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Anti-Aging Medicine, Anti-Aging Insights on Inflammation in 'Townsend Letter', Ronald Klatz, MD, DO, and Robert Goldman, MD, PhD, DO, FAASP, June 2015
Excerpts:
"The body deploys the inflammatory response as a defense mechanism to counter infection. However, unchecked chronic inflammation can be a deleterious process, contributing to conditions from heart disease to irritable bowel syndrome to cognitive decline. Chronic inflammation also reduces the number of vital, healthy years. Vishwa Deep Dixit, from Yale School of Medicine (Connecticut, US), and colleagues identified a compound, known as Nlrp3, as a trigger of aging-related inflammation. The team revealed that this compound causes a loss of function that manifests as insulin resistance, bone loss, frailty, and cognitive decline. The study authors are hopeful that future therapeutics targeted at lowering Nlrp3 might "delay multiple age-related chronic diseases."
Article at:
http://www.townsendletter.com/June2015/antiage0615.html
Researchers Pinpoint Chronic Inflammation In the Development of Skin Cancer in 'Melanoma News Today', Ana Pamplona, PhD, February 16, 2015
Excerpts:
"Inflammation is a process by which the immune system responds to a disease or injury. Chronic inflammation, however, has been linked to several types of cancers, such as basal cell carcinoma, lung, liver, colon cancer and others. Although this association is acknowledged, research has not been able to explain the cellular mechanisms that are involved in this process.
A new study entitled “Immature myeloid cells directly contribute to skin tumor development by recruiting IL-17–producing CD4+ T cells” was published in the Journal of Experimental Medicine by Dr. Myrna L. Ortiz, Dr. Vinit Kumar and Dr. Anna Martner, first co-authors, and led by Dr. Dmitry Gabrilovich from The Wistar Institute in Philadelphia, PA. In this study, researchers have shown that inflammatory conditions that favor the development of skin and colon tumors are linked to the accumulation of myeloid-derived suppressor cells in cancer tissues or to the accumulation of immature myeloid cells (IMCs) in individuals without tumors."
Article at:
http://melanomanewstoday.com/2015/02/16/researchers-pinpoint-chronic-inflammation-in-the-development-of-skin-cancer/
Chronic inflammation: is it the driver or is it paving the road for malignant transformation? in 'Genes and Cancer', Kambiz Afrasiabi1, Yi-Hong Zhou2, Angela Fleischman1
1 Department of Medicine, University of California, Irvine, CA, USA
2 Department of Surgery, University of California, Irvine, CA, USA,May 8, 2015
ABSTRACT:
"Chronic inflammation in well-defined mouse models such as Gia2 knock out mouse has been shown to trigger formation and expansion of hypoxic niches and also leads to up regulation of NF?B, offering cells which have adapted their genetic machinery to hypoxia a unique survival advantage. These adapted cells have been shown to acquire stem cell-like capabilities as shown by up regulation of stem cell markers. Such long lived cells become permanent residents in sub mucosa and acquire a malignant phenotype from long-term exposure to noxious environmental agents due to a barrier defect secondary to down regulation of barrier proteins such as Zo1 and Occludin. Indeed mitotic spindle disorientation in such mice has been proposed as another contributory factor to malignant transformation. Sterilization of bowel lumen of these mice through different techniques has prevented malignant transformation in the presence of chronic inflammation. These facts stand strongly against chronic inflammation as a true driver of carcinogenesis but clearly support its role in facilitating the emergence of the neoplastic clone.
Article at:
http://www.impactjournals.com/Genes&Cancer/index.php?abs=64
Chronic Inflammation – The Silent Killer of Men in 'The New Prime', Craig Cooper, April 4, 2015
Excerpts:
"Chronic inflammation is another matter. It’s like a runaway train, fueled by the cytokines that are continuously spilled out into the body’s circulation and causing inflammation of the tissues. Your immune system wants to put on the brakes and stop the cell and tissue damage and progression toward disease.
Stomping on those brakes however becomes more and more difficult as time goes on because the body gets tired. The cells sent by the immune system to fix the damage just can’t keep up with the demands. In addition, the aging process adds more fuel to the runaway train because as cells age, they become less efficient at repairing any injury but more likely to send out pro-inflammatory chemicals.
Therefore, as the train speeds along, it can cause an accumulation of damaged blood vessels, a buildup of fat (triggered by the secretion of adipokines, hormones that cause fat storage), plaque in your arteries and brain, excess body weight, and other injuries, all associated with chronic inflammation.
Consequences of chronic inflammation
Chronic low-level inflammation is like an insidious villain, running rampant throughout the body yet often without causing any symptoms until things get serious. In fact, left untreated, chronic inflammation can result in a wide range of serious health problems.
Cancer (e.g., colorectal, lung, lymphoma, ovarian, pancreatic, prostate)
Heart disease and stroke
Alzheimer’s disease and cognitive impairment
Nephritis and chronic kidney disease
Chronic lower respiratory disease
Osteoporosis
Age-related macular degeneration
Depression
Rheumatoid arthritis
Inflammatory bowel disease
Pancreatitis
Diabetes
Asthma
There are also a host of inflammation related disorders and diseases that come under the suffix of “…itis” – meaning “a disease characterized by inflammation”. I had three of them when I was young – pericarditis (heart inflammation), osteomyelitis (bone inflammation), and encephalitis (brain inflammation). A triple whammy between the ages of nine and eighteen years. Scary shit for a teenager. But it focused me on living a lifestyle of prevention and learning how to manage inflammation better."
"Causes of chronic inflammation
A variety of factors can cause chronic inflammation, a few of which you have no control over, but others are definitely ones you can take control of.
You are aging
You have bad genes
You don’t eat right.
You don’t exercise right
You are exposed to toxins
Your stress levels are high.
You smoke
Your sex hormone levels are low
You have periodontal disease
You have problems with sleep."
