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Category Archives: Parkinson’s Treatment
Posted: September 7, 2017 at 5:47 pm
Researchers have found evidence that an antidepressant drug could slow progression of Parkinsons disease.
A study by Michigan State University discovered that a drug – nortriptyline – can stop the growth of abnormal proteins that can build up in the brain.
The drug has been around for more than 50 years and is used to treat depression and nerve pain.
However, scientists believe it could have a new purpose.
Depression is a very frequent condition associated with Parkinson’s, so we became interested in whether an antidepressant could modify how the disease progresses,” said Tim Collier, lead study author of the research published in the journal Neurobiology of Disease.
Scientists looked at whether patients who had been on antidepressants needed to go on standard Parkinsons treatment later than people who hadnt used antidepressants.
Parkinsons sufferers are commonly prescribed a therapy called levodopa.
It increases levels of dopamine, which is a natural chemical in the body that sends signals to other nerve cells.
The disease can cause levels of dopamine to significantly decrease.
“We found that those on a certain class of antidepressant, called tricyclics, didn’t need the levodopa therapy until much later compared to those who weren’t on that type of antidepressant medication,” said Collier.
They discovered that the antidepressant decreased the amount of abnormal protein build up in the brain in rats.
The protein – called alpha-synuclein – can cause the brain’s nerve cells to die when in a clustered state.
Researchers believe that understanding how these proteins clump together could help them develop other drugs for Parkinsons.
“What we’ve essentially shown is that an already FDA-approved drug that’s been studied over 50 years and is relatively well tolerated could be a much simpler approach to treating the disease itself, not just the symptoms,” added Collier.
In the future they hope to test the antidepressant drug in a human clinical trial.
Parkinsons disease affects 127,000 people in the UK.
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Parkinson’s disease cure: THIS common drug could slow progression of condition – Express.co.uk
Posted: at 5:47 pm
The brain chemical missing in Parkinsons disease may have a hand in its own death. Dopamine, the neurotransmitter that helps keep body movements fluid, can kick off a toxic chain reaction that ultimately kills the nerve cells that make it, a new study suggests.
By studying lab dishes of human nerve cells, or neurons, derived from Parkinsons patients, researchers found that a harmful form of dopamine can inflict damage on cells in multiple ways. The result, published online September 7 in Science, brings multiple pieces of the puzzle together, says neuroscientist Teresa Hastings of the University of Pittsburgh School of Medicine.
The finding also hints at a potential treatment for the estimated 10 million people worldwide with Parkinsons: Less cellular damage occurred when some of the neurons were treated early on with antioxidants, molecules that can scoop up harmful chemicals inside cells.
Study coauthor Dimitri Krainc, a neurologist and neuroscientist at Northwestern University Feinberg School of Medicine in Chicago, and colleagues took skin biopsies from healthy people and people with one of two types of Parkinsons disease, inherited or spontaneously arising. The researchers then coaxed these skin cells into becoming dopamine-producing neurons. These cells were similar to those found in the substantia nigra, the movement-related region of the brain that degenerates in Parkinsons.
After neurons carrying a mutation that causes the inherited form of Parkinsons had grown in a dish for 70 days, the researchers noticed some worrisome changes in the cells mitochondria. Levels of a harmful form of dopamine known as oxidized dopamine began rising in these energy-producing organelles, reaching high levels by day 150. Neurons derived from people with the more common, sporadic form of Parkinsons showed a similar increase but later, beginning at day 150. Cells derived from healthy people didnt accumulate oxidized dopamine.
This dangerous form of dopamine seemed to kick off other types of cellular trouble. Defects in the cells lysosomes, cellular cleanup machines, soon followed. So did the accumulation of a protein called alpha-synuclein, which is known to play a big role in Parkinsons disease.
Those findings are direct experimental evidence from human cells that the very chemical lost in Parkinsons disease contributes to its own demise, says analytical neurochemist Dominic Hare, of the University of Technology Sydney. Because these cells churn out dopamine, they are more susceptible to dopamines potential destructive forces, he says.
