Parkinson's 'a risk factor for most cancers in Taiwan'

June 20, 2015

Parkinson's disease has identified a link between the neurodegenerative brain disorder and 16 different types of cancer, including lung cancer, cervical cancer and leukemia.

In Taiwan, researchers found patients with Parkinson's disease may be at greater risk of 16 different types of cancer.

According to the research team - including Dr. Pan-Chyr Yang, of the National Taiwan University College of Medicine in Taipei - more than 25 epidemiological studies have investigated the link between Parkinson's disease and cancer over the past 50 years.

While the majority of these studies have found a reduced risk of cancer among patients with Parkinson's disease, some studies have identified an increased risk of certain cancers among patients with the brain disorder, making the studies conflicting.

What is more, Dr. Yang and colleagues note that most of these studies were conducted in Western populations, with very few including East Asian populations.

As such, the team decided to investigate the association between Parkinson's disease and cancer among a Taiwanese population.

They publish their findings in JAMA Oncology.

Parkinson's patients in their 50s at greatest cancer risk

The researchers used the Taiwan National Health Insurance Database to identify 62,023 patients who had been diagnosed with Parkinson's disease between 2004 and 2010, alongside 124,046 individuals without Parkinson's.

All patients were followed until 31st December 2012 or until one of the following occurred: a cancer diagnosis, withdrawal from the Database, loss to follow-up or death.

Compared with participants free of Parkinson's, those with the condition were found to be at greater risk of 16 cancers, including brain, lung, colorectal, kidney, prostate and cervical cancers, as well as lymphoma/leukemia and skin cancers - including melanoma. The highest risk of cancer was found among Parkinson's patients aged 50-59.

However, Parkinson's disease was not associated with increased risk of breast, ovarian or thyroid cancers.

Based on these findings, the authors "conclude that Parkinson's disease is a risk factor for most cancers in Taiwan," noting that further studies are warranted to determine whether their results may apply to other populations in East Asia.

The authors add:

"The striking differences between our study and the previous studies in Western cohorts suggest the importance of ethnicity and environmental exposures in disease pathogenesis."

Though they are unable to explain why Parkinson's appears to be linked to greater risk of cancer in the Taiwanese population, they state that one explanation could be mutations in the PARK2 gene, explaining that mutations in these genes have been linked to both cancer and early-onset Parkinson's.

They point out, however, that further research is warranted to determine the exact mechanisms underlying the relationship between Parkinson's and increased cancer risk.

The team says there are some limitations to their study. For example, incidence of Parkinson's disease was identified through medical records, so it may have been underestimated. The researchers were also unable to identify the smoking status of participants - a factor that may have influenced cancer incidence.

Earlier this week, Medical News Today reported on a study published in JAMA Internal Medicine, in which researchers estimated that almost half of all deaths from 12 cancers are caused by smoking.

Written by Honor Whiteman

Copyright: Medical News Today

http://www.medicalnewstoday.com/articles/295553.php

Researchers develop drug delivery technique to bypass blood-brain barrier

 Wednesday 21 October 2015

Breakthrough could help countless patients with neurological conditions that are currently hard to treat

Researchers at Massachusetts Eye and Ear/Harvard Medical School and Boston University have successfully shown neuroprotection in a Parkinson's mouse model using new techniques to deliver drugs across the naturally impenetrable blood-brain barrier. Their findings, published in Neurosurgery, lend hope to patients around the world with neurological conditions that are difficult to treat due to a barrier mechanism that prevents approximately 98 percent of drugs from reaching the brain and central nervous system.

"We are developing a platform that may eventually be used to deliver a variety of drugs to the brain," said senior author Benjamin S. Bleier, M.D., of the department of otolaryngology at Mass. Eye and Ear/Harvard Medical School. "Although we are currently looking at neurodegenerative disease, there is potential for the technology to be expanded to psychiatric diseases, chronic pain, seizure disorders and many other conditions affecting the brain and nervous system down the road."

