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Nearly all my shares shown as a sell volume but never sold one.
Expecting News soon, IMO.
My Bags are Full, LOL
GLTA
ILNS
LoL! We will see...
2,65M shares
ILNS
Another 400k. Thanks!
Yep! LoL
Not enough funds to move forward with all ILNS technology.
Yes, ILNS needs much more Transparency, News, Updates and Marketing.
IMO
1,85M shares!
ILNS
Old news published today.
In german language..never found this bevor, it was my german language google search alert today..
http://www.prestigecars.de/automobile-magazin/2012/intellect-neurosciences-erhalt-fur-seine-immuntherapie-technologieplattform-antisenilin-zur-behandlung-von-alzheimer-die-patentankundigung-des-us-patent-und-markenamts/35680
It sounds like ELAN is interested in ILNS technology. LoL!
http://www.fiercebiotech.com/story/johnson-johnson-cashes-out-elan-shares-after-failed-alzheimers-trials/2013-04-18
Kelly Martin has proposed....
http://www.research-store.com/technologynetworks/News/intellect_neurosciences_files_appeal_for_alzheimers_drug?productid=253D5B3D-8DC2-4C3D-A732-558F1B08C214
Yesterday: Sell 100k, Short 416k
There's A Storm Brewing!
WHat's about inovacia.se?
Thanks for sharing!
1,85M and reloading!
I'm still here Ladies and Gentleman!
Seed and reap is the philosophy!
Hey Elis, there was a Xechem law regarding the assets in 2012 (01.04.2012 or 04.01.2012, can't remember) but i can't find it again...
The assets were sold on 24.August 2011...
Biotech Stocks Outperform the S&P 500
A Brief History of Biotechnology
By Brian Hicks
Monday, April 8th, 2013
"We have the means right now to live long enough to live forever. Existing knowledge can be aggressively applied to dramatically slow down aging processes so we can still be in vital health when the more radical life extending therapies from biotechnology and nanotechnology become available."
— Ray Kurzweil
The 19th century French chemist Louis Pasteur is widely regarded as the father of the modern-day biotechnology industry.
If you remember your grade school lesson, Pasteur was a microbiologist worshiped for his breakthroughs in the causes and preventions of diseases.
Pasteur's discoveries reduced mortality from puerperal fever, and he created the first vaccines for rabies and anthrax. But perhaps he's best known for inventing a method to treat milk and wine in order to prevent it from causing sickness, a process called pasteurization.
It may surprise you to learn Pasteur wasn't the first to use biotechnology. In fact, humans have been experimenting with "biotech" processes for thousands of years.
Before I go any further, here's a quick definition: Biotechnology is the use of living systems and organisms to develop or make useful products.
Yeast is probably the best-know unicellular organism in this regard. And of course, you know it's used to make bread and beer. Well, that's biotechnology.
Sounds rather scientific and simple at the same time, doesn't it?
That's because it is...
Nearly 10,000 years ago, humans were producing wine, beer, and bread by using fermentation, a natural process in which the biological activity of one-celled organisms plays a critical role.
It wasn't until the 20th century that the life-changing impact of biotechnology was fully realized, marked by the discovery of antibiotics through biotechnology...
Alexander Fleming discovered the mold Penicillium in 1928. His work led to the purification of the antibiotic penicillin by Howard Florey, Ernst Boris Chain, and Norman Heatley.
In 1940 penicillin became available for medicinal use to treat bacterial infections in humans, and for the next 40 to 50 years, penicillin was the drug of choice to treat a whole host of infections.
The next big milestone for biotechnology came in September 7, 1984, when Amgen went public. On that day, the biotechnology industry changed forever as it ushered in a massive inflow of capital investment for R&D to target the world's deadliest diseases.
Amgen has now returned investors who purchased its stock on that day over 100,000%!
And ever since, investors have tried to find the next Amgen. Because no other sector in the market offers the breathtaking returns biotechnology does.
Think about it like this: What's the cure for cancer worth? Or heart disease, diabetes, obesity?
It goes further than that...
As you read this, biotechs all across America are researching ways to make you live longer with a superior quality of life. They're growing limbs and organs in labs. And they're researching drugs to eradicate some of the most terrifying diseases known to man, like Alzheimer's.
Each of these drugs — if successful — could be worth tens of billions of dollars.
That's the promise of biotechnology.
