.
The findings could point to new ways to treat or prevent the chronic brain inflammation linked to cognitive disorders like Alzheimer's disease, autism and depression.
The study appears online in the journal Brain, Behavior, and Immunity.
Previous studies by Duke neuroscientist Staci Bilbo and colleagues showed that when rats get bacterial infections at a very early age, even elsewhere in the body, immune cells in their brains become hypersensitive to subsequent infections and pump out a continuous stream of messenger molecules called cytokines that can cause cognitive problems later in life."
"According to what scientists call the "Biome Depletion Theory," some autoimmune and inflammation-related diseases may be the result of too few of the life forms that once lived in and on the body -- particularly gut worms -- rather than too many.
Tapeworms, roundworms and other wormy companions have inhabited the warm wet folds of animal intestines for more than 100 million years, bathing in a constant supply of food and nutrients.
Over millions of years of co-existence, the theory goes, the immune system learned to tolerate these live-in guests, and eventually adapted to work with worms in mind.
The theory is that now, with worms gone from our guts, the body's natural defenses can spiral out of control.
"Our bodies are essentially an ecosystem," said Duke immunologist and study co-author William Parker.
Parker and Bilbo decided to see if restoring the internal ecosystem in the gut could bring the brain's immune cells back in balance."
"The worm-free rats responded to the second immune challenge with the same harmful outpouring of inflammatory cytokines seen in previous studies.
But the wormy rats, and also rats that were worm-free but born to worm-infested parents, responded differently.
Notably, the immune cells in their brains were able to respond to the second trigger without going into overdrive. They also didn't develop the same memory problems later in life that their worm-free counterparts did."
Article at:
http://www.medicalnewstoday.com/releases/297069.php?tw
Stanford scientists see iron-containing inflammatory cells in Alzheimer's brains in 'Medical News Today', 21 July 2015
Excerpts:
"Examining post-mortem tissue from the brains of people with Alzheimer's disease, Stanford University School of Medicine investigators identified what appear to be iron-containing microglia -- specialized scavenger cells that sometimes become inflammatory -- in a particular part of the hippocampus, a key brain structure whose integrity is critical to memory formation.
In post-mortem brain tissue from people not diagnosed with Alzheimer's, neither the iron deposits nor the scavenger cells engulfing them were present in that brain region."
"The bulk of microglia found in association with iron in the study were in an activated, inflammatory state. Alzheimer's is increasingly understood to involve brain inflammation, and groups led by Stanford researchers such as neurologists Katrin Andreasson, MD, and Tony Wyss-Coray, PhD, and neurobiologist Ben Barres, MD, PhD, have previously fingered microglia as potential suspects in the early inflammatory pathology of the disease. This study adds the new finding that inflamed, iron-associated microglia are present in the hippocampus in Alzheimer's and are observable by 7T MRI, which could advance the scientific community's understanding of the disease."
Article at:
http://www.medicalnewstoday.com/releases/297082.php?tw
Biotech Investing Hits An All-Time High--But Is It a Bubble? in 'Forbes', Arlene Weintraub, 7/21/2015
Excerpts:
"The biotechnology industry hauled in $2.3 billion worth of venture capital investments during the second quarter of this year—a 32% increase over the prior quarter, according to the newest MoneyTree Report from PricewaterhouseCoopers (PwC) and the National Venture Capital Association (NVCA). The 126 deals struck during the period marked the biggest quarterly investment in biotech since the MoneyTree report first came out in 1995, and it brought the total for the first half to $3.8 billion. That puts the biotech industry well on track to soar past 2014’s total of $6 billion of VC cash raised for the year, which will inevitably spark the question that comes up whenever any industry looks so frothy: Is this a biotech bubble or are the gains sustainable?
To best address that question, it helps to start by looking at some of the trends behind the dollar signs. First of all, after years of shying away from early-stage research, VCs have clearly regained their appetite for taking bets on unproven science. During the quarter, about $1.5 billion of VC cash went into early-stage companies, and $733 million of that went to startups receiving venture money for the first time. “In the biotech space, that’s an all-time high,” says Greg Vlahos, a life science partner at PwC."
Article at:
http://www.forbes.com/sites/arleneweintraub/2015/07/21/biotech-investing-hits-an-all-time-high-but-is-it-a-bubble/
Coffee drinking may lower inflammation, reduce diabetes risk in Reuters, KATHRYN DOYLE, July 20, 2015
Excerpts:
"Coffee drinkers in a long-term study were about half as likely to develop type 2 diabetes as those who didn't drink coffee, and researchers think an inflammation-lowering effect of the beverage might be the key."
"Habitual coffee drinkers were 54 percent less likely to develop diabetes compared to non-coffee drinkers, even after accounting for smoking, high blood pressure, family history of diabetes and intake of other caffeinated beverages, the researchers reported in the European Journal of Clinical Nutrition.
Levels of serum amyloid, one of the inflammatory markers in the blood, seemed to explain some of the relationship between coffee and diabetes, the authors write. Higher coffee consumption went along with lower amyloid levels."