When researchers treated neurons carrying a mutation that causes inherited Parkinsons with several different types of antioxidants, the damage was lessened. To work in people, antioxidants would need to cross the blood-brain barrier, a difficult task, and reach the mitochondria in the brain. And this would need to happen early, probably even before symptoms appear, Krainc says.
Without this human model, we would not have been able to untangle the pathway, Krainc says. In dishes of mouse neurons with Parkinsons-related mutations, dopamine didnt kick off the same toxic cascade, a difference that might be due to human neurons containing more dopamine than mice neurons. Dopamine-producing neurons in mice and people have some very fundamental differences, Krainc says. And those differences might help explain why discoveries in mice havent translated to treatments for people with Parkinsons, he says.
Over the past few decades, scientists have been accumulating evidence that oxidized dopamine can contribute to Parkinsons disease, Hastings says. Given that knowledge, the new results are expected, she says, but still welcome confirmation of the idea.
These toxic cellular events occurred in lab dishes, not actual brains. Cell cultures arent the perfect re-creation of whats going on in the human brain, Hare cautions. But these types of experiments are the next best thing for monitoring the chemical changes in these neurons, he says.
Sumitomo Dainippon Seeks Japanese Approval for Trerief to Treat Parkinsonism in Dementia Patients – Parkinson’s News Today
Posted: at 5:47 pm
Sumitomo Dainippon Pharma has asked Japanese authorities to approve itsTrerief (zonisamide) as a new therapy for parkinsonismin dementia patients with Lewy bodies, the company announced in a press release.
Trerief went on sale in Japan in March 2009 as a treatment for Parkinsonspatients who saw insufficient results with levodopa and other Parkinsons-specific drugs. After a 2013 expansion of its originalapproval, Trerief is now accepted as a treatment option inJapan, where a2014 Patient Surveyreported some144,000 patients suffering from vascular dementia and unspecified dementia,including dementia with Lewes bodies (DLB).
Parkinsonism is a general term used to describe a group of neurological disorders that cause movement problems similar to those observed in Parkinsons disease, like tremors, slow movement and stiffness.
The DLB form of dementia causes progressive cognitive impairment. Parkinsonism is one of the four core features of DLB, alongside fluctuating cognition, recurrent visual hallucinations and rapid eye movement (REM) sleep behavior disorder.
DLB is classified as part of the Lewy body disease spectrum, which also includes Parkinsons disease. Since symptoms of parkinsonism virtually mimic those of Parkinsons disease, Sumitomo Dainippon is now seeking approval for Trerief as another therapeutic option for treating parkinsonism in DLB, under the assumption that its action will be equally effective.
If approved, Trerief will be the worlds first drug to treatparkinsonism in DLB. Sumitomo Sainipponbased its application on data from a Phase 3, multicenter, placebo-controlled, randomized, double-blind, 12-week study of Trerief in patients with parkinsonism accompanying DLB. Topline results were disclosed in early April.
The study evaluated the efficacy and safety of Trerief in 351 patients randomized to receive the active compound at 25 mg/daily, 50 mg/daily, or placebo.
Using the Unified Parkinsons Disease Rating Scale a rating scale thatmeasures disability and impairment in Parkinsons and also the primary outcome measure in most clinical trials of Parkinsons therapeutics the primary endpoint of the study at 12 weeks was significantly higherin the groups receiving Trerief, compared to placebo.
According to the April report of topline results, the incidence of treatment emergent adverse effects was no different than those previously reported. Incidence at 25 mg/daily was 48.7 percent, rising to 54.5 percent at 50 mg/daily, while in the placebo group, it was 47.1 percent.
Posted: September 5, 2017 at 9:42 pm
(Left to right): Heidi and Hans-Juergen Koch/Minden Pictures; Zephyr/Science Source; Robert Blanken
By Giorgia GuglielmiSep. 1, 2017 , 3:05 PM
Something is changing the sex of Costa Rican crocodiles
After probing and peering at the genitalia of nearly 500 crocodiles in Palo Verde, Costa Rica, a team of ecologists found something odd: The sex ratio was way out of whack, with males outnumbering females four to one among hatchling crocs. The researcherslater discovered that the animals tissues are tainted with a synthetic hormone that may be causing them to switch sex.