Article at:
http://thenewprime.com/blog/inflammation-the-silent-killer-of-men/
Research finds link between chronic inflammation, tumor development in breast cancer in 'Local10.com', Jun 10 2015
Short News Video at:
http://www.local10.com/news/health/research-finds-link-between-chronic-inflammation-tumor-development-in-breast-cancer/33510556
Also, short clip on new Cholesterol drug
Has Biogen found the 'Goldilocks' dose for Alzheimer's drug? in NBC News, Meg Tirrell, 17 Jul 2015
Excerpts:
"Highly anticipated data due out next week on its experimental Alzheimer's medicine could show whether aducanumab will be among the first drugs to slow the cognitive declines associated with the disease.
If the medicine continues to perform the way the data have suggested so far, the impact would be enormous: Alzheimer's affects more than 5 million Americans now—a number expected to triple by 2050 without interventions. Analysts say the drug has a potential market opportunity of $20 billion a year."
""The key question is: Does the 6mg/kg look more similar to the 10mg/kg, which demonstrated profound benefit (but was toxic) or does it look more like the 3mg/kg dose, which was modestly effective.""
"Analysts say there are reasons to be optimistic, especially since Biogen has already made plans to move forward with large late-stage studies of the medicine. The Alzheimer's conference, which kicks off this weekend, will also bring data on a competing drug from Eli Lilly. If it or Biogen's is successful, they could be the first on the market to make an impact on the memory loss that Alzheimer's brings.
The drugs are being tested on patients with the earliest forms of Alzheimer's, so wouldn't be a panacea for the millions of patients with the disease today. But they could be a significant step forward in a massive disease with no effective treatment options."
Article at:
http://www.cnbc.com/2015/07/17/has-biogen-found-the-goldilocks-dose-for-alzheimers-drug.html
INFLAMMATION--food and information for thought, John Bergman, July 12, 2015
39 minute video on inflammation in practical, understandable terms, worth the watch for your understanding of inflammation. Stay tuned, more coming.
Video at:
New Antibody May Treat Brain Injury and Prevent Alzheimer’s Disease in Healthline.com, R. Sam Barcla, July 15, 2015
Excerpts:
"Previous research has pinpointed misfolded tau proteins as one of the causes of Alzheimer’s disease.
Normally, healthy tau proteins (called trans P-tau) work inside nerve cells to form the scaffolding that gives the cells their shape and allows them to function properly.
Brain Injures
However, when the protein folding process goes awry, the brain can instead form misshapen tau proteins (called cis P-tau).
These proteins malfunction and damage the energy generators inside nerve cells, eventually leading to toxicity and cell death.
Using a brain imaging technique called immunofluorescence, the researchers examined the brains of people with chronic injury-related brain damage. They found that, compared to healthy people, these people had much higher levels of cis P-tau.
The misfolded tau proteins were particularly concentrated in the axons of the nerve cells — the long stalks that nerves project to link up with other cells and form connections.
Mice as Models
To find the causal connection, the researchers turned to mouse models.
Mice that received a single, minor brain injury showed elevated levels of cis P-tau, but these levels dropped back to normal within two weeks.
Mice that received a single, major brain injury (simulating what a soldier surviving an explosion might experience) or a series of minor brain injuries (simulating what an athlete might experience) showed elevated cis P-tau levels that remained for at least six months.
In the severe or chronic brain injury groups, cis P-tau also spread throughout the brain, jumping from one cell to the next and leaving a swathe of cell death in its path. These proteins can spread to the hippocampus and the cortex, which are responsible for memory formation and executive control of emotions and behavior.
“Cis P-tau has the ability to kill one neuron after another, eventually leading to widespread neurofibrillary tangles and brain atrophy, which are the hallmark lesions of both Alzheimer’s disease and [chronic brain injury],” explained Kun Ping Lu, M.D., Ph.D., professor of medicine at Harvard Medical School and chief of the Division of Translational Therapeutics at Beth Israel Deaconess Medical Center, as well as senior co-author on the paper, in an interview with Healthline.
Physical brain injury wasn’t the only thing that could cause cis P-tau to form, either.
The researchers also subjected cultured nerve cells to stress. In particular, starving them of oxygen or brain growth factors, as might happen if blood flow is reduced in the brain after an injury.
The researchers homed in on an enzyme called Pin1, which converts toxic cis P-tau into beneficial trans P-tau. Oxygen starvation deactived Pin1, while lack of growth factor prevented the brain from building new Pin1.
Together, this model of reduced blood flow showed how brain injury and other forms of stress can lead to increased levels of cis P-tau and its toxic effects."
Article at:
http://www.healthline.com/health-news/new-antibody-may-treat-brain-injury-and-prevent-alzheimers-disease-071515#2
PENN SCIENTISTS MAKE BREAKTHROUGH IN ALZHEIMER'S DISEASE RESEARCH in ABC Action News, Monica Malpass, July 16, 2015
Excerpts:
"Now after years of analysis, and trial and error, they've had a breakthrough.
They discovered that Tau proteins get misfolded and cause tangled information to spread from cell to cell. Knowing that means it may be possible to stop the cell to cell spread.
"We target Tau, we target Sia Nuclein, we figure out a way to unfold it with a small molecule, drugs or a way to snag it with antibodies and throw it in the trashcan," said Dr. Trojanowski, Director of Penn Institute on Aging.
If they succeed with their theories on mice, it may one day lead to a human application.
That's exciting to this team because even if they just block the cell to cell spread for five years,that would effectively be a cure for Alzheimer's."
REMEMBER the RCPI paper on Tau protein in Brain Disorders & Therapy?