Etc.
http://www.wealthdaily.com/articles/biotech-stocks-outperform-the-sp-500/4148
The Nobel Prize in Physiology or Medicine 1945
Sir Alexander Fleming, Ernst B. Chain, Sir Howard Florey
Biography
Ernst Boris Chain was born on June 19, 1906, in Berlin, his father, Dr. Michael Chain, being a chemist and industrialist. He was educated at the Luisengymnasium, Berlin, where he soon became interested in chemistry, stimulated by visits to his father's laboratory and factory. He next attended the Friedrich-Wilhelm University, Berlin, where he graduated in chemistry in 1930. He was from an early age interested in biochemistry and after graduation he worked for three years at the Charité Hospital, Berlin, on enzyme research. In 1933, after the access to power of the Nazi regime in Germany, he emigrated to England. Here, his first two years were spent working on phospholipids at the School of Biochemistry, Cambridge, under the direction of Sir Frederick Gowland Hopkins, for whose personality and scientific ability he came to have a great admiration.
In 1935 he was invited to Oxford University where he worked in the Sir William Dunn School of Pathology, becoming, in 1936, demonstrator and lecturer in chemical pathology. In 1948 he was appointed Scientific Director of the International Research Centre for Chemical Microbiology at the Istituto Superiore di Sanità, Rome. He became Professor of Biochemistry at Imperial College, University of London, in 1961, which position he still holds.
His research has covered a wide range of topics in addition to those already detailed. From 1935 to 1939 he worked on snake venoms, tumour metabolism, the mechanism of lysozyme action and the invention and development of methods for biochemical microanalysis. In 1939 he began, with H. W. (now Sir Howard) Florey, a systematic study of antibacterial substances produced by micro-organisms. This led to his best known work, the reinvestigation of penicillin, which had been described by Sir Alexander Fleming nine years earlier, and to the discovery of its chemotherapeutic action. Later he worked on the isolation and elucidation of the chemical structure of penicillin and other natural antibiotics. Since 1948 his research topics have included carbohydrate-amino acid relationship in nervous tissue, a study of the mode of action of insulin, fermentation technology, 6-aminopenicillanic acid and penicillinase-stable penicillins, lysergic acid production in submerged culture, and the isolation of new fungal metabolites.
Professor Chain is author or co-author of many scientific papers and contributor to important monographs on penicillin and antibiotics. He was in 1946 awarded the Silver Berzelius Medal of the Swedish Medical Society, the Pasteur Medal of the Institut Pasteur and of the Societé de Chimie Biologique, and a prize from the Harmsworth Memorial Fund. In 1954 he was awarded the Paul Ehrlich Centenary Prize; in 1957 the Gold Medal for Therapeutics of the Worshipful Society of Apothecaries of London; and in 1962 the Marotta Medal of the Società Chimica Italiana. He was elected a Fellow of the Royal Society in 1949. He holds honorary degrees of the Universities of Liège, Bordeaux, Turin, Paris, La Plata, Cordoba, Brasil, and Montevideo, and is a member or fellow of many learned societies in several countries: these include the Societé Philomatique, Paris; the New York Academy of Medicine; the Accademia dei Lincei and the Accademia dei XL, Rome; the Académie de Médicine, Académie des Sciences, Paris; the Real Academia de Ciencias, Madrid; the Weizmann Institute of Science, Rehovoth, Israel; the National Institute of Sciences, India; the Società Chimica Italiana; and the Finnish Biochemical Society.
He is a Commander of the Légion d'Honneur and Grande Ufficiale al Merito della Repubblica Italiana.
Professor Chain married Dr. Anne Beloff in 1948. They have two sons, Benjamin and Daniel, and one daughter, Judith. Music is one of his recreations.
From Nobel Lectures, Physiology or Medicine 1942-1962, Elsevier Publishing Company, Amsterdam, 1964
This autobiography/biography was written at the time of the award and first published in the book series Les Prix Nobel. It was later edited and republished in Nobel Lectures. To cite this document, always state the source as shown above.
Ernst B. Chain died on August 12, 1979.
http://www.nobelprize.org/nobel_prizes/medicine/laureates/1945/chain-bio.html
ILNS
OX1/OXIGON/VP20629
$126M DEAL
Friedreich's Ataxia is the most prevalent inherited ataxia and affects about one in every 50,000. It affects both males and females equally and is an early-onset ataxia with symptoms usually appearing any age between 5 and 15 years.