Using nasal mucosal grafting, researchers delivered glial derived neurotrophic factor (GDNF), a therapeutic protein in testing for treating Parkinson's disease, to the brains of mice. They showed through behavioral and histological data capture that their delivery method was equivalent to direct injection of GDNF - the current gold standard for delivering this drug in Parkinson's disease despite its traumatic nature and high complication rates - in diffusing drugs to the brain.

The researchers chose to test their delivery method with GDNF because the therapy has been shown to delay and even reverse disease progression of Parkinson's disease in pre-clinical models. The study was funded by The Michael J. Fox Foundation for Parkinson's Research (MJFF).

"Brain diseases are notoriously difficult to treat due to the natural protections the body builds against intrusion," said Jamie Eberling, PhD, senior associate director of MJFF research programs. "Dr. Bleier's group has identified a potential avenue to pass that barrier, and we look forward to the next stage of research to further test its utility in people with Parkinson's disease ."

Nasal mucosal grafting is a technique regularly used in the ENT field to reconstruct the barrier around the brain after surgery to the skull base. ENT surgeons commonly use endoscopic approaches to remove brain tumors through the nose by making a window through the blood-brain barrier to access the brain. Once they have finished the treatment, they use adjacent nasal lining to rebuild the hole in a permanent and safe way. The safety and efficacy of these methods have been well established through long-term clinical outcomes studies in the field, with the nasal lining protecting the brain from infection just as the blood brain barrier has done.

Dr. Bleier saw an opportunity to apply these techniques to the widespread clinical dilemma of delivering drugs across the barrier to the brain and central nervous system. By functionally replacing a section of the blood-brain barrier with nasal mucosa, which is more than 1,000 times more permeable than the native barrier, surgeons may create a "screen door" to allow for drug delivery to the brain and central nervous system.

The technique has the potential to benefit a large population of patients with neurodegenerative disorders, where there remains a specific unmet need for blood-brain penetrating therapeutic delivery strategies.

"We see this expanding beyond Parkinson's disease, as there are multiple diseases of the brain that do not have good therapeutic options," Dr. Bleier said. "It is a platform that opens doors for new discovery and could enable drug development for an underserved population." 

Drugs used to treat a variety of central nervous system diseases may be administered through the nose and diffused through an implanted mucosal graft (A, in red) to gain access to the brain. Under normal circumstances, there are multiple layers within the nose that block the access of pharmaceutical agents from getting to the brain including bone and the dura/arachnoid membrane, which represents part of the blood-brain barrier (B). After endoscopic skull base surgery (C), all of these layers are removed and replaced with a nasal mucosal graft, which is 1,000 times more porous than the native blood-brain barrier. Consequently, these grafts may be used to deliver very large drugs, including proteins, which would otherwise be blocked by the blood-brain barrier.

Credit: Garyfallia Pagonis and Benjamin S. Bleier, M.D.

Gene could hold key to treating Parkinson's disease

Oct.20,2015

Researchers at King's College London have identified a new gene linked to nerve function, which could provide a treatment target for 'switching off' the gene in people with neurodegenerative diseases such as Parkinson's disease.

Parkinson's disease affects approximately 7-10 million people worldwide and is characterised by progressive loss of motor function, psychiatric symptoms and cognitive impairment.

Current treatments for Parkinson's only treat symptoms of the disease rather than its underlying causes, so these new findings in fruit flies could lead to novel preventative treatments if replicated in humans.

Previous research suggests that defects in mitochondria, which are tiny 'batteries' in cells that provide energy, play an important role in a number of diseases that affect the nervous system, including Parkinson's. However, until now the neuronal processes underlying the development of these conditions were unknown.

The study, published in PNAS, discovered that damaged mitochondria in fruit flies produce a signal which stops nerve cells from working. A gene called HIFalpha was found to regulate the nerve signals from damaged mitochondria and, when this gene was 'switched off' by the research team, nerve function in flies with Parkinson's disease was restored. By deactivating the HIFalpha gene, the early failure of nerve cells caused by mitochondrial damage was prevented.

An identical effect was observed in flies with Leigh syndrome, a rare neurological disorder caused by a severe mitochondrial defect, which typically arises in the first year of life in humans.

As the HIFalpha gene is also found in humans, this new finding could pave the way for new treatments in the future, according to the study authors.