Anatabine Attenuates Tau Phosphorylation and Oligomerization in P301S Tau Transgenic Mice
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, Gloucester, Massachusetts, USA
3The Longtine Center for Neurodegenerative Biochemistry, Banner Sun Health Research Institute, Sun City, Arizona, USA
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."[/b]
Paper at:
http://www.omicsgroup.org/journals/anatabine-attenuates-tau-phosphorylation-and-oligomerization-in-ps-tau-transgenic-mice-2168-975X.1000126.php?aid=26406
Change Your Brain, Change Your Life on YouTube, TEDxOrangeCoast, Daniel Amen, Oct 16, 2013
Interesting and informative 14 minute video on TBI and dementia using SPECT brain scans in their treatment.
Video at:
Nicotinic Acetylcholine Receptors and Your Brain at YouTube, Meg Rosenburg, Jun 16, 2014
Short 4 minute video explaining Nicotinic Acetylcholine Receptors. Excellent, easy to understand video for non-biological science types like me. Now, what Dr Mullan has been talking about becomes clearer. Well worth the watch.
Video at:
Is there a connection? ACETYCHOLINE??? In Dr Meschino's video, he says that as we age, dementia patients show a decline in Acetycholine in the brain. Current AD drugs "increase effectiveness of acetylcholine in the brain. If there is less acetycholine, is improving effectiveness enough? Does Anatabine increase the total actions of acetycholine in the brain? Is brain inflammation caused by reduced acetycholine levels the cause of AD? Maybe, maybe not? Dr Mullan probably has an idea. Maybe that's why he mentioned a combination of drugs for AD? What say you who are more knowledgeable than I on the subject???
From the Memory Loss website: http://www.memorylossonline.com/glossary/acetylcholine.html
"Acetylcholine (ACh)
Acetylcholine is a neurotransmitter, one of the chemicals that neurons use to communicate with each other."
"In the brain, acetylcholine is produced in several locations including the basal forebrain. It may promote learning. Acetylcholine-producing cells in the basal forebrain are damaged in the early stages of Alzheimer's disease, which may contribute to the memory impairments which are an early symptom of the disease. The drugs tacrine (brand name Cognex) and donepezil (trade name Aricept), currently marketed as Alzheimer's drugs, are cholinesterase inhibitors, meaning that they increase the effectiveness of acetylcholine in the brain."
From the RCPI website: http://www.rockcreekpharmaceuticals.com/pharmaceutical/research_areas
"Mechanism of Action
Our compounds are cholinergic receptor ligands that mimic the activity of the endogenous neurotransmitter acetylcholine. For instance, studies suggest that binding and activation of alpha-7 cholinergic receptors leads to an indirect inhibition of the intracellular transcription factors such as NF-kB. This subsequently reduces the expression of inflammatory cytokines, potentially leading to a reduction of inflammation relevant to chronic inflammatory conditions."
Vitamins for Your Brain at YouTube, Dr.James Meschino, Feb 3, 2012
10 minute video explaining connection of vitamins to brain health
Preventing Brain Loss with B Vitamins? video at Nutritionfacts.org, Dr. Greger'
Interesting 7 minute video on the relationship between vitamins B6-B12 to brain shrinkage and dementia.
Picturing the Body’s Immune Response in 'Memorial Sloan Kettering Cancer Center, Julie Grisham, MS, July 15, 2015
Excerpts:
"The immune system plays an important role in keeping us healthy. But an overactive immune response can lead to excess inflammation, characterized by an increase in fluids, immune cells, and other substances in the affected area. Inflammation is part of the body’s natural response to infection or wounds, but chronic inflammation can lead to a number of health diseases, including cancer."
"If a person has a chronic influx of white blood cells into certain tissues — like the gut, for example — this lasting inflammatory reaction can promote the development of tumors. In part this is because the toxic chemicals that are released by our white blood cells not only kill pathogens as they are supposed to but also unfortunately damage and mutate our own cells, which may enable tumors to form.
Persistent inflammation can promote the development of tumors.
In fact, we know that inflammatory conditions of the gastrointestinal tract such as Crohn’s disease and colitis increase the incidence of cancers in those organs. Acid reflux disease is another example: When stomach acid persistently injures the epithelial lining of the esophagus, white blood cells are constantly recruited to the site of damage to release toxic antimicrobial chemicals. If this goes on unchecked for a long time, esophageal cancer can result."
Article at:
https://www.mskcc.org/blog/picturing-body-s-immune-response
Stevia For Diabetes, Inflammation And Even Cancer in 'Natural Medicine Box', July 4, 2015
Excerpts:
"Stevia is a 100% natural sweetener extracted from the leaf of the Stevia plant where other sweeteners are chemically produced. Stevia rebaudiana is a South American shrub"
"The secret of its sweetness lies in the fact that the plant accumulates and contains a compound substance – stevioside. This substance is made of glucose, sucrose, steviol and other compounds. At the present time, stevioside is the sweetest natural product. In its pure form stevioside is 300 times sweeter than sugar. Until recently, the FDA has prohibited the sweetener from use in foods in the United States or Europe in order to promote the sales of aspartame, a artificial chemical sweetener, which has never been shown to be safe for human consumption. "
"Stevia was found to contain different antioxidants including apigenin, kaempferol and quercitrin. Researchers have discovered stevia extracts’ ability to protect DNA strands against damage by hydroxide radicals. Additionally, Webmd.com suggests that stevia could lower high blood pressure by using between 750-1500 mg of stevioside each day.
Also Stevia contains no calories and will not raise blood sugars. In fact, the research has showed that stevia is an insulin sensitizer that can aid in glucose tolerance and clearance after a meal. Stevia has been used by the Japanese for years in the treatment of type 2 diabeties. One of the most recent studies which was performed on fructose-fed rats, has showed that a single instance of oral stevioside increased insulin sensitivity and reduced postprandial blood glucose in a dose-dependent manner."