AMD $4B MARKET
AD $8B MARKET
Students lead awareness campaign for rare genetic disease,
YellowJackets contribute
By WILLIAM O'BRIEN · Published on April 04, 2013 6:38 AM · Last updated: April 04, 2013 6:09 PM
A semester-long effort to raise awareness and support for research Friedreich’s ataxia, spearheaded by seniors Galen Dole and Sarah Gelbard, is in full swing.
The Friedreich’s Ataxia Research Alliance (FARA) defines the disease as a “debilitating, life-shortening, degenerative neuro-muscular disorder.”
The most common symptoms of include loss of coordination, fatigue, and aggressive scoliosis. The disease, which is quite rare, affects about 1 in 50,000 people in the U.S.
Gelbard, in the hope of leaving her mark at UR, had the idea to start an annual fundraising campaign for Friedreich’s ataxia, a disease that has profoundly impacted the lives of her best friend and friend’s sister, Laura and Sara Ferrarone.
After the passing of 26-year-old Sarah last November, Gelbard’s passion for the cause was renewed. In addition to her fundraising and awareness goals, Gelbard wanted to cheer up her friend Laura.
Gelbard reached out to Dole, hoping that the YellowJackets, of whom Ferrarone was an avid fan, would make a music video of Jason Mraz’s “I Won’t Give Up.”
Unbeknownst to Gelbard, Dole was a prime ally: Dole’s younger sister Marlise also suffers from the disease.
The potential for collaboration put Gelbard’s goals of fundraising and awareness within reach.
Both Gelbard and Dole shared the experience of watching the impact of Friedreich’s ataxia on people they care about.
Dole watched as Marlise progressed from a walker, to a manual wheelchair, to an electric wheelchair. Gelbard shared a similar experience with the Ferrarone sisters.
They both found hope in the fact that their loved ones’ struggle did not impact their personalities and positive spirits.
“It affects coordination but in no way affects the mind,” Dole said.
The pair began collaborating on awareness and fundraising efforts through the webiste GoFundMe.com and social media. They reached out to FARA to find ways to help support and expand the organization’s research, an important undertaking since many researchers do not want to spend the money to study such a rare condition.
“Little stitches make a quilt, [and] little bills will find a cure,” Gelbard explained.
While they saw a gradual response and contributions of “little bills,” they were looking for a way to reach a broader larger population.
Their second round of efforts began with a letter-writing campaign and plans for a benefit concert. Gelbard sent letters to celebrities and politicians ranging from local Rochester officials to President Obama. Dole, along with his fellow YellowJackets, decided to donate the proceeds from their second-semester show, “Concert for a Cure,” taking place Friday, April 5.
Their efforts so far have raised both the awareness and funds they were hoping for. Dole succeeded in getting Friedreich’s ataxia included as part of the biochemistry curriculum at UR. Their fundraising efforts have reached almost $8,000.
In recognition of their efforts, both Dole and Gelbard have been offered positions to work with FARA over the summer.
Dole is optimistic about the impact of their semester-long efforts.
“More people know, more people care, and more can be done,” Dole said.
O’Brien is a member of the class of 2016.
http://www.campustimes.org/2013/04/04/students-lead-awareness-campaign-for-rare-genetic-disease-yellowjackets-contribute/
MY BAGS ARE FULL!
ILNS
" The vast majority of these meetings had to do with the strategic plan I outlined in my letter to you of February 13, 2013: namely, to move forward aggressively with our CONJUMAB-A and tau immunotherapy programs, which have attracted interest from the pharmaceutical industry and institutional investors, especially in Europe."
http://finance.yahoo.com/news/intellect-neurosciences-issues-letter-shareholders-133500705.html
Institutional Investors
Definition
Large organizations (such as banks, finance companies, insurance companies, labor union funds, mutual funds or unit trusts, pension funds) which have considerable cash reserves that need to be invested. Institutional investors are by far the biggest participants in securities trading and their share of stockmarket volumes have consistently grown over the years. For example, on a typical day, about 70 percent of the trading on the NYSE is on the behalf of institutional investors. Because they are considered knowledgeable and strong enough to safeguard their own interests, institutional investors are relatively less restricted by the security regulations designed to protect smaller investors.
http://www.businessdictionary.com/definition/institutional-investors.html
No dumping anymore?
http://finance.yahoo.com/mb/ILNS/
MY BAGS ARE FULL!