Dr Joseph Bateman from the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King's College London, said: 'Like their human counterparts flies with Parkinson's disease progressively lose motor function, which includes a negative impact on their ability to climb. Remarkably, we found that switching off a particular gene dramatically improved their motor function and climbing ability.

'The biggest surprise from our work is that damaged mitochondria produce a signal that actively prevents nerve cells from working properly. Thanks to this study we now have a much better understanding of how nerve cells function, which could transform the way in which neurological diseases such as Parkinson's are understood and treated.'

Claire Bale, Head of Research Communications at Parkinson's UK, said: 'Understanding how subtle changes in our genes may trigger brain cell death is one of the most promising avenues for the development of new treatments for Parkinson's.

'This discovery adds a new piece to the intricate jigsaw puzzle of genetic factors that play a part in Parkinson's.'

Image shows the larval stage of the fruit fly Drosophila. The nerve cells in this larva are genetically engineered to produce a green fluorescent protein (GFP), which helped researchers from King's College London see the nerves that had damaged mitochondria. By analysing nerves with damaged mitochondria in larvae and adult flies, they discovered that mitochondria produced a signal which blocked nerve function. 

Credit: King's College London

References:

This research was carried out in collaboration with Dr Sean Sweeney of the Department of Biology, University of York and Dr Marc Dionne of the Department of Life Sciences, Imperial College London.
The study was part-funded by the Wellcome Trust, the Biotechnology and Biological Sciences Research Council (BBSRC) and a Biomedical Research Studentship / Fellowship to study co-author Olivia Duncan from the National Institute for Health Research (NIHR) Biomedical Research Centre [and Dementia Unit] at South London and Maudsley NHS Foundation Trust and King's College London.
King's College London
http://www.medicalnewstoday.com/releases/301249.php?tw

New study provides insights into potential treatment of severe pain in Parkinson's disease with prolonged-release oxycodone/naloxone

 Tuesday 20 October 2015

A study published today in The Lancet Neurology has provided important insights into the analgesic effects of prolonged release oxycodone/naloxone (OXN PR) for Parkinson's disease patients with chronic, severe pain.ⁱ The primary endpoint of improved average 24-hour pain score with OXN PR versus placebo at week 16 was not met (p=0.058), however assessments at other time points as well as secondary endpoint data indicate some potentially positive treatment effects with OXN PR.ⁱ

The primary endpoint of the study was to demonstrate superiority of OXN PR compared to placebo for average 24-hour pain scores (11-point numerical rating scale, 0=no pain to 10=pain as bad as you can imagine) at week 16. Secondary endpoints included frequency of rescue medication intake, percentage of responders (defined by a ≥30% reduction from baseline) in average 24-hour pain at week 16, and percentage of responders ('much improved' or 'very much improved') for Clinical Global Impression - Improvement (CGI-I) and Patient Global Impression Improvement (PGI-I) at week 16.ⁱ

The study found that OXN PR was associated with numerical but not significant improvement at week 16 (p=0.058), however statistically significant differences were seen at week 4 (p=0.018), week 8 (p=0.011) and week 12 (p=0.021).ⁱFurthermore, the Per Protocol Population analysis revealed that when OXN PR was taken in line with the study protocol, this adherence resulted in significantly improved 24-hour average pain scores at week 16 with OXN PR as compared to placebo (p=0.010).ⁱ Secondary endpoints also demonstrated greater improvements with OXN PR including a greater responder rate for 24-hour pain control (p=0.021), less use of rescue medication and clinically relevant improvements in CGI-I (p=0.019) and PGI-I (P=0.022). OXN PR also provided significant improvements in severe musculoskeletal (p=0.023) and severe nocturnal pain (p=0.010) as compared to placebo.ⁱ Overall adverse events were similar between OXN PR and placebo. Treatment related adverse events seen more frequently with OXN PR compared to placebo were nausea (17% vs 9%) and constipation (17% vs 6%).ⁱ

"This study provides key learnings on the potential use of oxycodone/naloxone for the treatment of severe pain in Parkinson's disease. The encouraging secondary endpoint data suggest that further studies may help to uncover the potential role of OXN PR in this patient population", said Claudia Trenkwalder, principal investigator of the study. "This study adds to the very limited knowledge base on the efficacy and safety of opioid-based treatment of patients with Parkinson's disease suffering from complex pain."

