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Evidence Strengthening that Common Benzodiazepine Sedatives May Cause Dementia in 'Mad In America, June 11, 2015
Excerpts:
"Researchers from Chongqing Medical University in China analyzed six studies (involving 11,891 dementia cases and 45,391 participants) that provided risk estimates on the association of benzodiazepine use with dementia. They found that long-term benzodiazepine use was associated with about a 50% increase in risk of developing dementia. "The risk of dementia increased by 22% for every additional 20 defined daily dose per year," they added.
The authors noted that early symptoms of dementia such as sleep disturbance, anxiety and depression can often begin ten years before people receive a diagnosis of dementia. For this reason, they stated, some researchers do not believe that benzodiazepines are causing dementia, but instead believe that people's symptoms of dementia are motivating physicians to prescribe benzodiazepines.
The authors of the meta-analysis then put forth data and arguments to refute that perspective. Adjusting for the presence of symptoms of anxiety and depression did not change their findings, they noted. And comparing people who'd stopped taking benzodiazepines with people who were currently taking them also did not change their findings. Rates of developing dementia were about 50% higher for all of these different groups of past or present long-term users, the authors wrote, and the dose-response relationship they'd found persisted across all of the groups.
Such findings, they wrote, support arguments that there is "a causal relationship between benzodiazepine use and dementia.""
Reference data from benzo.org.uk:
"Worldwide sales of benzodiazepines (tranquillizers and sleeping pills) are estimated at in excess of $21 billion."
"Approximately 10% - 15% of the population use tranquillizers and sleeping pills with up to 30% of people over the age of 60 years using these drugs (often over many years having been prescribed them at a much earlier age) and who have become "accidental addicts""
Article at:
https://www.madinamerica.com/2015/06/evidence-strengthening-that-common-benzodiazepine-sedatives-may-cause-dementia/
6 inflammation-causing foods no one talks about in 'Well + Good', —Amanda Benchley
My comments: And there may be more.
Excerpts:
"There's a five-alarm fire sounding these days about inflammation, and with good reason. Heart disease, cancer, Alzheimer's, and acne are just some of the possible consequences of too much inflammation in the body.
According to Nicholas Perricone, M.D., the pioneering nutritionist and dermatologist (who wrote the book on anti-inflammation eating), our bodies actually depend on temporary inflammation to help fight off sudden injuries or infection. But when that inflammation becomes chronic, "the immune system mistakenly attacks normal cells, and the process that ordinarily heals becomes destructive."
Like so many health issues, the main culprit is too much sugar, which is why you've probably heard the sweet stuff singled out—as well as other well-known offenders, like dairy, booze, and trans-fat-filled fried foods. But inflammation can sneak up on you via lots of seemingly innocent foods. Here are six surprising sources you might want to approach with caution..."
"1. Agave
2. Frozen yogurt
3. Barley and Rye
4. Seitan
5. Peanuts
6. Seasoning mixes"
Article at:
http://wellandgood.com/2013/11/04/6-inflammation-causing-foods-no-one-talks-about/#6-inflammation-causing-foods-no-one-talks-about-1
My conjecture and guesses:
It also appears that they haven't given up on the 'food supplement' version. Their New Zealand clinical trials appears (to me) headed in that direction. This trial may allow them to put on the label 'reduces chronic inflammation' legally. New Zealand is a British Commonwealth country so I would suspect it's laws are similar to England. I noticed they chose a Chinese doctor to run the trials. Is it possible that they may look to introduce the supplement version in New Zealand/Australia/Hong Kong and maybe followed by mainland China? With what most of us know about the efficacy of Anatabine Citrate, the potential in China is many times that of the United States. The Chinese are hypochondriacs and anything that betters their health is welcome. ie why do you think TCM (Traditional Chinese Medicine) continues to be very popular there in spite of western medicine. The 'drug' version is being tested in England first and maybe they will pursue it's introduction in Europe first, bypassing the United States temporarily. It also seems to me that, just maybe, Mullan might be thinking of a combo drug application in the future. Maybe his Nilvadipine trials might be involved in his future research. If both of these things come true, it would seem to be easier to get an NDI here from the FDA??? I suspect both of these approaches are cheaper to do than doing these trials in the U.S. I know that many drug companies are choosing to run trials in China because of costs. If both of these guesses pan out, or some similar version, Mullan will be perceived by his admirers and peers as a great CEO. So what do others think RCPI/Mullan is headed?
Gene variants linked to MS disrupt key regulator of inflammation in 'Yale News', Bill Hathaway, June 10, 2015
Excerpts:
"With genetic roots of many autoimmune diseases pinpointed, scientists are zeroing in on the variety of molecular mechanisms triggered by these harmful variants. A team led by Yale School of Medicine researchers has implicated a central regulator of inflammation as a cause of many cases of multiple sclerosis (MS) — and intriguingly, the researchers note — ulcerative colitis as well."
"Last fall, a consortium of researchers identified genetic variants that play a role in onset of 21 different autoimmune diseases. Ninety-seven variants were associated with multiple sclerosis. The new Yale research led by Hafler and first author William J. Housley shows that 17 of these MS variants affect the NFkB pathway, which controls a host of immune system responses to environmental threats, and that one variant associated with MS near the NFkB gene profoundly increased gene activity.
The findings illustrate the complexity of individual diseases like MS, in which variants can contribute to small increases in risk of disease through different molecular mechanisms. They also illustrate how same molecular pathways, such as NFkB, can trigger a variety of autoimmune diseases with fundamentally different symptoms — such as MS and ulcerative colitis."
Article at:
http://news.yale.edu/2015/06/10/gene-variants-linked-ms-disrupt-key-regulator-inflammation
"Christopher Chapman, M.D., President of Rock Creek Pharmaceuticals (RCPI -12.7%) resigns to pursue other interests. Chairman and CEO Dr. Michael Mullan will assume his duties."
Notice at Seeking Alpha:
http://seekingalpha.com/news/2571835-rock-creek-pharma-president-bids-adieu?uprof=46&dr=1#email_link
calcineurin-blocking agents:
Re: tacrolimus
Ulcerative colitis[edit]
In recent years, tacrolimus has been used to suppress the inflammation associated with ulcerative colitis (UC), a form of inflammatory bowel disease. Although almost exclusively used in trial cases only, tacrolimus has shown to be significantly effective in the suppression of outbreaks of UC.[15][16]
Dermatological use[edit]
As an ointment, tacrolimus is used in the treatment of eczema, in particular atopic dermatitis. It suppresses inflammation in a similar way to steroids, and is equally as effective as a mid-potency steroid.