.... yes, for a wild ride!
"Our lead program, CONJUMAB-A, offers an important advantage to the AĂź antibodies currently in clinical development for both AD and AMD by several large pharmaceutical companies. This is because those antibodies (e.g. solanezumab, bapineuzumab, gantenerumab, crenzeumab, RN6G and GSK33766A) are designed for a single purpose, namely to clear AĂź, while none act on the important secondary neurotoxic mechanisms, such as oxidative stress that causes most of the damage from AĂź. By contrast, CONJUMAB-A is empowered with a potent antioxidant. An important step in establishing proof-of-principle was the initial data generated through our collaboration with iNovacia to evaluate compounds synthesized by Lonza for Intellect. The data demonstrated the conjugation of the antioxidant molecule to an amino acid does not reduce its antioxidant activity. Pending adequate financial resources, these studies, which are almost complete, will allow us to select a drug candidate to take into development, providing the trigger for us to move forward with LONZA into an expanded manufacturing project, bringing us closer to the submission of an Investigational New Drug application."
http://finance.yahoo.com/news/intellect-neurosciences-issues-letter-shareholders-173223118.html
"Traditionally, ADCs have been used to deliver a cytotoxic payload to kill cancer cells. By contrast, drugs based on CONJUMAB are comprised of antibodies targeting amyloidogenic polypeptides that would be linked chemically to a small molecule that is non-toxic and instead confers cytoprotective properties such as an antioxidant or anti-inflammatory molecule. CONJUMAB-A is comprised of a humanized monoclonal antibody against beta amyloid (AĂź) conjugated to melatonin, a potent antioxidant molecule with anti-amyloidogenic, anti-inflammatory and anti-apoptotic properties with the aim of preventing the accumulation of toxic AĂź in the retina and delivering on-site neuroprotection to reduce geographical atrophy and neovascularization."
http://finance.yahoo.com/news/intellect-neurosciences-present-bio-europe-143500108.html
"When amyloid is removed from brains using vaccines, it doesn't help patients. In fact, patients got slightly worse. This is true in all the studies. Further, when one sees amyloid deposition in the brain, oxidative damage decreases. So there's an inverse correlation. Whether oligomers or fibers, when we see amyloid increased, we see a decrease in the levels of oxidative damage."
http://archive.sciencewatch.com/ana/st/alz2/11junSTAlz2Perr/
Linking Poor Sleep and Alzheimer's
March 23, 2013
Alzheimers linked to poor sleep prior to cognitive problems
(dailyRx News) Poor sleep is linked to a wide range of possible ailments. However, it also works the other way around. Poor sleep can also be a sign that illness is contributing to the bad sleep.
In a recent study, researchers found that individuals with certain proteins in their spinal fluid had poor sleep quality, but not sleep quantity.
These findings suggest that poor sleep could be one symptom indicating possible development of Alzheimer's disease.
This finding does not mean that someone sleeping poorly has Alzheimer's. It means those with a risk of Alzheimer's might want to talk to a doctor if they notice their sleep quality changes.
"Talk to your doctor about sleeping problems."
The study, led by Yo-El S. Ju, MD, of the Department of Neurology at the Washington University School of Medicine in St. Louis, Missouri, aimed to discover whether changes in sleeping patterns might be related to symptoms of Alzheimer's disease.
The researchers tracked the sleep patterns of 145 individuals, all aged 45 and older, including 62 with at least one parent who developed late-onset Alzheimer's disease.
For two weeks, the participants wore actigraphs, devices that tracked their sleep and wake times. The researchers tracked how much time the participants slept in total and the quality of their sleep, based on how much time they spent in bed asleep.
The participants also kept sleep diaries to confirm the numbers and to note any naps.
Then, the researchers took samples of the participants' spinal fluid to look for evidence of beta-amyloid. Beta-amyloid is a molecule that indicates the likely development of Alzheimer's disease.
The researchers found beta-amyloid in 23 percent of the participants (32 individuals). The researchers then compared these individuals' sleep patterns with the patterns of those without beta-amyloid.
The participants with beta-amyloid deposits in their spinal fluid had worse sleep quality than those who did not have the amyloid deposits, though by only a small amount.