Article at:
http://www.naturalmedicinebox.net/stevia-for-diabetes-inflammation-and-even-cancer/
The inflammation epidemic: your number one health concern 2015 (and what sugar’s got to do with it) in 'High Fifty Health', Christine Morgan, 15 January 2015
Excerpts:
"Inflammation is an essential part of a healthy immune system that helps your body heal after an injury or infection. But when it becomes chronic – that is, when your immune system produces immune cells constantly – it can cause a wide range of health problems.
Such is its effect on health that some US experts describe chronic inflammation as an epidemic. Dr Sohere Roked, a London GP with a specialist interest in integrative medicine, says chronic inflammation is common in the UK too but the problem is, most people aren’t aware of it.
“Chronic inflammation can be common at any age, but the body can be less resilient when you’re in your 50s,” she says.
“Diseases that are obviously inflammatory in nature include asthma, Crohn’s disease, rheumatoid arthritis, tendonitis, bursitis, laryngitis, gingivitis, gastritis, otitis, coeliac disease, diverticulitis and inflammatory bowel disease,” says Dr Carolyn Dean.
Also linked with chronic inflammation are heart disease, cancer, diabetes, stroke, Alzheimer’s disease, osteoporosis and depression. So is premature ageing and some of the visible signs of getting older, including not-so-youthful skin."
"Many nutrition experts agree that where inflammation is concerned, the number one food enemy is sugar.
“Processed sugar is a major source of inflammation in the diet, and it is wreaking havoc,” says Renae Norton, a specialist in the treatment of eating disorders and obesity. “When you eat sugar, you deplete the enzymes that help you to digest protein. So the protein gets into the bloodstream as a partially digested protein, and is attacked by the immune system.”"
Article at:
http://www.high50.com/health/the-inflammation-epidemic-your-number-one-health-concern-2015
The Diabetes Epidemic and How Gut Inflammation is Playing a Key Role in 'Nuritas', Meaghan Lee-Erlandsen and Dr. Nora Khaldi, June 19, 2015
Excerpts:
"One may expect that diabetes goes hand in hand with inflammation as many diabetics suffer from gut inflammation. However, what is unexpected regarding this relationship between diabetes and inflammation is that inflammation may actually be a possible cause or play a major role in the development of diabetes."
"Obesity and insulin resistance are major global health concerns. When people become obese, their body’s tissues fail to respond well to insulin, a process called insulin resistance, which can lead to high blood sugar triggering type 2 diabetes, though the underlying causes are not well known. Our recent work has shown that the gut immune system is an important new player in controlling this process. Mice fed a high fat, high calorie diet were found to have an increase in the pro-inflammatory immune cells in the gut. Similar results were seen in a small cohort of 14 humans, half who were obese. This change in gut resident immune cells in mice was associated with worsened leakiness of bacterial products from the bowel into the blood, as well as abnormal immunity to food proteins, and exacerbated effects on inflammation in nearby fat tissue. These changes contribute to insulin resistance, which impacts blood sugar. Most excitingly, this cascade could be targeted and reversed with existing drugs like 5-aminosalicylic acid (5-ASA), which dampen down inflammatory changes in the gut. Such gut specific anti-inflammatory agents could represent a new class of potentially minimal side effect anti-diabetes medications that locally targets the immune system that lives in the gut"
Article at:
http://www.nuritas.com/the-diabetes-epidemic-and-how-gut-inflammation-is-playing-a-key-role/
Celgene to buy Receptos for $7.2 billion in 'Reuters News', Tue Jul 14, 2015 5:42pm
News Excerpts:
"Celgene Corp said on Tuesday it would buy Receptos Inc for $7.2 billion in a move that will give the U.S. biotechnology company a potential blockbuster drug in late stage development for inflammatory bowel disease and multiple sclerosis.
Celgene said it would pay $232 per share in cash for the smaller biotech. Receptos shares closed at $207.18 on Nasdaq on Tuesday."
"Receptos in April reported positive data in ulcerative colitis from a midstage trial of its experimental oral drug ozanimod, the medicine at the heart of the Celgene deal.
Phase III ozanimod trials are underway for both ulcerative colitis and relapsing MS. The drug could be approved for MS in 2018, Celgene said. Phase III colitis data are expected in 2018.
Celgene forecast peak annual ozanimod sales of $4 billion to $6 billion."
Article at:
http://www.reuters.com/article/2015/07/14/us-receptos-m-a-celgene-idUSKCN0PO2OB20150714
Body's response to injury and inflammation may hinder wound healing in diabetes in 'Eureka Alert', BOSTON CHILDREN'S HOSPITAL, 15-JUN-2015
Excerpts:
"One of the body's own tools for preventing wound infections may actually interfere with wound healing, according to new research from Boston Children's Hospital. In a study published online in Nature Medicine, scientists from the hospital's Program in Cellular and Molecular Medicine (PCMM) found they could speed up wound healing in diabetic mice by keeping immune cells called neutrophils from producing bacteria-trapping neutrophil extracellular traps (NETs).'
"When the skin is cut or broken, the body mobilizes a complicated array of cells and proteins to stop bleeding, prevent infection by triggering inflammation and start the healing process. As part of the inflammatory response, neutrophils, which ingest and destroy bacteria, expel their own chromatin (a mix of DNA and associated proteins) in the form of NETs within the wound.
While possibly beneficial as a tool for keeping bacteria out of the body, NETs also have a dark side. 'NETs predispose patients to inflammation, heart disease and deep vein thrombosis [dangerous blood clots that form within veins deep inside the body], all of which are elevated in patients with diabetes,' says Wagner, who is also the Edwin Cohn Professor of Pediatrics at Harvard Medical School."