Re: cyclosporine
"ciclosporin is also used in severe atopic dermatitis, Kimura disease, pyoderma gangrenosum, chronic autoimmune urticaria, acute systemic mastocytosis, and, infrequently, in rheumatoid arthritis and related diseases, although it is only used in severe cases.[citation needed]
Ciclosporin has also been used to help treat patients with acute severe ulcerative colitis that do not respond to treatment with steroids.[13] This drug is also used as a treatment of posterior or intermediate uveitis with noninfective etiology"
My comments:
Excerpts from Wikipedia, notice that these drugs are also anti-inflammatory and are used similar to how anatabine citrate might be used to reduce inflammation. So, maybe Mullan is on the right track, ie this is like doing a phase III clinical trial of an anti-chronic inflammatory drug. (reduces NF-kB?) It looks like it reduces the incidences of dementia/Alzheimers.
New study may have found drug to prevent Alzheimer's disease
Jun 9, 2015 18:28 IST
Excerpts:
"A drug that suppresses the immune system to prevent transplant patients' bodies from rejecting their new organs may also protect against Alzheimer's disease, a new study has found.
It is known that toxic protein aggregates called Amyloid beta oligomers selectively target and disrupt the points of communication between brain cells, impairing memory in people suffering from Alzheimer's disease.
Calcineurin is an enzyme that regulates communication between brain cells and memory formation.
Researchers have shown previously that this enzyme plays a central role in the harmful effects of the Amyloid beta oligomers and that elevated calcineurin is found in the nervous system of Alzheimer's patients.
However, the question of whether blocking calcineurin would prevent the onset and progression of Alzheimer's in people is challenging because treatment with a calcineurin-blocking agent suppresses the immune system."
"In the new study, researchers from the University of Texas Medical Branch (UTMB) at Galveston analysed data from the medical records of 2,644 patients who received organ transplants and and must take calcineurin inhibitor-based medications, such as Tacrolimus or cyclosporine, for the rest of their lives to prevent rejection of the transplanted organ."
"The study data was compared with national data obtained from the 2014 Alzheimer's Association Facts and Figures dataset on age-matched patients to compare the prevalence of Alzheimer's in the US.
"These data clearly show that the prevalence of dementia and Alzheimer's in our transplant patient group is significantly lower, in fact almost absent, when compared to national data from the general population," said senior author Luca Cicalese, professor in the department of surgery.
"In patients over 65 years, 11 per cent of the general population had dementia compared with 1.02 per cent of the study subjects.
"In Americans over 75 years, 15.3 per cent of the population had dementia compared with 0.6 per cent of the study subjects. Among Americans over 85 years, 32 per cent had dementia, although we did not have any patients in this age group with dementia," Cicalese said.
The researchers are currently working on devising treatment strategies to obtain the same beneficial effects in humans with the disease using low doses of calcineurin inhibitors that result in minimal or no immunosuppression, thus limiting possible undesired side effects."
Article at:
http://www.firstpost.com/living/new-study-may-have-found-drug-to-prevent-alzheimers-disease-2287160.html
Hmmmm? How to Live Forever?--New video taunts anti-aging therapy market. Huge potentials! Could this have been today's trigger that caused RCPI to rise? Video talks about Telomerase/telemorese. Pitch is to sell an advisory newsletter on new technology. Maybe the time has come? Are investors relooking at RCPI? Remember Patrick Cox's newsletter re anti-aging and Anatabloc? Looks to me like anatabine citrate might be a cheaper solution than the $40,000 solution proposed in this video. See excerpts below.
How to Live Forever video at:
http://pro.moneymappress.com/NVXHCX/PNVXR636/?iris=373971&ad=4-hsca25ytl-btr&h=true
Patrick Cox excerpts (MARCH 6, 2015):
"The healthcare industry is in the midst of a transition from the old model of medicine (treating diseases) to the new (delaying or preventing the age-related conditions that cause diseases)."
"It seems that with almost anything that activates NF-?B, if you reduce it, it improves aging,” says Paul Robbins of the Scripps Research Institute in this feature article “How We Age.” I’m personally glad to see this new area of research hitting a more mainstream audience, because I’ve been alone reporting these developments for too long. There have been lots of journal articles supporting this view that NF-?B accelerates aging, but for some reason, nothing in the journals seems to penetrate the public consciousness. The article in The Scientist, by the way, cites this great journal piece.
The reality is that NF-?B over-activation, which is autoimmune syndrome, is a major accelerator of the aging processes. Essentially, the body recognizes normal aging as signs of injury and invasion, prompting an emergency innate immune response. A cytokine storm ensues and aging accelerates.
One alkaloid, which I’ve talked about incessantly here, has been shown in animal as well as human studies to moderate NF-?B and the associated accelerated aging. It’s not on the market at present, but I’m confident that others will be soon simply because the gene target is now known.
My confidence is based on the increased pace of discovery resulting from Moore’s Law and its impact on biological tools. It is orders of magnitude easier today to screen potential molecules for therapeutic activities. If I were a young, smart molecular biologist, like my son, I’d be looking for molecules in nature that mimic the alkaloid known to moderate NF-?B. "
Patrick Cox newsletter at:
https://www.mauldineconomics.com/tech/tech-digest/breakthroughs-in-anti-aging-science-appear-in-the-scientist
And this input from: Role of the Nervous System in deciding How Long we Live, Josh Mitteldorf, May 5, 2013
Excerpts:
"This brings us to the results published this week in Nature from the lab of Dongsheng Cai at Einstein College of Medicine in New York. Excess inflammation has been recognized for a long time as a direct mechanism of aging. Inflammation increases cancer risk, destroys arteries, and plays a role in Alzheimer’s disease (here is my blog post on the subject).
The new study shows that there is also an indirect effect of inflammation that magnifies its pro-aging effect. Inflammation is detected in the hypothalamus*, and pro-aging signals are sent out as a result. Since these signals further increase inflammation, this could be one of those self-reinforcing loops that accelerate our demise, and are relatively easy to disrupt via medical intervention. (Cai spoke of ‘cascading benefits’.) The mechanism described in Cai’s paper involve two more ingredients from the genetical alphabet soup: NF-kappa-B is emitted in response to danger, and switches on the gene transcription in a cell in a manner appropriate to emergency response. NF-kappa-B increases with age and promotes higher levels of inflammation — Boooo! GnRH is a signal that commands the reproductive cycle (M as well as F) and incidentally works to protect the body from aging — Yeaaa! Inflammation increases NF-kappa-B in the hypothalamus, and this, in turn, reduces the flow of GnRH.
When the researchers added GnRH to the hypothalamuses of old mice, they saw that it promoted adult neurogenesis. When they injected mice with GnRH, the mice showed reduced signs of aging. (from The Scientist)
The one-line take-home is that blocking NF-kappa-B in the hypothalamus increased the life span of mice by 20% (press release). And that’s as close as I can come to a simple story with a single magic bullet."
Article at:
http://joshmitteldorf.scienceblog.com/2013/05/05/role-of-the-nervous-system-in-deciding-how-long-we-live/
Fusion of normal cells may trigger genetic changes leading to cancer in 'Medical News Today', Monday 8 June 2015
Excerpts:
"As the number two leading cause of death in the US, cancer touches just about everyone in some way. There are many factors involved in the formation of cancer, and genetic changes are a key culprit. Now, a new study sheds light on how the fusion of one normal cell with another can trigger genomic events that turn normal cells cancerous, allowing tumors to form."