Anti-inflammatory cuts risk of heart attack
A clinical trial of more than 10,000 heart attack patients supports a novel way to protect them from a stroke or a second attack: with drugs that stop inflammation. The approach has been advanced by some scientists for years, but this is the first trial to conclusively show that it works. Cardiologists hailed the study, reported this week, as vindication for the heart attackinflammation link, which hadnt been provedin people.
Modified T cells that attack leukemia become first gene therapy approved in the United States
The U.S. Food and Drug Administration this week approved a new cancer therapy that involves genetically modifying a patients immune cells to kill leukemia cells. The therapy, developed by the pharma giant Novartis, is the first such treatment to be approved in the United States.
Asthma drug may thwart Parkinsons disease
When people with asthma have trouble breathing, they may reach for an inhaler containing salbutamol, a drug that expands the airways. Salbutamol may have another beneficial effectprotecting against Parkinsons disease. Individuals who inhaled the highest doses of salbutamol were about half as likely to develop the devastating neurological condition as those who didnt take the drug, a new study reveals.
Why some baby bees are destined to become workersor queens
The saying you are what you eat is particularly true for female honey bees, which grow up to be either small, sterile workers or large, fertile queens depending on their diet. Previously, researchers thought that something in the food fed to young queensa secretion called royal jellywas what made the difference. Now, a study suggests its signaling molecules in the grub of young worker bees that keeps their sexual development in check.
Originally posted here:
Top stories: Why Costa Rica’s crocodiles are changing sex and an … – Science Magazine
Posted: September 3, 2017 at 8:46 am
A treatment that could reverse some of the main symptoms of Parkinsons disease potentially enabling patients to recover enough control of their movements to play tennis is set to be trialled in humans for the first time.
In what was described as a major leap forward, scientists in Japan managed to significantly improve the condition of monkeys given an artificially induced version of the disease.
They did this by taking tissue from adult humans and turning it into stem cells, which are capable of becomingany kind of cell. These were then used to create new brain cells in the monkeys, with dramatic results.
Parkinsons involves a progressive loss of brain cells that release a chemical called dopamine, causing the trademark uncontrollable shaking and loss of balance.
The success of the experiment raises hopes of reproducing astonishing results achieved by transplanting brain tissue from foetuses into Parkinsons patients in the 1990s. This appeared to be hugely successful, until major sideeffects were discovered and the trials had to be stopped.
The scientists in Japan monitored the monkeys for signs of cancer and other feared sideeffects, but have concluded it was now safe to proceed to clinical trials in people.
Writing in the journal Nature, the researchers said they had found a 40 to 55 per cent improvement in the motor skills of the monkeys after the new brain cells were transplanted.
One of the scientists, Professor Jun Takahashiof Kyoto University, said the treatment had helped the monkeys movementcontrol and balance.
Judging from our data and previous clinical trials using foetal mid-brain tissues, I think a stem cell-based therapy is effective for Parkinsons disease, he told The Independent in an email.
However, Parkinsons disease also causes dementia and cognitive problems.
In this study, we did not evaluate their memory, because memory function is not deteriorated in this [disease] model. So, I have no idea about the effect of this therapy on memory function, Professor Takahashi said.
Asked how close science was to a complete cure, he said: It depends on the definition of complete cure. A stem cell-based therapy can replace lost neurons, but cannot delete a cause of the disease.
If somebody finds the way to delete the cause of the disease and a stem cell-therapy is combined, it will be a complete cure.
Dr Tilo Kunath, of Edinburgh University, said the extremely promising research demonstrated that a safe and highly effective cell therapy for Parkinsons can be produced in the lab.
Asked what it would mean if it worked as well in human as in the monkeys, he said: I think it would be a huge deal for the patients that it works for. It would be the first therapy that can reverse symptoms and reduce the need for medication.