Article at:
http://www.eurekalert.org/pub_releases/2015-06/bch-brt060915.php
Molecular Link between Obesity and Type 2 Diabetes Reveals Potential Therapy in 'UC San Diego Health', Heather Buschman, PhD, February 23, 2015
Excerpts:
"Oesity causes inflammation, which can in turn lead to type 2 diabetes. What isn’t well established is how inflammation causes diabetes — or what we can do to stop it. Researchers at University of California, San Diego School of Medicine have discovered that the inflammatory molecule LTB4 promotes insulin resistance, a first step in developing type 2 diabetes. What’s more, the team found that genetically removing the cell receptor that responds to LTB4, or blocking it with a drug, improves insulin sensitivity in obese mice. The study is published Feb. 23 by Nature Medicine."
"Here’s what’s happening in obesity, according to Olefsky’s study. Extra fat, particularly in the liver, activates resident macrophages, the immune cells living there. These macrophages then do what they’re supposed to do when activated — release LTB4 and other immune signaling molecules to call up an influx of new macrophages. Then, in a positive feedback loop, the newly arriving macrophages also get activated and release even more LTB4 in the liver.
This inflammatory response would be a good thing if the body was fighting off an infection. But when inflammation is chronic, as is the case in obesity, all of this extra LTB4 starts activating other cells, too. Like macrophages, nearby liver, fat and muscle cells also have LTB4 receptors on their cell surfaces and are activated when LTB4 binds them. Now, in obesity, those cells become inflamed as well, rendering them resistant to insulin."
Article at:
http://health.ucsd.edu/news/releases/Pages/2015-02-23-type-2-diabetes-and-obesity-molecular-link.aspx
Link between inflammation and type 2 diabetes identified in 'Science Daily', February 5, 2015, Yale University
Excerpts:
"Scientists have identified the molecular mechanism by which insulin normally inhibits production of glucose by the liver and why this process stops working in patients with type 2 diabetes, leading to hyperglycemia"
"Yale researchers hypothesized that insulin suppressed glucose production by the liver by inhibiting the breakdown of fat, which would result in a reduction in hepatic acetyl CoA, a key molecule that they showed was critical in regulating the conversion of amino acids and lactate to glucose. They also found that reversal of this process, due to inflammation in adipose (fatty) tissue, led to increased hepatic glucose production and hyperglycemia in high-fat-fed rodents and obese, insulin-resistant adolescents. "These studies identify hepatic acetyl CoA as a key mediator of insulin action on the liver and link it to inflammation-induced hepatic insulin resistance and type 2 diabetes," Shulman explained.
This new insight into insulin resistance paves the way for exploring new treatments. "None of the drugs we currently use to treat type 2 diabetes target the root cause," said Shulman. "By understanding the molecular basis for hepatic insulin resistance we now can design better and more effective drugs for its treatment.""
Article at:
http://www.sciencedaily.com/releases/2015/02/150205123018.htm
Diabetes and Inflammation in'WebMD'
Excerpts:
"Researchers discovered that in people with type 2 diabetes, cytokine levels are elevated inside fat tissue. Their conclusion: Excess body fat, especially in the abdomen, causes continuous (chronic), low levels of abnormal inflammation that alters insulin's action and contributes to the disease.
As type 2 diabetes starts to develop, the body becomes less sensitive to insulin and the resulting insulin resistance also leads to inflammation. A vicious cycle can result, with more inflammation causing more insulin resistance and vice versa. Blood sugar levels creep higher and higher, eventually resulting in type 2 diabetes."
Article at:
http://www.webmd.com/diabetes/guide/inflammation-and-diabetes
Scientists catch brain damage in the act in the 'University of British Columbia News', March 13, 2014
Excerpts:
"Scientists have uncovered how inflammation and lack of oxygen conspire to cause brain damage in conditions such as stroke and Alzheimer’s disease.
Microglia are part of a newly discovered mechanism that contributes to Alzheimer's disease.
The discovery, published today in Neuron, brings researchers a step closer to finding potential targets to treat neurodegenerative disorders.
Chronic inflammation and hypoxia, or oxygen deficiency, are hallmarks of several brain diseases, but little was known about how they contribute to symptoms such as memory loss.
The new study shows that the combination of inflammation and hypoxia activates microglia in a way that persistently weakens the connection between neurons. The phenomenon, known as long-term depression, has been shown to contribute to cognitive impairment in Alzheimer’s disease."
Article at:
http://news.ubc.ca/2014/03/13/macvicar/
Study: Type 2 Diabetes Reduces Brain Function Within Just Two Years in 'Forbes Health', David DeSalvo, 7/13/2015
Excerpts:
"A new study published in the journal Neurology shows that Type 2 diabetes triggers a significant reduction in cognitive ability within just a two-year period. The main culprits appear to be increased tissue inflammation and decreased blood flow to the brain."
Article at:
http://www.forbes.com/sites/daviddisalvo/2015/07/13/study-type-2-diabetes-reduces-brain-function-within-just-two-years/
Hyperglycemia modulates extracellular amyloid-ß concentrations and neuronal activity in vivo in 'the Journal of Clinical Investigation', Shannon L. Macauley1, Molly Stanley1, Emily E. Caesar1, Steven A. Yamada1, Marcus E. Raichle1,2, Ronaldo Perez1, Thomas E. Mahan1, Courtney L. Sutphen1, and David M. Holtzman1, May 4, 2015
Excerpts:
"Epidemiological studies show that patients with type 2 diabetes (T2DM) and individuals with a diabetes-independent elevation in blood glucose have an increased risk for developing dementia, specifically dementia due to Alzheimer’s disease (AD)"
Article at:
http://www.jci.org/articles/view/79742
Scientists find key to ageing process in hypothalamus | Science (guardian.co.uk) in Reddit, egocentrism04
Excerpts:
"Neuroscientist here! This is both interesting and unsurprising (which is good! We don't need to overturn a bunch of science!). NF-?B is a known immune system modulator - we know it's relevant in a whole host of diseases because most diseases trigger an inflammatory response, and NF-?B is how they do it. NF-?B is also important for cell survival! Blocking NF-?B activation (like they do in this paper) has been show to help in a bunch of different diseases, including Alzheimer's disease and various cancers. So it's unsurprising that NF-?B is involved. The surprising thing is that just blocking activity in the hypothalamus is enough to see large differences in lifespan, though I'll have to take a closer look at this paper. We neuroscientists tend to focus on the cortex, which is just the outer layer of the brain - there's a lot about the inner layers that we don't know about, because we just haven't had time to get there yet!"