Prof. Dr. Karen Reimer, Managing Director, Mundipharma Research, added: "To our knowledge, this is the first randomised, double-blind, controlled trial specifically designed to investigate treatment in Parkinson's disease pain. At Mundipharma, it is our vision to set ourselves apart as pioneers in pain management. We have a proven track record of bringing pain treatment innovations to market and want to build on this heritage, in an effort to continue to provide novel treatment options that really make a difference to people living in pain."

Parkinson's disease is the second most common neurodegenerative disease after Alzheimer's disease^{ii, iii}, affecting over 4 million people in the world's most populous nations.^iv Pain is a common symptom, with approximately 60% of patients affected, and is one of the non-motor symptoms of Parkinson's disease associated with a depressed mood and reduced quality of life.^{v, vi, vii} There is little awareness of the different types of Parkinson's disease pain from both medical and patient perspectives, with disease-related pain commonly only being treated by increasing the doses of dopaminergic therapy.

OXN PR is currently available in 23 countries across Europe as well as other territories in Asia, North America and Oceania (Targin®/ Targinact®/Targiniq®) and its efficacy and safety profiles have been demonstrated in a variety of non-malignant and cancer-related pain settings.^{viii, ix, x, xi}

This multi-centre, double-blind randomised placebo controlled study was funded by Mundipharma GmbH & Co.KG. 

Adapted by MNT from original media release

http://www.medicalnewstoday.com/releases/301272.php?tw

Parkinson's victims 'brought back to life': Cancer drug's amazing effect echoes Awakenings film

• Leukaemia drug nilotinib helped advanced Parkinson's disease patients
• 
  
• Scientists said those given it for a research study had 'come back to life'
• 
  
• One wheelchair-bound patient able to walk again, others regained speech
• 
  
• Researchers now hope ‘life-changing’ drug will help those with Alzheimer's

By FIONA MACRAE SCIENCE CORRESPONDENT FOR THE DAILY MAIL 

19 October 2015   

Patients with advanced Parkinson’s disease have ‘come back to life’ after being given a cancer drug, said scientists.

In dramatic scenes reminiscent of the Robin Williams film Awakenings, in which a drug was used to awaken catatonic patients, one wheelchair-bound patient was able to walk again.

Others regained the ability to speak or were able to enjoy pleasures such as reading a book once more after taking the drug during a study.

+2

Breakthrough: Scientists say patients with advanced Parkinson’s disease have ‘come back to life’ after being given the cancer drug nilotinib, which is used to treat leukaemia (file photo)

Researchers now hope the ‘life-changing’ drug – a leukaemia treatment called nilotinib – will also work for those with brain conditions such as Alzheimer’s.

The fact the drug has already gone through extensive testing in cancer patients should speed up the approval process for its use treating other conditions whether the results are too good to be true.

More than 125,000 Britons have Parkinson’s, in which the death of the brain cells that produce a chemical called dopamine leads to tremors, stiffness and a gradual slowing of the body.

There is no cure and existing drugs can only provide temporary relief. In contrast, it is thought nilotinib spares the key brain cells from death.

+2

In dramatic scenes reminiscent of the Robin Williams film Awakenings (pictured), in which a drug was used to awaken catatonic patients, one wheelchair-bound patient was able to walk again

The team from Georgetown University in Washington DC gave nilotinib to 12 men and women who had Parkinson’s disease or a similar condition called dementia with Lewy bodies. 

The daily dose of the drug for six months had dramatic effects, with some of their worst symptoms being reversed, the Society for Neuroscience’s annual conference heard. 

Three patients regained the ability to talk, one was able to walk again and another could feed herself once more.

One patient, retired lecturer Alan Hoffman, said: ‘Before nilotinib, I did almost nothing around the house. Now, I empty the garbage, unload the dishwasher ... I read a book for the first time in a couple of years. My wife says it is life-changing.’