I think people are not wanting to call it a cure because Parkinsons is still ongoing, and still can cause a lot of the non-motor problems such as cognitive decline and dementia, but serious motor symptoms can be solved with this.
The patients that had foetal grafts in the 1990s, where it worked well;the patients lives were transformed, they got their lives back and could do a lot of things play tennis.
But some of them ended up in disaster very serious sideeffects. Foetal grafts had to stop because of sideeffects that made patients worse.
Professor David Dexter, director of the Parkinsons UK Tissue Bank, sounded a similarly optimistic note.
Stem cells and talk about cures for Parkinsons have been around for a long period of time, but this is now a major leap forward, he said.
For the first time, patient-derived stem cells from healthy volunteers, and also from people affected by Parkinsons, have been transplanted into a primate model of Parkinsons. In the past, stem cells have been plagued by a number of problems.
It had been thought that a patients own cells could be reprogrammed to become stem cells and then replacement brain cells, but doing this on an individual basis has proved prohibitively expensive.
Instead, Professor Dexter said it was thought that a bank of cells could be built up from about 150 people who were a good match for some 90 per cent of the UK population.
This would mean patients would probably have to take immune suppressing drugs. One sideeffect in the trial involving monkeys was a very mild immune response.
Professor Tom Foltynie, a consultant at the UKs National Hospital for Neurology & Neurosurgery, said the study provided reassurance that brain cells made from stem cells could survive and function for a significant period after they were transplanted.
Most importantly, the team found no evidence for tumour development, at least until the two-year time point, he said.
However, Professor Foltynie cautioned that the model of Parkinsons created in the monkeys did not get progressively worse as the real disease does in humans.
As such, there will be concerns about how transplants might fare in the long term in humans with Parkinsons disease, which was also the case for the previous foetal cell trials, although long-term improvements in movement have been previously reported in two patients who had foetal cell transplants in the 1990s, he said.
Overall, the results they report in the shortterm are encouraging, and provide some reassurance that these cells can function as sources of dopamine to address those movement symptoms of Parkinsons disease that relate to dopamine loss.
Noone expects that transplants will address the non-dopamine, non-movement aspects of Parkinsons disease, such as dementia and falls, which ultimately emerge with very long-term follow up.
However, by conducting this research, the authors have confronted most of the major issues associated with the development of a cell therapy for Parkinsons disease its safety, the main factors predictive of efficacy,andthe availability of adequate tissue.
Current medications can only help manage the symptoms of the disease.
Parkinsons UKs website says: We dont yet have any treatments that can cure, slow, stop or reverse the progression of Parkinsons. This means the condition continues to progress as do the symptoms and side effects of taking more medication.
An Advance in Treatment of Parkinson’s Disease | American Council … – American Council on Science and Health
Posted: September 1, 2017 at 6:49 pm
Parkinsons disease can be very visible; one need only think of Mohammed Ali or Michael J Fox. But in terms of commanding our medical and economic attention is seems to be more of an orphan disease. It affects approximately 1 million Americans, dwarfed heart disease that affects 28.4 million or diabetes affected 29 million. So this weeks major advance in treating Parkinsons may have been overlooked in the media. The FDA has approved amantadine  in a new formulation for the dyskinesia in Parkinsons patients based on a Phase 3 study reported in JAMA Neurology. The study was a randomized, double-blind, placebo controlled it doesnt get much better, that demonstrated
Lets unpack some of what they found. Parkinsons Disease is a degenerative disease of the central nervous system that primarily affects motor nerves. It manifests itself with rigidity, shaking and a general slowing of movement. It is, in some ways being trapped in a body that doesnt respond well to commands and as a consequence can increase depression and anxiety in patients. It’s cause is unknown and involves the usual suspects, genetics and the environment. With no cure available, symptomatic relief is the only relief possible. Parkinsons is manifested on brain imaging by the death of cells in the midbrain  resulting in a deficiency of dopamine. For that reason, treatment involves supplying L-Dopa and when that begins to lose efficacy, adding dopamine agonists (drugs that act similarly to dopamine).