"Good question! To be honest, it's not known why NF-?B is important for aging, but we have a few guesses. The most popular hypothesis is that NF-?B triggers inflammation, and inflammation is what actually causes a lot of what we associate with aging! As you age, you generate more and more reactive oxygen species (ROS) - basically, damage-causing particles that are generated from normal metabolism. These ROS cause damage, which activates your immune system through NF-?B (because most damage triggers inflammation). The problem is that your immune system is built to destroy things that are hurting you - so if your body is damaging itself, inflammation just causes more damage! Blocking NF-?B doesn't change the fact that you're accumulating more and more ROS, but it at least prevents the additional damage that inflammation causes.
Telomere shortening is a real phenomena, but it doesn't play much of a role in normal aging - it just means that, unless we figure out a way around it, there is an absolute limit on our cellular lifespans! Most people die before their telomeres are depleted."
"You have several questions, so let me answer them point by point.
It's definitely possible that cells with high levels of ROS will have increased levels of mutations! That by itself doesn't really mean anything, though, because any cells that turn cancerous would still be destroyed by the immune system through non-NF-?B modulated pathways.
The cells would be unlikely to die from asphyxiation. ROS can cause mitochondrial failure, but to consistently cause mitochondrial failure you'd have to have incredibly high levels! It's more of a "higher levels of ROS lead to higher probabilities of cell death" - it's not a threshold effect.
So there are two assumptions in your NF-?B inhibition question - that killing cells with high ROS levels is better than leaving them alive, and that NF-?B-mediated inflammation causes less damage than letting ROS build up. Killing cells is really a measure of last resort - cells with high ROS levels are still functional, even at low levels, and by keeping them, you reduce stress on other cells! Additionally, NF-?B-mediated inflammation has been shown to cause several diseases to progress more quickly - the mechanisms are unknown as to how inflammation damages cells, but it's true that blocking NF-?B-induced inflammation is usually helpful in disease conditions. Remember, ROS is building up at the same rate in normal mice as well! I guess you could argue that these older mice are less healthy than normal mice right before they die, but the older mice are alive, so I would argue that being alive is healthier!"
"There's actually quite a lot of controversy on what Alzheimer's disease is caused by! From my experience, I would say that people would agree that NMDAR inhibition by A-beta oligomers is involved, but the estimates on how much of disease pathology is caused by that range from 5%-100%, which I would not call consensus! My institution is pushing the neuroinflammatory response as a cause - the idea that A-beta triggers inflammation, and then the chronic inflammatory response is actually what drives neurodegeneration. However, this idea itself is controversial as well! Furthermore, given the number of posters at conferences, I would guess that around 20%-30% of the field believes that A-beta isn't even involved in causation - it's just some sort of response to the actual pathological mechanism. Again, correlation is not causation!"
Comments at:
http://www.reddit.com/r/science/comments/1dhz93/scientists_find_key_to_ageing_process_in/
Biogen Plunges After Cowen Says Alzheimer’s Drug Data Pose Risk
in Bloomberg Business, by Doni Bloomfield, July 10, 2015
Excerpts:
"Biogen Inc. dropped the most since April after Cowen & Co. said the biotechnology company’s stock price faces risk from data coming later this month on a drug to treat Alzheimer’s disease."
"Also Friday, Biogen’s head of research and development, Douglas Williams, said he would leave the company at the end of the month to become chief executive officer of an undisclosed biotech company. Chief Medical Officer Alfred Sandrock and Chief Scientific Officer Spyros Artavanis-Tsakonas will take over Williams’s responsibilities, the company said in a statement."
Article at:
http://www.bloomberg.com/news/articles/2015-07-10/biogen-plunges-after-cowen-says-alzheimer-s-drug-data-poses-risk
Chronic Ills May Add Up to a Shortened Life Span
Study finds combination of diabetes, heart disease and stroke can cut up to 15 years of life expectancy in 'Medline Plus', July 7, 2015
Excerpts:
"Smokers and people with HIV have been found to lose about 10 to 11 years of life expectancy, the study authors said. By comparison, having two cardiometabolic risk conditions at age 60 was linked to a 12-year drop in life expectancy, while having three conditions was linked to a 15-year drop, the researchers said. And those numbers could go even higher among patients whose diseases first strike before the age of 40, they added."
Article at:
http://www.nlm.nih.gov/medlineplus/news/fullstory_153457.html
Diabetes Takes a Toll on the Brain in'New York Times, Well.blog', NICHOLAS BAKALAR JULY 8, 2015
Excerpts:
"The study, published in Neurology, included 40 people whose average age was 66, half of whom had been in long-term treatment for Type 2 diabetes. All were tested at the start of the study and then two years later with M.R.I. scans, various blood tests and several tests of cognitive ability.
At the end of two years, people with diabetes had greater declines in gray matter volume, composite scores on mental tests, and in rates of blood flow to the brain than those in the control group. They also had greater increases in blood measures of inflammation. Among the group with diabetes, those with more severe declines in cerebral blood flow had correspondingly greater declines on tests of mental skills.
“There is currently no treatment for cognitive decline in diabetes,” said the lead author, Dr. Vera Novak, an associate professor of neurology at Harvard. “Even tighter glycemic control did not improve things. We are doing a new trial to assess whether injecting insulin into the brain through the nose could improve cognitive function or slow down cognitive decline.”