The sleep efficiency of those with the beta-amyloid deposits was about 80.4 percent. The sleep efficiency of those without the deposits was about 83.7 percent.
In particular, those who had sleep quality/efficiency percentages below 75 percent were more than five times more likely to have "preclinical" Alzheimer's disease.
"Preclinical" refers to having the deposits but not showing outward symptoms of the disease.
These differences held true after the researchers made adjustments to account for the participants' age and sex and whether the participants carried a particular genetic marker for Alzheimer's.
The total amount of sleep among the participants was not different, regardless of whether they had beta-amyloid deposits or not.
However, 31 percent of those with the deposits took naps three or more days a week, compared to only 15 percent of those who did not have the deposits.
The researchers therefore concluded that having beta-amyloid deposits – which indicates an early stage of Alzheimer's disease before the clinical symptoms of cognitive problems show up – is associated with poor sleep. However, having the deposits is not linked to getting less sleep.
The study was published March 11 in the journal JAMA Neurology. The research was funded by the National Institutes of Health and the Ellison Medical Foundation Senior Scholar Award.
One author has consulted for Jazz Pharmaceuticals and received research support from UCB. Another author is involved in clinical trials related to medications for dementia which are sponsored by Janssen Alzheimer Immunotherapy Program and Pfizer. He has also received consulting or speaking fees from seven other pharmaceutical companies.
http://www.dailyrx.com/alzheimers-linked-poor-sleep-prior-cognitive-problems
Viropharma Inc (NASDAQ:VPHM): Are Hedge Funds Right About This Stock?
By RONALD JAY SY in News
Published: March 22, 2013 at 10:17 pm
Viropharma Inc (NASDAQ:VPHM) has experienced an increase in support from the world's most elite money managers recently.
To the average investor, there are many indicators shareholders can use to monitor publicly traded companies. A duo of the most useful are hedge fund and insider trading interest. At Insider Monkey, our research analyses have shown that, historically, those who follow the best picks of the top fund managers can outpace the S&P 500 by a significant amount (see just how much).
Equally as important, bullish insider trading sentiment is another way to parse down the marketplace. Just as you'd expect, there are many incentives for an upper level exec to sell shares of his or her company, but only one, very obvious reason why they would initiate a purchase. Several academic studies have demonstrated the impressive potential of this method if shareholders know what to do (learn more here).
With these "truths" under our belt, we're going to take a glance at the key action surrounding Viropharma Inc (NASDAQ:VPHM).
Hedge fund activity in Viropharma Inc (NASDAQ:VPHM)
Heading into 2013, a total of 20 of the hedge funds we track were long in this stock, a change of 11% from one quarter earlier. With hedgies' sentiment swirling, there exists a few noteworthy hedge fund managers who were increasing their holdings meaningfully.
Of the funds we track, Julian Baker and Felix Baker's Baker Bros. Advisors had the most valuable position in Viropharma Inc (NASDAQ:VPHM), worth close to $205 million, accounting for 5.4% of its total 13F portfolio. Coming in second is William Leland Edwards of Palo Alto Investors, with a $87 million position; 0.1% of its 13F portfolio is allocated to the company. Other hedgies that hold long positions include Israel Englander's Millennium Management, Ken Griffin's Citadel Investment Group and Sean Cullinan's Point State Capital.
Consequently, key money managers were leading the bulls' herd. Columbus Circle Investors, managed by Donald Chiboucis, created the biggest position in Viropharma Inc (NASDAQ:VPHM). Columbus Circle Investors had 10 million invested in the company at the end of the quarter. Jim Simons's Renaissance Technologies also initiated a $6 million position during the quarter. The other funds with new positions in the stock are Mike Vranos's Ellington, Charles Davidson's Wexford Capital, and David Harding's Winton Capital Management.
What do corporate executives and insiders think about Viropharma Inc (NASDAQ:VPHM)?
Insider buying is best served when the company we're looking at has experienced transactions within the past 180 days. Over the latest half-year time frame, Viropharma Inc (NASDAQ:VPHM) has experienced 1 unique insiders purchasing, and 5 insider sales (see the details of insider trades here).
With the results exhibited by the aforementioned tactics, retail investors must always keep an eye on hedge fund and insider trading sentiment, and Viropharma Inc (NASDAQ:VPHM) applies perfectly to this mantra.
http://www.insidermonkey.com/blog/viropharma-inc-nasdaqvphm-are-hedge-funds-right-about-this-stock-95537/
It's Time to buy ILNS!