"Results reveal that fused cells can replicate - 19% of fused IEC-6 cells generated clones - and with replication, the chromosomes from the two separate cells fused together."
"They say their findings suggest that after cells fuse, a chromosomal instability might result in DNA damage and, therefore, genetic changes that underpin cancer."
""The frequency of cell fusion events in vivo is not known, although cell fusion is thought to occur under some circumstances such as cell injury, inflammation and viral infection. Although fusion of normal cells in vitro and in vivo may be a rare event, this study shows that cell fusion between normal cells can have pathological consequences."
Article at:
http://www.medicalnewstoday.com/articles/294976.php
Bacteria may cause type 2 diabetes in 'World Pharma News,' 02 JUNE 2015
Excerpts:
"Bacteria and viruses have an obvious role in causing infectious diseases, but microbes have also been identified as the surprising cause of other illnesses, including cervical cancer (Human papilloma virus) and stomach ulcers (H. pylori bacteria). A new study by University of Iowa microbiologists now suggests that bacteria may even be a cause of one of the most prevalent diseases of our time - Type 2 diabetes.
The research team led by Patrick Schlievert, PhD, professor and DEO of microbiology at the UI Carver College of Medicine, found that prolonged exposure to a toxin produced by Staphylococcus aureus (staph) bacteria causes rabbits to develop the hallmark symptoms of Type 2 diabetes, including insulin resistance, glucose intolerance, and systemic inflammation."
""What we are finding is that as people gain weight, they are increasingly likely to be colonized by staph bacteria - to have large numbers of these bacteria living on the surface of their skin," Schlievert says. "People who are colonized by staph bacteria are being chronically exposed to the superantigens the bacteria are producing."
Schlievert's research has previously shown that superantigens - toxins produced by all strains of staph bacteria - disrupt the immune system and are responsible for the deadly effects of various staph infections, such as toxic shock syndrome, sepsis, and endocarditis."
Article at:
http://www.worldpharmanews.com/research/3100-bacteria-may-cause-type-2-diabetes
What's giving bees dementia? in 'CNN News', June 6, 2015
Excerpts:
"From pesticides to possible cell phone radiation, the causes of bee population decline are an on-going debate.
Now there's another thing the buzzy little insect has to fear, dementia.
A new study, published on PLoS ONE, says aluminum, "one of the most significant environmental contaminant of recent times," could be responsible in the pollinators decline.
Aluminum, a widely known ecotoxicant, has already been linked to the elimination of entire fish species due to acid in bodies of water, deforestation due to nutrient deficient soil, and crop production problems due to soil acidity."
"Bees have pretty complex brains, and there's evidence to support that there's presence of memory, a high-level cognitive function. Although aluminum is considered a neurotoxin, and was initially linked to Alzheimer's disease in humans, the Alzheimer's Society in the United Kingdom advises a direct link has not been proven "despite continuing investigation."
Article at:
http://us.cnn.com/2015/06/06/us/aluminum-bees-dementia-irpt/index.html
Inflammation Seems to Underlie Concussion Symptoms in 'Psych Central', Traci Pedersen, 2015
Excerpts:
"Inflammation appears to be the underlying factor behind the symptoms of traumatic brain injuries, according to a new study by researchers at McMaster University in Canada.
The findings provide an explanation for why many people with very mild head injuries, or even injuries to other parts of their bodies, still suffer from debilitating post-concussion-like syndromes. These symptoms include headaches, dizziness, cognitive impairment, and other neuropsychiatric symptoms such as irritability, anxiety, and insomnia."
"“It’s inflammation that they have in common,” said Michel Rathbone, M.D., Ph.D., a professor of medicine for McMaster’s Michael G. DeGroote School of Medicine and a lead author of the paper. “Rather than a concussion, we’d like to propose a unifying umbrella term of post-inflammatory brain syndromes or PIBS.”
He added that their new findings will encourage scientists to open up new lines of research into understanding the cause of post-concussion symptoms. So even in a situation where there is no obvious visible brain injury on conventional imaging scans, physicians may be able to still offer treatments that target inflammatory mediators."
"He added that the results could provide hope for individuals suffering from cognitive dysfunction after major infections, surgeries, and traumas, as these individuals may benefit from similar treatments as people with concussions."
Article at:
http://psychcentral.com/news/2015/05/09/inflammation-underlies-concussion-symptoms/84448.html
What causes brain problems after traumatic brain injury? Studies have a surprising answer in 'Eureka Alert', UNIVERSITY OF MARYLAND SCHOOL OF MEDICINE, 15-JAN-2015
Excerpts:
"A new paper by researchers at the University of Maryland School of Medicine (UM SOM) argues that there is a widespread misunderstanding about the true nature of traumatic brain injury and how it causes chronic degenerative problems.
In a perspective article published in the latest issue of Neurotherapeutics, the two authors - Alan Faden, MD, a neurologist and professor of anesthesiology, and David Loane, PhD, an assistant professor of anesthesiology, propose that chronic brain damage and neuropsychiatric problems after trauma are to a large degree caused by long-term inflammation in the brain. In their view, this inflammation is a key culprit behind the myriad symptoms that have been linked with traumatic brain injury and mild traumatic brain injury, including brain atrophy, depression and cognitive decline.
Dr. Faden and Dr. Loane also say that there has been too much emphasis on a specific diagnosis known as chronic traumatic encephalopathy (CTE), the set of symptoms and pathology that has been found in some former professional football players. They argue that this may deflect focus from other mechanisms, which may be more important and treatable. They say that although chronic traumatic encephalopathy is a serious problem, relatively few people have been diagnosed with this condition. Instead, they contend, researchers and journalists should focus more on the fact that even repeated concussive impacts or mild traumatic brain injury may trigger chronic brain inflammation that can persist for years and cause lasting damage.
"Brain inflammation is a key issue, and it has been under-emphasized," says Dr. Faden. "Recent brain imaging studies, including those in former professional football players, indicate that persistent brain inflammation after a single moderate head injury or repeated milder traumatic brain injury may be very common, and may contribute to cognitive problems. In addition, larger studies indicate that brain inflammation persists for many months or years in many people with traumatic brain injury."
The paper also points out that chronic brain inflammation related to traumatic brain injury may be treatable. Dr. Faden and Dr. Loane say recent research shows that some experimental drugs, as well as carefully controlled exercise programs, can block brain inflammation caused by traumatic brain injury. They maintain that these avenues should be pursued vigorously."
Article at:
http://www.eurekalert.org/pub_releases/2015-01/uoms-wcb011515.php
New Research May Help Prevent Alzheimer's, Associated Press, May 25, 2015
My comments:
Short 2 minute video discussing efforts to understand more about the tau tangles.