Lead author Dr Charbel Moussa said: ‘We’ve seen patients at end stages of the disease coming back to life. 

'We had people as stiff as a board at the start of the study who were walking around, sitting down and bending their legs by the end.’

It is thought nilotinib clears away toxic proteins that accumulate in the brain cells of Parkinson’s patients, so freeing them to make dopamine. 

Researcher Dr Fernando Pagan said the drug seemed to be the first to reverse some of the symptoms – but that larger studies were needed to determine its true impact.

Parkinson’s UK has cautioned that the study’s failure to include untreated patients made it impossible to say how well the drug had really worked, warning that ‘just someone’s belief that they are taking a new drug could produce these results’.

Professor Carl Clarke, a neurologist at Birmingham University, added: ‘It seems too good to be true. I dearly hope I am wrong.’

Further trials are now planned.

Read more: http://www.dailymail.co.uk/health/article-3278525/Parkinson-s-victims-brought-life-cancer-drug.html#ixzz3p40W9KQs
Follow us: @MailOnline on Twitter | DailyMail on Facebook

http://health.einnews.com/article/292336681/zOsnByhc8xBFd15N

Blood Cancer Drug Giving Hopes For Parkinson's Patients

10/19/2015 7:36 AM ET 

A short-term trial of blood cancer drug Nilotinib in patients with Parkinson's disease with dementia recorded dramatic improvement in memory and limb movements. It also helped in checking tremor and neuromotor freezing in Parkinson's patients with Lewy body dementia, a type of progressive memory loss. 

Scientists at the Georgetown University Centre in Washington believe that the drug would be useful in removing neurotoxic proteins in the brain, blood and spinal fluid.

The six-month safety trial in 12 patients was too short for a conclusion and there was no comparison with placebo. However, the researchers are excited to continue with the studies using the Novartis drug. 

Nilotinib or Tasigna is a kinase inhibitor capsules for oral use, and is indicated for the treatment of chronic myeloid leukemia in adult patients. 

In vitro studies and trial in transgenic mice paralyzed by Parkinson's disease have shown that the drug in small quantities helped in rescuing the brain from unwanted proteins. The Phase 1 study was presented at the Neuroscience 2015, the annual conference of the Society for Neuroscience in Chicago. 

More than 10 million people around the globe are found to be suffering from Parkinson's disease. 

by RTT Staff Writer

http://health.einnews.com/article/292320694/F6wg6Y85uQw2WNDG

Novartis's Tasigna is FDA-approved to treat leukemia.Courtesy of Novartis

Some of the improvements were dramatic.

Researchers at Georgetown University Medical Center on Saturday revealed what could be a major breakthrough in the treatment of Parkinson’s disease.

A study unveiled at the Society for Neuroscience’s annual meeting found that 11 patients with Parkinson’s disease with dementia who were given nilotinib, an FDA-approved drug for leukemia that’s sold by Novartis as Tasigna, experienced improved cognition, motor skills and non-motor function in a 12-patient, six-month trial.

Fernando Pagan, a GUMC associate professor of neurology who directs the Movement Disorders Program at MedStar Georgetown University Hospital, said that to his knowledge, the study “represents the first time a therapy appears to reverse—to a greater or lesser degree depending on stage of disease—cognitive and motor decline in patients with these neurodegenerative disorders.”

In some patients, the results of the treatment were rather dramatic. A release from GUMC says that one patient who was confined to a wheelchair was able to walk again and that three other patients who could not speak were able to hold conversations.

One patient in the trial, Alan Hoffman, a professor emeritus of social science education at Georgia State University, was diagnosed with Parkinson’s disease in 1997. Before taking nilotinib, he said he didn’t do much around the house. “Now,” he told GUMC, “I empty the garbage, unload the dishwasher, load the washer and the dryer, set the table, even take responsibility for grilling.”

Pagan said that a larger, more comprehensive study must be done before determining the drug’s true impact, but if the drug’s effectiveness is confirmed in such tests, nilotinib could become the first treatment to impede the killing of brain cells that’s consistent with Parkinson’s, according to NPR. GUMC says its researchers are now planning larger clinical trials with nilotinib for patients with Parkinson’s and other similar diseases including Alzheimer’s disease, likely to begin in 2016.