Article at:
http://well.blogs.nytimes.com/2015/07/08/diabetes-takes-a-toll-on-the-brain/?ref=health
Latest Presentation update June 10, 2015, see at:
http://investors.rockcreekpharmaceuticals.com/presentations-and-webinars#past:2015:7
FDA Strengthens Warning of Increased Chance of Heart Attack or Stroke Non-aspirin-Nonsteroidal Anti-inflammatory Drugs (NSAIDs),
in 'Drugs.com', July 9, 2015
Excerpts:
"Prescription NSAID labels will be revised to reflect the following information:
The risk of heart attack or stroke can occur as early as the first weeks of using an NSAID. The risk may increase with longer use of the NSAID.
The risk appears greater at higher doses.
It was previously thought that all NSAIDs may have a similar risk. Newer information makes it less clear that the risk for heart attack or stroke is similar for all NSAIDs; however, this newer information is not sufficient for us to determine that the risk of any particular NSAID is definitely higher or lower than that of any other particular NSAID.
NSAIDs can increase the risk of heart attack or stroke in patients with or without heart disease or risk factors for heart disease. A large number of studies support this finding, with varying estimates of how much the risk is increased, depending on the drugs and the doses studied.
In general, patients with heart disease or risk factors for it have a greater likelihood of heart attack or stroke following NSAID use than patients without these risk factors because they have a higher risk at baseline.
Patients treated with NSAIDs following a first heart attack were more likely to die in the first year after the heart attack compared to patients who were not treated with NSAIDs after their first heart attack.
There is an increased risk of heart failure with NSAID use."
Article at:
http://www.drugs.com/fda/non-aspirin-nonsteroidal-anti-inflammatory-nsaids-safety-communication-fda-strengthens-warning-13732.html?utm_source=ddc&utm_medium=email&utm_campaign=Today%27s+news+summary+-+July+9%2C+2015&utm_content=Non-aspirin+Nonsteroidal+Anti-inflammatory+Drugs+%28NSAIDs%29%3A+Drug+Safety+Communication+-+FDA+Strengthens+Warning+of+Increased+Chance+of+Heart+Attack+or+Stroke
Could anti-inflammatory agents be the Alzheimer's connection? (my comments)
High blood pressure linked to reduced Alzheimer's risk, meds may be reason in 'World Pharma News', 26 JUNE 2015
Excerpts:
"A new study suggests that people with a genetic predisposition to high blood pressure have a lower risk for Alzheimer's disease. However, authors conclude the connection may have more to do with anti-hypertension medication than high blood pressure itself."
Article at:
http://www.worldpharmanews.com/research/3123-high-blood-pressure-linked-to-reduced-alzheimers-risk-meds-may-be-reason
Anti inflammatory effects of statin in COPD in 'Science Direct'
Excerpts:
"Statins are now becoming recognized as powerful antiinflammatory agents that exert beneficial effects beyond low-density lipoprotein cholesterol reduction"
Article at:
http://www.sciencedirect.com/science/article/pii/S0422763813000083
Making vitamins and supplements---Contract Pharmaceuticals is one of many companies that manufacture vitamins and supplements for various retailers and distributors. Contract is probably one of the biggest, if not the biggest in the industry. Take a look at their list of clients and products. I wonder if RCPI had Anatabloc made here?
http://cpc.com/
Catabasis Pharmaceuticals Receives FDA Fast Track Designation for CAT-1004 for the Treatment of Duchenne Muscular Dystrophy in 'Business Wire', July 06, 2015 08:00 AM Eastern Daylight Time
CAMBRIDGE, Mass.--(BUSINESS WIRE)--Catabasis Pharmaceuticals, Inc. (NASDAQ: CATB), a clinical-stage drug development company built on a pathway pharmacology technology platform, today announced that CAT-1004 has received Fast Track designation from the U.S. Food and Drug Administration (FDA) for the treatment of Duchenne muscular dystrophy (DMD). CAT-1004 is designed to inhibit activated NF-kB, which has the potential to reduce muscle inflammation and degeneration, and promote muscle regeneration for patients with DMD regardless of the underlying mutation. DMD is a rare disease that involves progressive muscle degeneration that eventually leads to death and for which there are no approved therapies in the United States.
Article at:
http://www.businesswire.com/news/home/20150706005248/en/Catabasis-Pharmaceuticals-Receives-FDA-Fast-Track-Designation#.VZsHWhtVhHw
What you are describing is the PRE-market trading price and volume. The AFTER-hours trades were only 401 shares up .08 to 1.73, with only 1 share hitting that high. 400 shares traded at 1.69. Check at Nasdaq RCPI pre/after market quites at:
http://www.nasdaq.com/symbol/rcpi/premarket
http://www.nasdaq.com/symbol/rcpi/after-hours
Let's hope it continues to rise with more news coming.
Evotec AG (EVTG.F), Roche (RHHBY)'s Alzheimer's Hopeful Fails Another Trial, uly 1, 2015, Mark Terry, BioSpace.com Breaking News Staff
Excerpts:
"Swiss-based Roche (RHHBY) and Hamburg, Germany-based Evotec AG announced yesterday that its Phase IIb clinical trial of Sembragiline in Alzheimer’s patients failed to meet its primary endpoint.
Sembragiline was licensed from Roche to Evotec in 2006 for a different indication. In 2011 the two companies inked an exclusive global agreement to develop and commercialize the monoamine oxidase type B (MAO-B) inhibitor for Alzheimer’s disease. Evotec received an upfront fee of $10 million with potential milestones up to $820 million and double-digit royalties on sales, which now seems very unlikely. "
"On Dec. 19, 2014, Roche announced it was discontinuing Scarlet RoAD, a Phase III study of gantenerumab on pre-dementia Alzheimer’s disease patients.
In July 2014, Roche announced that its drug crenezumab failed to meet its co-primary endpoints in Alzheimer’s patients. Those findings were not completely disappointing, because they did indicate a trend in cognition for individuals with mild disease who received a high dose of the drug intravenously.