Excerpt:
"An ambitious study is testing if an experimental drug might help healthy but at-risk people stave off Alzheimer's. In addition to brain scans checking for amyloid build up, researchers are looking for tangles of a protein named tau. (May 26)"
Video at:
Mechanisms and secrets of Alzheimer's disease: exploring the brain
LECMA Vaincre Alzheimer
My comments:
Excellent short 6 minute video explaining Alzheimers and where we stand today.
Video at:
Identifying Pathways that Lead to the Development of Alzheimer's Disease in Peer Reviewed Alzheimer's Research Program', Kalipada Pahan, Ph.D., Rush University Medical Center, January 7, 2015
Excerpts:
"The nuclear factor kappa B (NF-?B) transcription factor is an important regulator of neuro-inflammation. Dr. Pahan and his team hypothesized that peptides which block specific binding domains important in NF-?B activation would modulate neuro-inflammatory cascades and block further damage to the neurons. "After intranasal administration, the peptide enters into the brain, inhibits microglial activation, protects neurons, and improves memory and learning in mice with AD-like pathology", said Dr. Pahan. Using animal modeling, treatment with the peptide improved cognitive function in animals predisposed to Alzheimer's disease. In a separate study, Dr. Pahan showed that increased activation of NF-?B in the cortex and hippocampus of Alzheimer's patients negatively affects cognitive function. Therefore, it is conceivable that these peptides may help Alzheimer's patients maintain or recover lost cognitive function."
Article at:
http://cdmrp.army.mil/prarp/research_highlights/15pahan_highlight.shtml
Herbs and Supplements References at:
http://www.nlm.nih.gov/medlineplus/druginfo/herb_All.html
Biotech and Pharma mergers and acquisitions---Good website to keep track of who is doing what with whom:
http://www.biospace.com/news_subject_all_results.aspx?CatagoryId=3
The Biggest Health Breakthrough Since the Discovery of Penicillin---I thought it was Anatabloc---Pitch that eeeirly sounded like anatabine citrate. Dr trying to peddle a book but interesting to read:
http://www.alsearsmd.com/Landing/JVOut_Pescatore_CC_Penicillin_20150603.html?utm_source=pescatore&utm_medium=jvout&A13utm_term=solo-email&utm_content=buyer&utm_campaign=ccgold-20150603
Unknown: see Clinical Trials.gov for 'public' info on trials
https://clinicaltrials.gov/ct2/show/NCT02432313?term=ANATABINE&rank=2
I can't believe you can't look up this info for yourself. You can find all the 'anatabine' clinical trials here if you searched the website for 'anatabine':
https://clinicaltrials.gov/ct2/results?term=ANATABINE&Search=Search
New Research Suggests That Pre-Existing Inflammation May Promote the Spread of Cancer in 'Newswise', 2-Jun-2015, Source Newsroom: Florida Atlantic University
Excerpts:
" Although normal inflammation plays an important role in helping to fight off infections, there is mounting evidence that chronic inflammation is linked to increased risk of tumor development. A new study conducted by researchers in the Charles E. Schmidt College of Medicine at Florida Atlantic University is helping to shed light on the important link between inflammation and cancer, and how pre-existing inflammation may aid in the metastatic process.
In an article titled, “Allergen Induced Pulmonary Inflammation Enhances Mammary Tumor Growth and Metastasis: Role of CH13L1,” featured on the cover of the current issue of the Journal of Leukocyte Biology, this new research suggests inflammation raises the level of a known biomarker of cancer, called “chitinase-3-like-1” or “CHI3L1,” in the inflamed tissue, which leads to increased metastasis and faster cancer growth in that tissue. Metastasis is responsible for 90 percent of breast cancer deaths despite significant improvements in diagnosis and treatments."
"“In this study, we found that CH13L1 was an important inflammatory protein that promoted tumor growth and metastasis, providing the necessary ‘soil’ or the proper environment for the ‘seeds,’ that is the circulating breast tumor cells,” said Iragavarapu-Charyulu. “We are encouraged by the results of our study and hopeful that it will help us to better develop targeted therapeutics to treat cancer.”"
Article at:
http://www.newswise.com/articles/new-research-suggests-that-pre-existing-inflammation-may-promote-the-spread-of-cancer
Bacteria may cause type 2 diabetes in 'World Pharma News', 02 JUNE 2015
Excerpts:
"Bacteria and viruses have an obvious role in causing infectious diseases, but microbes have also been identified as the surprising cause of other illnesses, including cervical cancer (Human papilloma virus) and stomach ulcers (H. pylori bacteria). A new study by University of Iowa microbiologists now suggests that bacteria may even be a cause of one of the most prevalent diseases of our time - Type 2 diabetes."
""What we are finding is that as people gain weight, they are increasingly likely to be colonized by staph bacteria - to have large numbers of these bacteria living on the surface of their skin," Schlievert says. "People who are colonized by staph bacteria are being chronically exposed to the superantigens the bacteria are producing."
"The team's latest study, published recently in the journal mBio, shows that superantigens interact with fat cells and the immune system to cause chronic systemic inflammation, and this inflammation leads to insulin resistance and other symptoms characteristic of Type 2 diabetes. In examining the levels of staph colonization on the skin of four patients with diabetes, Schlievert's team estimate that exposure to the bacterial superantigens for people who are heavily colonized by staph is proportional to the doses of superantigen that caused the rabbits to develop diabetes symptoms in the team's experiments."
""I think we have a way to intercede here and alter the course of diabetes," Schlievert says. "We are working on a vaccine against the superantigens and we believe that this type of vaccine could prevent the development of Type 2 diabetes.""
Article at:
http://www.worldpharmanews.com/research/3100-bacteria-may-cause-type-2-diabetes
Alzheimer's-Linked Brain Proteins Tied to Poor Sleep in Study at 'Drugs.com, June 1, 2015
Excerpts:
"Poor sleep in old age may be linked to the brain-clogging plaques thought to contribute to Alzheimer's disease, new research suggests.
"Sleep appears to be a missing piece in the Alzheimer's puzzle, and enhancing sleep may lessen the cognitive burden that Alzheimer's disease imparts," said study author Bryce Mander, a postdoctoral fellow at the University of California, Berkeley."
"Those patients with the highest levels of amyloid plaques in one part of the brain -- the medial prefrontal cortex -- had lighter sleep and higher levels of memory problems, the researchers found"
"The study was published in the June 1 issue of Nature Neuroscience."
Article at:
http://www.drugs.com/news/alzheimer-s-linked-brain-proteins-tied-poor-sleep-study-57015.html?utm_source=ddc&utm_medium=email&utm_campaign=Today%27s+news+summary+-+June+1%2C+2015&utm_content=Alzheimer%27s-Linked+Brain+Proteins+Tied+to+Poor+Sleep+in+Study
Take your pick: Dilution of shares or bankruptcy. Big Pharma could buy RCPI at a fire sale.
RCPI says: it's "principal focus is on cholinergic anti-inflammatory pathways, in particular osteoarthritis, ulcerative colitis, psoriasis, smoking cessation, and Hashimoto's thyroiditis". Roskamp scientist keep publishing papers on AD using anatabine, but you never know, they could change their mind.