In a typical day, a Parkinsons patient may be symptom-free for eight hours, with an additional four hours when the symptoms are present but there is good benefit. Amantadine in its new extended release form increased the symptom-free time by 4 hours, 50%. That is a big deal from a functional point of view.
As with any medication, there are side effects. In this instance, the most common (seen in greater than 10% of patients and greater than in the placebo group) were hallucinations, dizziness, dry mouth, peripheral edema, constipation, falls, and orthostatic hypotension. 20% of patients stopped the medication because of these side effects indicating that the new therapy may not help all patients.
On line pricing for generic fast acting, amantadine runs between $1-3.00 per day, pricing for the reformulated version has not been released. Heres hoping that we will see a fair price and not some of the recent profiteering that has brought media attention and headlines.
 Amantadine was initially approved as an anti-viral medication, and its use in nursing homes serendipitously uncovered its impact upon the dyskinesia of Parkinsons.
 More specifically the substantia nigra, an area involved in eye movement, motor function, and interestingly enough, learning and addiction.
UPDATE: Acorda Therapeutics shares crater 26% premarket after FDA rejects application for Parkinson’s treatment – MarketWatch
Posted: at 6:49 pm
Acorda Therapeutics Inc. shares ACOR, +4.33% slid 26% premarket Tuesday, after the company said it has received a Refusal to File letter from the U.S. Food and Drug Administration regarding its new drug application for inbrija, an investigational treatment for symptoms of Parkinson’s disease. The FDA said the NDA was not complete enough to permit a substantive review. Specifically, it questioned the date by which the manufacturing site would be ready for inspection, as well as the submission of the drug master production record. The company said it will seek a meeting with the FDA and that it believes the issues can be addressed. “We will work with the FDA as quickly as possible to address the open issues and to clarify the path to successfully re-file our application,” Chief Executive Ron Cohen said in a statement. “We remain confident in INBRIJA’s data package and its promise as an important new therapy for people with Parkinson’s disease.” Shares have gained 37% in 2017, while the S&P 500 SPX, +0.20% has gained 9%.
Posted: at 6:49 pm
A collaboration has been announced between AstraZeneca and Takeda Pharmaceutical Company for the development and commercialisation of an alpha-synuclein antibody, MEDI1341, as a potential treatment for Parkinsons disease.
Today there are no medicines that can slow or halt the degenerative progress of Parkinson’s disease so this remains a large area of unmet medical need, emphasized Mene Pangalos, executive vice president, Innovative Medicines & Early Development Biotech Unit and Global Business Development at AstraZeneca. Takeda has an excellent track record in neuroscience research and we are excited to be working together. By combining our scientific expertise and sharing the risks and cost of development, we hope to accelerate the advancement of MEDI1341 as a promising new approach to support the treatment of people with Parkinsons disease around the world.
Despite modest advancements in maintenance therapies, Parkinsons disease continues to represent a devastating diagnosis and a burdensome challenge for therapeutic discovery, added Emiliangelo Ratti, head, Global CNS Therapeutic Area Unit, Takeda. Our collaboration with AstraZeneca is a sophisticated one that will enable us to efficiently advance a validated target in a new modality, with the aim of improving the lives of patients.
MEDI1341 is an antibody that has a lower interaction with the immune system and is differentiated from other alpha-synuclein antibodies as is reported to have the potential to offer a better efficacy and safety profile. It is due to enter Phase I clinical trials later this year.
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Collaboration announced for development of Parkinson’s treatment – EPM Magazine
Titan to Start Phase 1/2 Study of Subdermal Implant to Deliver Requip to Parkinson’s Patients – Parkinson’s News Today
Posted: at 6:49 pm
The U.S. Food and Drug Administration (FDA) has given a green light to Titan Pharmaceuticals to begin a first-in-human clinical trial testing an implant that provides continuous release of ropinirole to treatParkinsons signs and symptoms.