New evidence on how deep brain stimulation works

Published: Monday 19 October 2015

Deep brain stimulation is known to treat the symptoms of stiffness, slow movement, and tremor in people with Parkinson's disease. Researchers are now a step closer to understanding exactly how this electrical stimulation of specific areas in the brain works.

It is thought that part of the underlying problem for people with Parkinson's is the overactivity of certain nerve cells. This overactivity affects the way that information flows from one circuit within the brain to another. In a paper published in the Journal of Neuroscience, researchers describe an experiment using deep brain stimulation that has demonstrated how the technique improves information flow between circuits, probably by calming down the overactive cells.

The researchers tested eye movements in 14 patients and 10 healthy controls. They electrically stimulated an area of the brain called the globus pallidus interna. They showed that this deep brain stimulation partially reverses deficits in voluntary control of eye movements, restoring some control.

The experiment showed improvement in information transfer between higher, cognitive, brain circuits and lower-level motor systems. This may mean that stimulation of the globus pallidus interna could have a positive effect on those symptoms of Parkinson's disease that are not directly movement-related.

Research: Pallidal Deep Brain Stimulation Improves Higher Control of the Oculomotor System in Parkinson's Disease, Chrystalina A. Antoniades, Pedro Rebelo, Christopher Kennard, Tipu Z. Aziz, Alexander L. Green, and James J. FitzGerald, Journal of Neuroscience, doi: 10.1523/JNEUROSCI.2317-15.2015, published 23 September 2015.

Adapted by MNT from original media release

http://www.medicalnewstoday.com/releases/301200.php?tw

Mechanism that 'melts' protein clumps may lead to new Parkinson's treatments

Published: Monday 19 October 2015

A new study provides fresh insights into a possible molecular method for reducing Lewy bodies - protein clumps found in the region of the brain that loses dopamine cells in people with Parkinson's disease.

The study proposes two ways that a protein complex may influence the formation of Lewy bodies found in the brains of people with Parkinson's disease.

The research, from Wayne State University School of Medicine in Detroit, MI, is published in The Journal of Biological Chemistry.

There are more than a million people in the US with Parkinson's disease, a devastating and currently incurable brain-wasting disorder that affects movement and coordination. As it progresses, the disease gradually diminishes one's ability to walk, talk and live an independent life.

While nobody has yet discovered the causes of Parkinson's disease, we know that they kill dopamine cells in the brain. Dopamine is a chemical messenger that is essential for sending brain signals that control a number of functions, including movement.

The dopamine-releasing cells most affected by Parkinson's disease are located in a midbrain region known as the substantia nigra pars compacta. A hallmark of Parkinson's disease is the accumulation and progressive spread of protein clumps called Lewy bodies in this region. Lewy bodies contain several proteins, the most common one is called alpha-synuclein.

Because studies show strong links between the presence of Lewy bodies and clinical symptoms of Parkinson's disease, many scientists are coming to the conclusion that they accelerate the disease, which has spurred the search for ways to prevent or get rid of the protein clumps.

The new study, led by Assia Shisheva, a professor of physiology, describes a step forward in the search for a possible way to "melt" the Lewy bodies found in Parkinson's disease.

For some years, Prof. Shisheva's lab has been researching how the behavior of three proteins inside cells are involved with disease. The proteins are two enzymes called PIKfyve and Sac3, and an accessory protein called ArPIKfyve.

The researchers found that these proteins are involved in controlling the traffic of material to the digestive system of the cell. They also found that if the Sac3 enzyme is not bound and protected by ArPIKfyve, it speeds to a hasty death in the cell.

Other discoveries show that mutations in Sac3 are linked to brain degenerating disease in humans, while mutations in PIKfyve are linked to a relatively benign disease in the cornea of the eye.

Two potential ways the protein complex triggers Parkinson's

Putting all these discoveries together led Prof. Shisheva and colleagues to conclude that the double ArPIKfyve-Sac3 complex has separate functions in the brain, and they set out to look for proteins that interact specifically with it.