See their website:
http://rockcreekpharmaceuticals.com/pharmaceutical/research_areas
My bet: The famous Bernanke formula, 'Quantitative Easing'---another private placement from the big believers with lotsa newly minted money. Or, maybe a 'Sugar Daddy' in the wings? Anyone else betting?
Details of Nilvadipine Phase III trials can be found here:
https://clinicaltrials.gov/ct2/show/NCT02017340
I should emphasize the issue of safety:
Excerpt from Roskamp:
"9. What is Nilvadipine? What are its components?
Nilvapdipine is a calcium channel blocker currently used to treat hypertension (high blood pressure) and is available in Ireland on prescription. It has been used for many years and is associated with a good safety profile (few side effects).
10. Who manufacturers Nilvadipine?
Nilvadipine is manufactured by pharmaceutical company Astellas Pharma US.
11. Are there any serious side-effects of Nilvadipine?
Nilvadipine has been used for the treatment of high blood pressure for over 10 years and has a very good safety profile. The main side effect, which is of concern to us in this trial, is that it may lower subjects’ blood pressure, and we have established a protocol to monitor for this closely. Nilvadipine can also cause headache, flushing, palpitations and swelling of the legs infrequently."
Webpage at:
http://www.rfdn.org/news_release_090806_faq.html
My Comments:
Safety MIGHT BE the big thing for anatabine. It's efficacy and wide-ranging application potential are also important. So what is the safety record for anatabine? We'll find out more after the phase I/II studies, but Anatabloc users have not reported any serious side effects that I have seen. (only some reaction to their 'sweetened' version at the beginning of sales.) Nilvadipine is a complex synthetic molecule: C19H19N3O6, Molecular mass 385.370 g/mo. Anatabine citrate is a small 'natural' molecule: C10H12N2, Molecular mass 160.22 g/mol. RCPI has a patent on the synthetic manufacture of anatabine. Roskamp reports that Nilvadipine does cross the blood brain barrier as does anatabine, thus making them potential candidates for AD. Clearly, in any drug, the fewer and less traumatic the side effects, the better. My opinion: As with any 'man-made' molecule, there is a long term risk that unforeseen problems can arise. For example, the risks of GMO's are highlighted, but no major problems have yet been cited. Almost all drugs are 'man-made' molecules or compounds, many have some serious adverse effects. I, personally, would trust a natural medicine more than a 'man-made' one. In China, TCM (Traditional Chinese Medicine) is a big deal. Followers truly believe in the efficacy and potency of it's compounds. It has been practiced for thousands of years. (without clinical trials--or more correctly, from the trials and errors of a long history) To western eyes, it verges on witch craft. As more becomes known, western medicine is recognizing the value of many of it's natural constituents and more and more 'natural' medicine is becoming popular in the west. Can you imagine the potential of anatabine sales in China if the efficacy being projected become true? Chinese are hypochondriacs, Most hospitals practice both western and TCM. Some hospitals only practice TCM.---from 5 in the morning, before the hospital opens at 8am, until the hospital closes, standing room only!
My thoughts and opinion:
Re Alzheimer's Research at RCPI, a scientist by the name of Ryan Lanier is the Chief Scientific Officer, and has been for the last 6 years. He appears to be the one heading up efforts on anatabine applications and research. Having said that, RCPI says it's principal focus is on cholinergic anti-inflammatory pathways, in particular osteoarthritis, ulcerative colitis, psoriasis, smoking cessation, and Hashimoto's thyroiditis.
Archer's scientific staff is led by Michael Mullan, who is the CEO and Chief Scientific Officer there. He is the CEO and Chairman of the Board at RCPI. Fiona Crawford, who is the CEO and President of Roskamp, is the Chief Technical Officer and Assistant Chief Scientific Officer at Archer. Daniel Paris is the Head of Research and Development at Archer and is a Senior Scientist at Roskamp. Ghania Ait-Ghezala is the Head of Molecular Biology at Archer and is also a Senior Scientist at Roskamp. Ven Kat Mathura is the Head of Bioformatics and Cheminformatics at Archer and a Senior Scientist at Roskamp. Archer's focus is on Nilvadipine as applied to Alzheimer's (ARCO 29)
It appears to me that Archer will be the (private) company that will see the fruits of Nilvadipine if is a commercial success. Implied in the current research of Nilvadipine is that it reduces inflammation, amiloyd plaque, and tau tangles. This is betting that this trio-attack will do what no other drug has been able to do and that is to reverse the effects of Alzeimers. Up to now the effort has been focused on amyloid and nothing has really worked. Astra Zenica hopes it's BACE1 inhibitor that reduces amyloyd will be AD's solution. The experimental monoclonal antibodies (mAbs), Biogen’s aducanumab, Eli Lilly’s solanezumab and Roche’s gantenerumab and crenezumab are betting that AD reduction is by reducing Tau. Mullan thinks that a drug that reduces amyloid, tau, and inflammation is the eventual solution and that Nilvadipine may be it. A parallel effort at RCPI is ongoing and some of the same scientists are looking at anatabine because, it too, reduces amyloid, tau, and inflammation. I think Mullan is 'double downing' his bet on his theory about AD. No where has it been said how effective Nilvadipine reduces the 3 issues. No mention has been made how effective anatabine reduces these issues also. Remember, anatabine AD tests were never completed and is now probably a year or more behind Nilvadipine in the clinical trial sequence. Mullan was lucky to find Nilvadipine because it's safety was already established so he went directly to phase III at the beginning. Those of us betting on RCPI have to wait until probably year end to 'officially' document safety and hopefully some efficacy results on anatabine with the trials in England.
So, is anatabine still in the running? You bet! If Nilvadipine proves successful, Mullan's theory will be vindicated. If anatabine proves successful, everybody's uncle will be racing towards this target(s). Only Mullan and his team have any insight on the real potential for anatabine as applied to AD. Some questions you might ask yourself: Why did Mullan leave Roskamp when he was already riding the Archer horse? Why is RCPI only (officially) focused on cholinergic anti-inflammatory pathways as it applies to osteoarthritis, ulcerative colitis, psoriasis, smoking cessation, and Hashimoto's thyroiditis when Mullan's whole professional life has been focused on AD? They asked Willie Sutton why he robbed banks? He said: "Because that's where the money is!" (just kidding, I think Mullan is a great scientist and his experience and insight will dictate his direction. Let's hope he is right and the banks are Big Pharma or ?. (Remember also that the official targets RCPI cites are large medical needs in their own right.)
We almost forgot about Archer---
Archer "Products & Research" page:
"ARC029 (Nilvadipine) is Archer’s first compound to be selected for clinical development. With Archer’s worldwide rights to ARC029 for its use in Alzheimer’s disease, it is our intention to fast track its development to deliver a first-in-class drug.
ARC029 was selected from approximately 2,000 chemicals in the same class as our first-line treatment of Alzheimer’s for several reasons:
The compound was one of the most proficient at lowering amyloid levels in the pre-clinical tests and models of Alzheimer’s disease.