Alla scoperte dei titoli speculativi del mercato OTC: Oggi tocca a Intellect Neurosciences (ILNS.PK)
Scritto il 20 marzo 2013
Raccolgo sempre molto volentieri le segnalazione dei vari titoli biotech, sopratutto di aziende che non conosco. L’amico Franco mi segnala due company quotate nel mercato OTC. Raccogliere informazioni in questo mercato diventa a volte complicato, sopratutto avere aggiornamenti e opinioni magari da chi ne capisce più di noi.
Iniziamo con la prima segnalazione ovvero Intellect Neurosciences, Inc. (ILNS.PK) (OTCBB:ILNS). Come segnalava non ricordo più chi sul blog che fine fanno le scoperte che spesso sentiamo ai telegiornali di vaccini, molecole o meccanismi innovativi?. Spesso si rivelano dei buchi nell’acqua altre invece danno l’inizio a studi clinici o interessamento da parte di qualche grossa biotech che fiuta “l’affare”.
Potremmo dire che forse questo potrebbe essere il caso dell’azienda oggetto dell’articolo di oggi. Partiamo non dall’inizio ma dalla fine. Proprio nel mese di Marzo il ceo dell’azienda è stato impegnato in alcune conference a Barcelona al Centre Convencions Internacional e a Firenze all’ 11th Annual Conference on Alzheimer’s disease and Parkinson’s disease.
Vediamo cosa ci dice il ceo “”Abbiamo scoperto un nuovo modo per attaccare alcuni tipi di malattie complesse mediante l’uso di anticorpi coniugati in cui due molecole diverse – un anticorpo rivolto ad un polipeptide amiloidogenica e una piccola molecola neuroprotettiva – sono combinati chimicamente in un’unica entità,” ha detto il dottor Daniel Chain, l’inventore del CONJUMAB. “L’anticorpo ha un chaperone-like (esiste non è una parolaccia) ruolo nel tenere la amiloide mentre la piccola molecola riduce la neurotossicità causata dal peptide. Il nostro farmaco CONJUMAB-A, capitalizza recenti intuizioni che collegano i meccanismi che contribuiscono alla patogenesi di AMD e malattia di Alzheimer , in particolare il ruolo di stress ossidativo e beta amiloide (a ²) che si ritiene essere un mediatore fondamentale nella progressione della AMD secca a AMD umida (con AMD parliamo di maculopatie degenerative).
L’amico Franco che è stato davvero professionale mi ha mandato diversi link. Il primo riguarda la pipeline davvero interessante con tre farmaci e con diversi partner ma solo uno può portare $, al momento, ovvero l’accordo con Viropharma. Il farmaco in questione è il VP 20629 (OX1 or indole-3-propionic acid (IPA) per la malattia friedreich’s ataxia. Per chi non conoscesse Viropharma (VPHM) vi posso dire che è un ottima azienda che si muove bene nel mondo biotech e che ha alcuni farmaci già approvati (che vendono) e altri promettenti in sviluppo.
ViroPharma is conducting Phase 2-enabling toxicology studies with VP 20629; the company expects to initiate Phase 2 clinical testing in late 2012/early 2013. Questo è il farmaco che ci interessa.
Intellect could receive in excess of $100 million in milestone payments from ViroPharma and, if approved, royalties from sales over many years. Viropharma ha già pagato 6,5 M di $. E’ vero il mercato per questa malattia non è grosso, è una malattia ereditaria che a oggi non ha una cura però i 100 M di $ che l’azienda potrebbe ottenere sono a vari raggiungimenti di obbiettivi e poi vi è una parte legata alle vendite del farmaco. Mi pare un ottimo accordo.
L’azienda ha inoltre un accordo con Lonza azienda quotata nel mercato svizzero per il farmaco CONJUMAB-A che abbiamo visto all’inizio dell’articolo. In base a questo accordo Lonza ha un opzione per il futuro sviluppo e la produzione del farmaco anticorpo coniugato CONJUMAB-A.
Per il momento direi di fermarmi qui. Ho altro materiale da analizzare, ma si possono già tirare delle conclusioni. L’azienda non è in grado di portare avanti sviluppi clinici con i propri mezzi e quindi cerca di vendere le proprie molecole ad altri. L’accordo con Viropharma è un ottimo accordo che potrebbe portare nelle casse dell’azienda diversi dollari.