In the open-labelPhase 1/2 trial (NCT03250117), which is nowrecruiting, roughly 20 Parkinsons disease patients taking levodopa along with oral ropinirole (marketed as Requip) will be switched to the subdermal, or under the skin, implant for three months. They will continue using levodopa.
This study will measure how muchropiniroleis released in the blood during the three months, and evaluate possibleside effects caused by the new drug delivery route. It will also look for evidenceof treatment efficacy through changes inthe severity of Parkinsons disease in participants. The trial will take place at three or more U.S. sites, although only one in Michigan is currently registered.
New treatments that offer continuous delivery of medication providing non-pulsatile stimulation of dopamine receptors in the brain appear to have some advantages over oral formulations, Dr.Aaron Ellenbogenof the Michigan Institute of Neurological Disorders said in a press release.
The ProNeura implants with ropinirole could potentially offer an important treatment option for continuous drug delivery that overcomes the fluctuating drug levels associated with oral administration of ropinirole, and we look forward to conducting this study, said Ellenbogen, the studys principal investigator at the site nearDetroit.
Requip, a dopaminergic agent, is approved in the U.S. as immediate-release and extended-release tablets to treat suchsigns and symptoms of Parkinsons asstiffness, tremors, muscle spasms, and poor muscle control. The immediate release formulation is also approved to treatrestless leg syndrome.
But some Parkinsons patients develop motor complications and dyskinesia, or uncontrolled and jerky movements, after taking oral Requipfor several years, due to fluctuations in blood levels of the medication. Dyskinesia can be anything from a slight tremor of the hands to an uncontrollable movement of the upper body or lower limbs.
The implant is based on Titans ProNeura technology, and is designed to continuously release a consistent dose of ropinirole for three months or more, avoiding the shiftsin bloodconcentrations when ropinirole istaken as a tablet.
While oral formulations of ropinirole have greatly benefitted those suffering from Parkinsons disease, many patients develop serious motor complications and dyskinesias after several years, due to the peak-trough fluctuations of medication in the blood, said Kate Beebe, PhD, executive vice president and chief development officer at Titan.
Our ropinirole implant is designed to provide continuous, non-fluctuating therapeutic levels of medication for up to three months, potentially offering patients and clinicians a more effective treatment option, Beebe said. We thank the FDA for their timely review and comments on the IND and clinical protocol.
Posted: August 25, 2017 at 5:41 pm
Last year, I reported on Titan Pharmaceuticals and partner Braeburn Pharmaceuticals’ milestone Food and Drug Administration (FDA) approval for an implant to treat opioid addiction. Using Titan’s “ProNeura” platform technologycomposed of matchstick-sized implants inserted in the upper armthe companies won marketing approval for Probuphine, which dispenses a medication called buprenorphine for up to six months. This therapy both treats pain while weaning users off of more powerful addictive opioids and presents one option for tackling the opioid crisis.
Now, Titan has been given the FDA go-ahead to launch trials for a long-acting implant with a commonly used Parkinson’s disease drug called ropinirole. The automated delivery system could be particularly useful for Parkinson’s patients, as the company explains, since a drop-off in symptom control medication levels can make life extremely difficult for people suffering from the disease. Parkinson’s symptoms may include tremors, stiffness, and loss of balance.
“While oral formulations of ropinirole have greatly benefitted those suffering from Parkinson’s disease, many patients develop serious motor complications and dyskinesias after several years, due to the peak-trough fluctuations of medication in the blood,” said Titan executive vice president and chief development officer Kate Beebe in a statement. “Our ropinirole implant is designed to provide continuous, non-fluctuating therapeutic levels of medication for up to three months, potentially offering patients and clinicians a more effective treatment option.”
The business strategy is an interesting one. Rather than focusing on the costly and risk-fraught endeavor of new drug development, Titan is essentially looking to make existing treatments more effectivein essence, building a better medical mousetrap.
This essay appears in today’s edition of the Fortune Brainstorm Health Daily. Get it delivered straight to your inbox.
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We May Be Able to Treat Parkinson’s Disease With an Implant – Fortune