Very importantly ARC029 easily crosses the blood brain barrier, and there is evidence that it accumulates in the brain, which is important for targeting Alzheimer’s disease.
Other drugs in the class do not cross the blood brain barrier.
Importantly, ARC029 acts to lower the soluble forms of amyloid before they become deposits in the brain. We believe that the soluble forms (rather than the deposited forms) are the real culprit in the disease, and so reducing them is our goal with ARC029.
Current Findings in Mild Cognitive Impairment- Based on current studies, Archer has extensive safety data and a mechanism of action for how ARC029 works in the brain. Nilvadipine has been shown to have beneficial effects, such as inhibiting amyloid production, increasing amyloid clearance across the blood brain barrier, and decreasing neuroinflammation (Paris et al., 2010; Bachmeier et al., 2011). Independent research has shown that Nilvadipine may prevent cognitive decline in patients with mild cognitive impairment (MCI) and act as a disease modifying agent (Hanyu et al., 2007).
Since posteromedial hypoperfusion suggests the presence of underlying Alzheimer’s disease pathology and predicts conversion to Alzheimer’s disease (Hirao et al., 2005), most patients with MCI in this study (Hanyu et al., 2007) were at high risk of progression to Alzheimer’s disease and may also have included a portion of patients with prodromal Alzheimer’s disease. This study then suggests that ARC029 may stabilize cognitive function over time.
Archer’s open label Phase I/IIa trial of Nilvadipine in Alzheimer’s patients demonstrated its safety and tolerability, and also showed APOE-genotype dependent stabilization of cognition and improvement in executive function over the 6 week duration (Kennelly et al., 2011a & b).
These promising findings led to the creation of the NILVAD consortium to evaluate the effects of 18 months of treatment with Nilvadipine in Alzheimer’s patients in a double-blind placebo controlled Phase III trial study being conducted in nine European countries, currently underway.
ARC031 – Follow-up Compound Archer data suggest that nilvadipine and related compounds can have direct effect on lowering soluble amyloid levels independently of their impact on calcium channels. Critically, this has allowed the development of non-calcium channel blocking derivatives of nilvadipine, including ARC031. ARC031 is not a calcium channel blocker but works in the same way as ARC029 to lower soluble amyloid levels. This compound has the advantage of not having antihypertensive effects in comparable doses to ARC029, which may be an additional advantage in Alzheimer’s disease."
Webpage at:
http://www.archerpharma.com/products&research.html
NILVAD – a clinical study for a new treatment in Alzheimer's disease:
"On January 1, 2012 the international European research project NILVAD (A European multicentre double-blind placebo-controlled phase III trial of nilvadipine in mild to moderate Alzheimer’s disease) started, coordinated by the Trinity College Dublin, Ireland. The European Commission funds NILVAD for five years, with an amount of 6 million Euros. Alzheimer’s disease (AD) is an ever-increasing public health concern among the aging population and is the most common form of dementia affecting more than 15 million individuals worldwide and around 5 million Europeans. The direct and indirect costs of AD and other dementias amount to more than €440,000 million each year (www.alz.org, 2010).
There is therefore an imperative to develop new treatments for AD that have disease modifying effects. NILVAD performs a double-blind placebo controlled study that will test the efficacy and safety of nilvadipine in 500 subjects with mild to moderate AD over a treatment period of 18 months. Male and female patients with mild to moderate AD aged between 50 and 90 with a range of medical morbidities and frailty will be included in the study. If this trial is successful, nilvadipine would represent an advance in the treatment of AD patients and would have a major impact on the health and social care costs incurred in Europe by this neurodegenerative disorder."
NILVAD Website at:
http://www.nilvad.eu/#
My Comments:
The clinical trials appear to be from 2 to 5 years (18 month treatment period). Since the trials started in 2012, it would seem that preliminary info should be coming out soon. Nilvadipine ARC029 acts to lower the soluble forms of amyloid. Results should be forthcoming before the Biogen trials (hopefully) and if positive, give Archer a head start before BigPharma. Is it possible that Mullan is thinking about Nilvadipine and anatabine? Or maybe already investigating? Could he be thinking of merging Archer and RCPI? Your thoughts?
Vitamin D: Can it help prevent Alzheimer's or dementia? at WPTZ.com, May 28, 2015
Excerpts:
"It is still unclear what role vitamin D has in brain function"
"New research suggests people with very low levels of vitamin D in their blood, known as vitamin D deficiency, are more likely to develop Alzheimer's disease and other forms of dementia.
For example, a large 2014 study published in Neurology showed people with extremely low blood levels of vitamin D were more than twice as likely to develop Alzheimer's disease or other types of dementia than those with normal vitamin D levels. But it's important to point out that the association between vitamin D deficiency and dementia risk is only observational at this point. More research is needed to show cause and effect.
Vitamin D is vital to bone metabolism, calcium absorption and other metabolic processes in the body. Its role in brain function, cognition and the aging process is still unclear. Some studies suggest vitamin D may be involved in a variety of processes related to cognition, but more research is needed to better understand this relationship."
Article at:
http://www.wptz.com/vitamin-d-can-it-help-prevent-alzheimers-or-dementia/33264046
Re Signum Biosciences, here's what they say: "Spearheading a novel, disease modifying mechanism for neurodegenerative disorders"
"Research has largely focused on pathological hallmarks seen at the endpoint of disease. Until now."
"The amyloid hypothesis has dominated the field and is being tested in a number of advanced clinical trials with small molecules and biological approaches. To date these trials have not demonstrated convincing efficacy. It is likely that amyloid deposition is a late phenomenon, and additional pathways contribute to the disease, therefore amyloid modulation is not sufficiently central to affect disease course. Additional strategies are targeting other hallmarks such as the abnormally aggregated tau protein in Alzheimer’s disease or alpha-synuclein in Parkinson’s disease. Such approaches are still to be evaluated in the clinic. Signum targets PP2A, a master regulator of tau, acting centrally in the disease process for maximal potential efficacy."
Remarks at Signum website:
http://www.signumbiosciences.com/pp2a
Don't forget about Tau---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, May 21, 2014
My Comments:
Big effort on inhibiting BACE1 and monoclonal antibodies to reduce amyloid by BigPharma. Some researchers think that the tau tangles are to blame for AD. Not many are chasing this.(maybe Signum Biosciences ) Anatabine appears to reduce both!!! Could anatabine be the BIG KAHUNA that no one seems to notice?
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://omicsgroup.org/journals/anatabine-attenuates-tau-phosphorylation-and-oligomerization-in-ps-tau-transgenic-mice-2168-975X.1000126.php?aid=26406
Some Immune Cells Change To Prolong Inflammation in Science 2.0,By News Staff, May 27th 2015
Excerpts:
"Researchers have unraveled one of the mysteries of how a small group of immune cells work: That some inflammation-fighting immune cells may actually convert into cells that trigger disease.