Per concludere tenendo conto della quotazione di ieri 0.0093$, e della capitalizzazione bassa ( circa 1M di $) ogni buona notizia che arriva da Viropharma può far esplodere la quotazione di Intellect Neurosciences . Il farmaco ha da poco iniziato la phase 2. Non sappiamo quando arriveranno altri soldi alla piccola azienda, di solito il grosso arriva alla fine della phase 3 e alla commercializzazione ma ci vorranno anni. Quindi per chi ha una piccola somma da poter puntare e dimenticandosela per anni potrebbe essere una buona giocata speculativa. A voi.
http://finanzanostop.finanza.com/2013/03/20/alla-scoperte-dei-titoli-speculativi-del-mercato-otc-oggi-tocca-a-intellect-neurosciences-ilns-pk/
I strongly agree! :)
How stress triggers Alzheimer's disease decoded
18 MAR, 2013, 02.37PM IST, PTI
LONDON: Chronic stress elevates steroids in the brain which inhibit cognitive activity and lead to an increased risk for Alzheimer's disease, a new study has found.
Researchers from Umea University, Sweden found that chronically elevated levels of allopregnanolone, a steroid seen in the brain during stress, accelerated Alzheimer's in two mice models.
The Alzheimer's mice responded with impaired learning and memory. They had also increased brain levels of beta-amyloids, the proteins that form plaques in Alzheimer's disease.
Alzheimer's is a neurodegenerative disease that destroys brain cells. Symptoms include having difficulty remembering things, making decisions and performing everyday activities.
One of the hallmarks of the disease is the accumulation of protein amyloid plaques between nerve cells in the brain.
Beta-amyloid is a protein fragment that normally is broken down and eliminated in a healthy brain. With Alzheimer's, these fragments form hard, insoluble plaques.
The study found that high levels of beta-amyloids corresponded to dysfunction among brain synapses, the connections between nerve cells.
This was seen after a period of chronically elevated levels of allopregnanolone, but not after placebo treatment.
The effects were identified early in the disease development when the animals normally have intact memory function.
http://economictimes.indiatimes.com/news/news-by-industry/et-cetera/how-stress-triggers-alzheimers-disease-decoded/articleshow/19034869.cms
GEORGE PERRY ON THE ROLE OF OXIDATIVE STRESS IN ALZHEIMER'S DISEASE
SPECIAL TOPIC OF ALZHEIMER'S DISEASE INTERVIEW, JUNE 2011
According to our Special Topics analysis on Alzheimer's Disease, the work of Dr. George Perry ranks at #2 by total papers and #7 by total cites, based on 292 papers cited a total of 11,180 times during the analysis period. Two of these papers appear on the top 20 papers lists.
Perry's work also ranked among the top 20 in our 2003 Special Topic on Alzheimer's, ranking at #2 by papers, #11 by cites, and #5 by cites/paper based on 164 papers cited a total of 4,572 times. His work also appears among the top 1% of scientists in the fields of Neuroscience & Behavior, Biology & Biochemistry, Clinical Medicine, and Pharmacology & Toxicology in Essential Science IndicatorsSM from Thomson Reuters.
Perry is Dean of Sciences and Professor of Biology at the University of Texas at San Antonio. He is a former President for the American Association of Neuropathologists, and the Editor-in-Chief of the Journal of Alzheimer's Disease, as well as on the editorial board of over 150 other journals.
BELOW, HE TALKS WITH SCIENCEWATCH.COM CORRESPONDENT GARY TAUBES ABOUT HIS HIGHLY CITED WORK IN ALZHEIMER'S.
By studying the role of oxidative stress in Alzheimer's disease, you are one of the few highly cited researchers not focusing on amyloid or tau. What is it about your approach that has led you off the beaten track in this field?
I have a pretty diverse background, and it plays a major role in the way I approach problems. I was trained initially as a classical biologist with a strong emphasis in chemistry. I was very interested in understanding environmental biochemistry, and I ended up working with sea urchins as a model system. I did a post-doctoral fellowship in cell biology and there I learned more about applied research. I was studying cytoskeletal abnormalities in disease processes.
Why cytoskeletal abnormalities?