On April 21, 2015, Massachusetts-based Biogen (BIIB) reported positive results from a Phase Ib clinical trial for aducanumab, which showed a significant reduction in amyloid plaque in patient’s with Alzheimer’s disease. Amyloid plaque is one of the substances found in the brains of AD patients that are linked to the disease. "
Article at:
http://www.biospace.com/News/evotec-ag-roches-alzheimers-hopeful-fails-another/383223
Flashback: FDA abused power of federal government to smear whistleblowers and protect corporations in 'NaturalNews.com, May 01, 2015, Ethan A. Huff, staff writer
Article:
"(NaturalNews) To be an honest person and also hold a high position within the government is a paradox, especially at the federal level. And if its the U.S. Food and Drug Administration (FDA) you're working for from a position of integrity, don't plan on keeping your job for long, as the agency has an extensive history of targeting whistleblowers who object to its institutionalized crime racket.
You either go along to get along or you get axed, as many an FDA scientist has learned the hard way over the years. One of the most recent cases of this was a group of FDA scientists who became targets of illegal agency spying, which ultimately led to their dismissal. What was their "crime"? Learning the truth about dangerous, FDA-approved medical devices and talking about it.
According to a 2012 report in The New York Times (NYT), the FDA tapped both the work and personal email accounts of at least five of its scientists after the agency employees expressed concerns about the safety and design of certain FDA-approved medical devices. In retaliation, the FDA installed spy software on their computers to intercept all emails, documents and even key strokes.
The NYT admitted at the time that the "extraordinary surveillance effort" was a type of revenge by the higher-ups at the FDA against the agency's lower-level scientists, who warned that FDA-approved medical imaging devices for mammograms and colonoscopies "exposed patients to dangerous levels of radiation."
A special review by the Office of Special Counsel, which deals specifically with concerns expressed by government workers, confirmed that these warnings were accurate, which should have prompted a full investigation into what the scientists had deemed "a substantial and specific danger to public safety." Instead, the FDA targeted the scientists simply for doing their jobs with honest intent.
Top FDA senior scientist admits agency is built on corruption, robbing human life for profit
Sadly, U.S. District Court Judge Reggie B. Walton also proved to be in on the fix when he dismissed a lawsuit filed by the FDA scientists against the agency for illegally monitoring their online activity.
Legally speaking, government agencies are prohibited from intimidating, threatening or otherwise targeting whistleblowers. And yet the FDA appears to have gotten away with targeting its own scientists, thanks to a corrupt legal system that clearly sides with corporations and government bureaucracy rather than the people.
The Pentagon has also been caught targeting whistleblowers, including journalists and other "dissenters" who attempt to expose the Department of Defense and other government departments for corruption and treason. This was one of the big issues surrounding the Cyber Intelligence Sharing and Protection Act, or CISPA, which threatens to greatly increase surveillance and spying activity by the government against citizens.
During an exclusive interview with Life Extension Magazine, Dr. David Graham, a senior drug safety researcher at the FDA, revealed how the FDA has essentially turned the human body into "a profit-generating machine," largely through deceit and coercion. Those at the agency who approve pharmaceutical drugs, he admitted, are the same people who oversee the post-marketing regulation of them, which means they are incentivized to hide any dangers associated with FDA-approved drugs from the public.
"The people who approve a drug when they see that there is a safety problem with it are very reluctant to do anything about it because it will reflect badly on them," stated Dr. Graham. "As currently configured, the FDA is not able to adequately protect the American public. It's more interested in protecting the interests of industry.""
Article at:
http://www.naturalnews.com/049557_FDA_whistleblowers_pharmaceutical_corporations.html#ixzz3YsvJb15N
How the FDA Went Bad: Health Serfdom and the Rise of Tyranny in 'Healthkeepers Magazine, Jonathan W. Emord
My comments: Worth reading entire article
Excerpts:
"...the FDA’s costliest failings
have nothing to do with the agency’s
budget and everything to do with
the efforts of political appointees
at the agency to pave the way
for lucrative post-government
employment by doing the bidding
of the agency’s most powerful
regulatees, the world’s largest drug
companies. For those agency
heads and political managers who
play their cards right and keep the
pressure on for approval of drugs,
even unsafe drugs, prospects for
obtaining high paying jobs in a drug
company or drug company lobbying
firm are very good indeed. "
"As FDA medical reviewers have
repeatedly stated in congressional
testimony, FDA views the drug
industry as its “client” and does its
client’s bidding when it approves
unsafe drugs. Many of those
reviewers have said that they and
their colleagues have been silenced
by FDA management, have been
coerced into altering their reports
to remove findings of harm, have
been kept from testifying of harms
before drug review panels, have
had their reports suppressed
to prevent them from reaching
drug review panels, or have been
ostracized and reassigned, replaced
with those who will conform to the
political managers’ desires. The
FDA Commissioner has operated
an Office of Internal Affairs that has
repeatedly forced agency scientists
who identify risks of drugs to be
the subject of investigations and
threats of prosecution. Some have
also been the victims of character
assassination in the academic
publishing community and on
Capitol Hill. "
Article at:
http://www.emord.com/how-the-fda-went-bad.pdf
News from the Broad Institute:
Study demonstrates central role for NFkB in driving pathophysiology of MS
June 15th, 2015
A central regulator of inflammation, nuclear factor kappa B (NFkB), has been implicated as a driver of the autoimmune disease multiple sclerosis (MS). A team led by David Hafler, of the Broad Institute and Yale School of Medicine, demonstrated that MS-associated variants alter NFkB signaling pathways, leading to increased activation of NFkB and making cells more responsive to inflammatory stimuli. The work, featured in Science Translational Medicine, suggests that rapid genetic screening for variants associated with NF?B signaling may identify individuals amenable to therapeutics targeting this pathway.
Article at:
https://www.broadinstitute.org/news?page=1#