White blood cells, called T-cells, iare one of the body's critical disease fighters. Regulatory immune cells, called "Tregs," direct T-cells and control unwanted immune reactions that cause inflammation. They are known to produce only anti-inflammatory proteins to keep inflammation caused by disease in check.
But using mouse models, the researchers studied how the body fights off a common oral fungus that causes thrush. They found that these harmful invaders activate a mechanism in Tregs that could transform the inflammation-fighting cells into cells that allow the disease to flourish"
"Other researchers have reported the presence of these cells in many human inflammation conditions, such as psoriasis, periodontitis and arthritis. Until now, however, the mechanisms of how these cells developed were not completely understood, Pandiyan said.
The findings will help researchers understand the origin of cells they suspect may keep the disease active or, at a minimum, don't battle inflammation. Pandiyan believes the knowledge could lead to new ways to fight diseases, such as:
(1) Using the converting Tregs (Treg-17) to identify chronic inflammation, including oral inflammation.
(2)Using the persistence of Treg-17 cells to indicate an excessive amount of the inflammatory proteins.
(3) Using the presence of the binding agent that triggers the cell's conversion as a point to use medicines to block its connection to Tregs."
Article at:
http://www.science20.com/news_articles/some_immune_cells_change_to_prolong_inflammation-155711
Bigger Share of Deaths Worldwide Now Due to Cancer in 'Drugs.com', May 28, 2015
Excerpts:
" A greater percentage of deaths worldwide are now caused by cancer, a new report shows.
Between 1990 and 2013, the proportion of all deaths caused by cancer rose from 12 percent to 15 percent. During that time, years of healthy life lost to cancer increased 29 percent, the report found.
In total, there were 15 million new cases of cancer, 8 million deaths and 196 million years of a healthy life lost in 2013, the researchers said.
Between birth and age 79, one in three men and one in five women developed cancer, the findings showed. The leading cause of cancer death in 2013 was tracheal, bronchus (the main passageway to the lungs) and lung cancer, which caused 1.6 million deaths.
Breast cancer was the leading cause of lost years of healthy life among women, and for men it was lung cancer, according to the study by the Global Burden of Disease Cancer Collaboration group.
The team analyzed data on 28 types of cancer in 188 countries between 1990 and 2013. The study was published online May 28 in the journal JAMA Oncology."
Article at:
http://www.drugs.com/news/bigger-share-deaths-worldwide-now-due-cancer-56965.html?utm_source=ddc&utm_medium=email&utm_campaign=Today%27s+news+summary+-+May+28%2C+2015&utm_content=Bigger+Share+of+Deaths+Worldwide+Now+Due+to+Cancer
Alzheimer's Disease Treatment Market Value Will Exceed $13 Billion in 'Drug Development and Delivery', 5/7/2015
"The global market for Alzheimer’s Disease (AD) treatment will more than double in value from $4.9 billion in 2013 to reach an estimated $13.3 billion by 2023, representing a Compound Annual Growth Rate (CAGR) of 10.50%, according to research and consulting firm GlobalData."
"Following the anticipated approval and launch of first-in-class BACE1 inhibitors and passive immunotherapies in 2018 and 2019, respectively, the AD treatment market will undergo rapid expansion, as several blockbuster drugs are expected to come from these two potentially disease-modifying therapeutic classes. The experimental monoclonal antibodies (mAbs), Biogen’s aducanumab, Eli Lilly’s solanezumab and Roche’s gantenerumab and crenezumab, will compete with the BACE1 inhibitors, Merck’s MK-8931 and AstraZeneca/Eli Lilly’s AZD-3293, as both treatment approaches are designed to prevent the formation of senile amyloid plaques.”"
Article at:
http://www.drug-dev.com/Main/Back-Issues/Alzheimers-Disease-Treatment-Market-Value-Will-Exc-926.aspx
Currently there are no remedies that prevent or halt the progression of these diseases at Signum Biosciences
Article:
"Neurodegenerative disorders are a dire public health problem
AD is arguably the most dire health problem facing the Western World. It is estimated that 50% of people over 85 will have or acquire Alzheimer’s; this translates into a huge market as advances in medicinal technology have extended life expectancy of the US population.
A multi-billion dollar drug market
The current size of Alzheimer’s-drug market is an estimated $3 billion, with up to 12 million people suffering from the condition in the U.S., Europe and Japan. The market could possibly surpass $20 billion with the approval of a disease-modifying drug. The key growth driver for Alzheimer’s drugs is undoubtedly an aging population.
Development of disease modifying therapeutics requires an understanding of the most basic mechanisms underlying these disorders. The drugs that are currently prescribed to treat AD do not affect the course of the disease; they only treat symptoms, leaving the underlying cause and inevitable attack of this devastating disorder. Signum’s approach has the promise to transform Alzheimer’s disease therapeutics to make a huge impact in a critical market"
Article at:
http://www.signumbiosciences.com/therapeuticmarkets
Blockbuster potential for AZ's Alzheimer's drug
Jeff Mordock, The News Journal, May 2, 2015
Excerpts:
"AstraZeneca is currently testing a potential Alzheimer's disease treatment the company estimates could generate peak sales of $5 billion, if approved."
"AstraZeneca, a British company with its U.S. headquarters in Fairfax, is attempting to meet that demand with AZD3293. The drug is viewed as unique because it may treat the underlying cause of the disease by preventing the build up of plaque that forms in the brain creating Alzheimer's disease.
Current medicines work to lessen the disease's symptoms by boosting patients' levels of acetylcholine, a chemical messenger needed for alertness, memory and thought."
"AZD3293 is part of a class of drugs known as a BACE inhibitor and works to block the accumulation of protein fragments called B-amyloids, which forms the Alzheimer's plaque in the brain. BACE inhibitors are relatively new in the field of Alzheimer's Disease.
"A BACE inhibitor is a new approach," Day said. "There has not been much emphasis placed on this."
""The BACE inhibitor treats the underlying cause of the disease," he said. "If it is effective and approved, it would be a new kind of treatment."
But whether the drug will be effective, or approved, remains a challenge. AstraZeneca, which has partnered with Eli Lilly Co. to develop AZD3293, said the drug has a 9 percent chance of surviving clinical trials."
"The Alzheimer's drug market is expecting to flatten or decrease by 2017 because of a lack of effective therapeutics, according to BCC Research, a publisher of technology market reports. BCC estimates the global market for Alzheimer's disease medicines, which was $10.2 billion in 2012, could fall by 1.5 percent to $9.5 billion in 2017. An increased need for treatment as the population ages will likely prevent the market from declining at an even faster rate.
"The less drugs you have in a class, the more lucrative it is going to be," said Joseph Fuhr, a professor of economics and adjunct assistant professor of pharmaceutical and healthcare business at Widener University. "If you are the only drug in market you have control of the price you are charging."
For now, AZD3293 remains in Phase II/III clinical trials studying its results on 22,000 patients who are in the early stages of the disease. The trials are taking place in many countries throughout the world. AstraZeneca's Alexander said he expects the study to be completed sometime in 2019."