Article at:
http://www.reuters.com/article/2015/07/20/us-health-diabetes-coffee-drinkers-idUSKCN0PU1NJ20150720?feedType=nl&feedName=healthNews
RANKL Signaling Pathway in Oncology Drug Pipeline Update 2015 at:
http://www.prnewswire.com/news-releases/rankl-signaling-pathway-in-oncology-drug-pipeline-update-2015-300114854.html
My comments: Everything you want to know about the NF-kB race (Probably for a price)
How to Avoid or Heal from Autoimmune Disorders at YouTube, John Bergman, April 2, 2015
IMPORTANT watch for your family's health. You decide. If true, this has to be the greatest fraud perpetrated against mankind. You thought sugar was bad, watch this video. Sugar plus plus. Is it the FDA again? Unbelievable! 43 minutes of your time well worth spent.
Video at:
New saliva test may catch Alzheimer's disease early in 'CNN', Liza Lucas, Special to CNN, July 20, 2015
Excerpts:
"A test detecting Alzheimer's disease early may become easily available thanks to one plentiful bodily substance: saliva, a recently released study shows.
The saliva test was presented at the 2015 Alzheimer's Association International Conference in Washington this week. Though research is still in its infancy, the saliva test represents the exciting future of diagnostic tools in development for the detection of the neurodegenerative disease."
"Researchers from the University of Alberta in Canada analyzed saliva samples of fewer than 100 people, divided into three groups based on cognitive ability: 35 with normal aging cognition, 25 with mild cognitive impairment and 22 with Alzheimer's disease.
Using protein analysis technology, researchers examined the saliva of each individual, analyzing nearly 6,000 metabolites, which are small molecules that are byproducts of chemical reactions in the brain.
The team then discovered specific biomarkers (or patterns of metabolites) in the groups with known Alzheimer's or mild cognitive impairment, in comparison with the natural aging group, and tested the biomarkers as predictors of cognitive performance."
"Experts say they will be looking for such an easy-to-use, affordable option like the saliva test for the day when that magic pill or drug treatment becomes available.
"When that blockbuster drug comes," said Isaacson. "A test like this is what we're all looking for.""
Article at:
http://us.cnn.com/2015/07/20/health/saliva-test-may-catch-alzheimers-disease/index.html
Alzheimer's Drugs In The Works Might Treat Other Diseases, Too in 'All Things Considered, WTVF Radio', JON HAMILTON • JUL 20, 2015
My comments: If you review RCPI's research, you will find that anatabine appears to reduce amaloyd plaque and tau tangles. What are we waiting for?
Excerpts:
"Previous efforts to treat Alzheimer's have focused on a single target — usually the protein called beta-amyloid, says Maria Carrillo, chief science officer of the Alzheimer's Association. "The one-target approach is probably not going to be the answer," Carrillo says.
Instead, several teams of scientists reporting their work at the Alzheimer's Association International Conference in Washington, D.C., this week are targeting a process in the brain that leads to toxins involved in several different diseases.
The biotechnology company Treventis is working on one of these potential drugs.
"Our ultimate goal is to discover a pill that can be taken once a day that could either stop or slow Alzheimer's disease," says Marcia Taylor, the company's director of biological research. Treventis hopes to do that with a drug that prevents the build-up of two toxic proteins.
These toxic substances, called beta-amyloid and tau, are the result of a process that begins when a healthy protein inside a brain cell somehow gets folded into the wrong shape."
Article at:
http://wvtf.org/post/alzheimers-drugs-works-might-help-other-diseases-too#stream/0
Inflammatory link discovered between arthritis and heart valve disease in 'Medical Press', Provided by: Walter and Eliza Hall Institute, July 20, 2015
Excerpts:
"Australian researchers have used models to identify a potential link between excess production of inflammatory proteins that cause rheumatoid arthritis and the development of heart valve disease.
The research team discovered that a critical inflammatory protein involved in rheumatoid arthritis could also lead to inflammation and disease of the heart valves, including aneurysms. The research could lead to improved treatments for rheumatoid arthritis, and suggests investigating existing medicines that dampen inflammation to treat heart valve diseases, such as rheumatic heart disease."
"The link between TNF overproduction and the development of rheumatoid arthritis has been known for many years. However Dr Bouillet's team has identified new regions of the DNA critical for destabilising the molecule.
"People with rheumatoid arthritis have too much TNF in their joints and in their blood," Dr Bouillet said. "We have identified a previously unknown way that the body destabilises the molecules during the process of TNF production to stop too much of the protein being made. We could essentially develop agents that put a spanner in the works, stopping the factory production of TNF."
Treating rheumatoid arthritis patients with drugs that 'mop up' excess TNF has been very effective in managing the disease, Dr Bouillet said. However they do have a downside.
"Up to 50 per cent of patients become unresponsive to anti-TNF drugs because they develop immunity to this foreign protein," he said. "We think targeting the regions of the DNA that destabilise the molecule could be an innovative way to interfere with protein production to dampen the amount of TNF being made.""
Article at:
http://medicalxpress.com/news/2015-07-inflammatory-link-arthritis-heart-valve.html