From the late 1970s to the early 1990s, there was a lot of interest in calcium regulating oxidative stress and cytoskeletal interactions. So I moved from oxidative stress to the cytoskeleton because of this calcium link. When I was looking for a faculty position, I got employed because of my understanding of the cytoskeleton. And that is how I got into Alzheimer's disease.
The actual work I do isn't that different from what I used to do in marine biology. It's just that I don't do work in marine organisms anymore; I work in the human brain. But because I was trained as a marine biologist and not a biologist studying marine organisms, this made a difference in how I approach problems.
How would you define that difference?
Annual reception honoring recipients of scholarships in the College of Sciences. View additional images of this event.
It has to do with whether you understand organisms in the context of their environment. If you go to a zoo and see a tiger and you go to India and see a tiger, you're seeing a tiger in both cases. But the only time you really appreciate a tiger as an organism is when you go to India. Organisms respond to the context they're in. It's true for people, too. And that's relevant to how one thinks about Alzheimer's. People develop these changes in their brains as they get older. They're not just imposed by genes.
Are you implying that the environment plays a major factor in influencing the disease process?
There are environmental influences, but the important point is that people's brains change as they get older all the time. As you get older in life, you realize you're not the same person you were when you were young. I don't mean you're the same but diminished. You're different. Everything is changed.
A lot of my work relates to the biology of Alzheimer's disease. That's been the central focus. Even though the publications are about oxidative stress, they're related to what type of changes people undergo as they get older and how they adjust during Alzheimer's disease.
Is oxidative stress a by-product of the disease process?
Some of it is, but not all of it, because we see it in everybody after the age of 35.
Is oxidative stress the earliest event you see in Alzheimer's disease?
It's one of the earliest events. It occurs prior to disease initiation, prior to the onset of symptoms. And during mild cognitive impairment, oxidative damage is actually higher than later in Alzheimer's disease. Although we haven't published that observation yet.
So you don't think amyloid accumulation triggers the disease process as Dennis Selkoe suggests?
His view and ours are diametrically opposite.
OK, tell us yours.
Ours is that amyloid is a response to the disease, not the cause of the disease. Amyloid is not irrelevant. It's very, very important. So I don't differ from Dennis in that sense, because we both believe amyloid is important.
Why? There are several reasons. One is vaccines. When amyloid is removed from brains using vaccines, it doesn't help patients. In fact, patients got slightly worse. This is true in all the studies. Further, when one sees amyloid deposition in the brain, oxidative damage decreases. So there's an inverse correlation. Whether oligomers or fibers, when we see amyloid increased, we see a decrease in the levels of oxidative damage. One important mechanism for amyloid's apparent antioxidant activity is that it binds copper and redox silences it.
With my colleague Mark A. Smith, also a highly cited person who unfortunately died in December, we've written probably about 100 publications questioning the amyloid-cascade hypothesis.
"If I had to make one guess at this point, I'd say Alzheimer's disease is a metabolic disease."
The amyloid cascade hypothesis is a very simplistic view that was useful to consolidate many observations under testable hypotheses. Failure of those tests has now put the hypothesis in question. Unfortunately the cascade hypothesis is fundamentally an abiological concept. It goes against evolutionary selection; it does so by proposing a well-adjusted organism would produce a response that has but a detrimental effect. For a response to develop in the body it must have some adaptive value.
So you're presuming it's a response to oxidative stress?
Exactly. I'm proposing amyloid is an adaptive response, based on some of what we already discussed.
That oxidative stress goes down when amyloid accumulation goes up?
That's one—oxidative stress goes down when amyloid goes up, and when we remove amyloid people actually get worse. Again, I'm not proposing the amyloid is irrelevant. And we're not the only ones who question the amyloid cascade hypothesis. Many people do. Most say it's secondary. Some say it's irrelevant. I think it's a critical part of the disease process, but not the trigger.
So your hypothesis would be that oxidative stress triggers the disease process?
Not exactly. Our hypothesis is that oxidative stress is a window for looking at the disease, just as amyloid is also a window. People elicit a number of responses as Alzheimer's develops. The key thing to determine is where the oxidative stress originates. There has to be an abnormality that predates oxidative damage. Amyloid is not the primary abnormality because amyloid, if anything, reduces oxidative stress.
http://archive.sciencewatch.com/ana/st/alz2/11junSTAlz2Perr/
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