"AstraZeneca and Eli Lilly partnered in September to jointly develop and sell the drug, if approved. Under the agreement, Lilly will pay AstraZeneca up to $500 million in development and regulatory milestone payments. AstraZeneca expects to receive the first milestone payment of $50 million sometime this year. The companies will equally share all future development and commercialization costs as well as net global revenues if the product is launched.
Lilly will lead the clinical development working with researchers from AstraZeneca's Innovative Medicines Unit for neuroscience, while AstraZeneca will be responsible for manufacturing. The commercialization expenses will be split by both companies.
As both companies monitor the drug's impact on Alzheimer's patients, researchers remain cautiously optimistic that a new treatment could hit the market within the next decade."
Article at:
http://www.delawareonline.com/story/money/business/2015/05/02/blockbuster-potential-azs-alzheimers-drug/26729877/
May 26, 2015 /PRNewswire Re Golimumab
Excerpts:
"MSD, known as Merck & Co., Inc. in the United States and Canada,- today announced that SIMPONI®(golimumab) has received CHMP positive opinion for the treatment of adult patients with severe, active non-radiographic axial spondyloarthritis (nr-axial SpA) with objective signs of inflammation as indicated by elevated C-reactive protein (CRP) and/or magnetic resonance imaging (MRI) evidence, who have had an inadequate response to, or are intolerant to nonsteroidal anti-inflammatory drugs (NSAIDs).[1] Once the EU commission issues their EC decision, and if approved, nr-axial SpA patients can be considered for the once-monthly subcutaneous injection with SIMPONI® (golimumab)."
"SIMPONI® is a human monoclonal antibody that targets and neutralises tumour necrosis factor (TNF)-alpha, a protein that when overproduced in the body due to chronic inflammatory diseases can cause inflammation and damage to bones, cartilage and tissue. Licensed indications for golimumab include: moderate to severe, active RA in adults, in combination with methotrexate, when the response to disease-modifying anti-rheumatic drug (DMARD) therapy including methotrexate has been inadequate; severe, active and progressive RA, in combination with methotrexate, in adults not previously treated with methotrexate; active and progressive PsA in adult patients, alone or in combination with methotrexate, when the response to previous DMARD therapy has been inadequate; and severe, active ankylosing spondylitis in adults who have responded inadequately to conventional therapy. Once approved, SIMPONI®will be indicated for the treatment of adults with severe, active nr-axial SpA with objective signs of inflammation as indicated by elevated C-reactive protein (CRP) and/or magnetic resonance imaging (MRI) evidence, who have had an inadequate response to, or are intolerant to nonsteroidal anti-inflammatory drugs (NSAIDs).
Golimumab is also the first and only subcutaneous anti-tumor necrosis factor (TNF)-alpha treatment administered as an every-four-week maintenance therapy for the treatment of adult patients with moderately to severely active ulcerative colitis who have had an inadequate response to conventional therapy, including corticosteroids and 6-mercaptopurine or azathioprine, or who are intolerant to or have medical contraindications for such therapies. Golimumab is available either through the SmartJect® autoinjector/prefilled pen or a prefilled syringe as a SC administered injection."
Article at:
https://www.virtualpressoffice.com/publicsiteContentFileAccess?fileContentId=2014721&fromOtherPageToDisableHistory=Y&menuName=News&sId=&sInfo=
How Scientists Plan to Hack Your Nervous System in 'Gizmodo', Gaia Vince, 26 May 2015
Excerpts:
"One nerve connects your vital organs, sensing and shaping your health. If we learn to control it, the future of medicine will be electric"
"Kevin Tracey, a neurosurgeon based in New York, is a man haunted by personal events – a man with a mission. “My mother died from a brain tumour when I was five years old. It was very sudden and unexpected,” he says. “And I learned from that experience that the brain – nerves – are responsible for health.” This drove his decision to become a brain surgeon."
"In the late 1990s, Tracey was experimenting with a rat’s brain. “We’d injected an anti-inflammatory drug into the brain because we were studying the beneficial effect of blocking inflammation during a stroke,” he recalls. “We were surprised to find that when the drug was present in the brain, it also blocked inflammation in the spleen and in other organs in the rest of the body. Yet the amount of drug we’d injected was far too small to have got into the bloodstream and travelled to the rest of the body.”
After months puzzling over this, he finally hit upon the idea that the brain might be using the nervous system – specifically the vagus nerve – to tell the spleen to switch off inflammation everywhere.
It was an extraordinary idea – if Tracey was right, inflammation in body tissues was being directly regulated by the brain. Communication between the immune system’s specialist cells in our organs and bloodstream and the electrical connections of the nervous system had been considered impossible. Now Tracey was apparently discovering that the two systems were intricately linked."
"The vagus nerve starts in the brainstem, just behind the ears. It travels down each side of the neck, across the chest and down through the abdomen. ‘Vagus’ is Latin for ‘wandering’ and indeed this bundle of nerve fibres roves through the body, networking the brain with the stomach and digestive tract, the lungs, heart, spleen, intestines, liver and kidneys, not to mention a range of other nerves that are involved in speech, eye contact, facial expressions and even your ability to tune in to other people’s voices. It is made of thousands and thousands of fibres and 80 per cent of them are sensory, meaning that the vagus nerve reports back to your brain what is going on in your organs."
"Research shows that a high vagal tone makes your body better at regulating blood glucose levels, reducing the likelihood of diabetes, stroke and cardiovascular disease. Low vagal tone, however, has been associated with chronic inflammation. As part of the immune system, inflammation has a useful role helping the body to heal after an injury, for example, but it can damage organs and blood vessels if it persists when it is not needed. One of the vagus nerve’s jobs is to reset the immune system and switch off production of proteins that fuel inflammation. Low vagal tone means this regulation is less effective and inflammation can become excessive,"
"Other patients on the trial had similar transformative experiences. The results are still being prepared for publication but Tak says more than half of the patients showed significant improvement and around one-third are in remission – in effect cured of their rheumatoid arthritis. Sixteen of the 20 patients on the trial not only felt better, but measures of inflammation in their blood also went down. Some are now entirely drug-free. Even those who have not experienced clinically significant improvements with the implant insist it helps them; nobody wants it removed.
“We have shown very clear trends with stimulation of three minutes a day,” Tak says. “When we discontinued stimulation, you could see disease came back again and levels of TNF in the blood went up. We restarted stimulation, and it normalised again.”"
"The implications of being able to simply and cheaply improve vagal tone, and so relieve major public health burdens such as cardiovascular conditions and diabetes, are enormous. It has the potential to completely change how we view disease. If visiting your GP involved a check on your vagal tone as easily as we test blood pressure, for example, you could be prescribed therapies to improve it. But this is still a long way off: “We don’t even know yet what a healthy vagal tone looks like,” cautions Kok. “We’re just looking at ranges, we don’t have precise measurements like we do for blood pressure.”"
Article at:
http://www.gizmodo.co.uk/2015/05/how-scientists-plan-to-hack-your-nervous-system/