The new study describes a previously unknown interaction between ArPIKfyve-Sac3 and Synphilin-1, a protein already known to be involved in the development of Parkinson's disease through its interaction with alpha-synuclein, and because like alpha-synuclein, it is also one of the proteins found in Lewy body deposits. Prof. Shisheva notes:

"Our study revealed that the ArPIKfyve-Sac3 complex is an effective inhibitor of aggregate formation by Synphilin-1."

The team also found that if Sac3 levels become excessive, then they trigger protein self-aggregation and clumping by Synphilin-1. This confirms recent research from Japan that found excessive Sac3 accumulates in Lewy bodies, they note.

The researchers therefore conclude there are two ways in which the ArPIKfyve-Sac3 complex may trigger Parkinson's disease. One way is when levels of ArPIKfyve-Sac3 are too low and the other is when levels of Sac3 are too high.

They propose that increasing levels of the ArPIKfyve-Sac3 complex may have a beneficial effect in Parkinson's disease.

Prof. Shisheva suggests that the ArPIKfyve-Sac3 complex works by shifting Synphilin-1 from a clumping form to a more soluble form. 

Meanwhile, Medical News Today recently reported how scientists have mapped the path Parkinson's takes as it spreads from affected to healthy brain tissue in the early stages of the disease. In a study published in ELife, the team from McGill University shows how the disease progresses from cell to cell through the brain along networks.

Written by Catharine Paddock PhD

Copyright: Medical News Today

http://www.medicalnewstoday.com/articles/301186.php?tw

Researchers close in on a blood test for Alzheimer's disease

Published: Monday 19 October 2015

Early detection presents new opportunities to slow or perhaps even halt disease progression

Researchers from the Rowan University School of Osteopathic Medicine are nearing development of a blood test that can accurately detect the presence of Alzheimer's disease, which would give physicians an opportunity to intervene at the earliest, most treatable stage.

Robert Nagele, PhD, presented his team's most recent findings October 18 at OMED 15 in Orlando. Dr. Nagele's work focuses on utilizing autoantibodies as blood-based biomarkers to accurately detect the presence of myriad diseases and pinpoint the stage to which a disease has progressed. By detecting Alzheimer's disease long before symptoms emerge, Dr. Nagele hopes those with disease-related autoantibody biomarkers will be encouraged to make beneficial lifestyle changes that may help to slow development of the disease.

"There are significant benefits to early disease detection because we now know that many of the same conditions that lead to vascular disease are also significant risk factors for Alzheimer's. People found to have preclinical disease can take steps to improve their vascular health, including watching their diet, exercising and managing any weight and blood pressure issues to help stave off or slow disease progression," Nagele said.

While the cause of Alzheimer's remains elusive, it is clear that maintaining a healthy blood-brain barrier is a critical preventative measure. Diabetes, high cholesterol, high blood pressure, stroke and being overweight jeopardize vascular health. As blood vessels in the brain weaken or become brittle with age, they begin to leak, which allows plasma components including brain-reactive autoantibodies into the brain. There, the autoantibodies can bind to neurons and accelerate the accumulation of beta amyloid deposits, a hallmark of Alzheimer's pathology.

The blood test developed by Dr. Nagele has also shown promise in detecting other diseases, including Parkinson's disease, multiple sclerosis and breast cancer. His team's research on the role of autoantibodies explains that:

• All humans possess thousands of autoantibodies in their blood;
• These autoantibodies specifically bind to blood-borne cellular debris generated by organs and tissues all over the body;
• An individual's autoantibody profile is strongly influenced by age, gender and the presence of specific diseases or injuries; and
• Diseases cause characteristic changes in autoantibody profiles that, when detected, can serve as biomarkers that reveal the presence of the disease.

In Alzheimer's, the brain begins to change years before symptoms emerge. Detecting Alzheimer's antibodies at the preclinical stage would give patients an opportunity to work with their physician to make lifestyle changes or receive available treatments before they become symptomatic. Potentially, this early intervention could help those with preclinical Alzheimer's avoid or delay the most devastating symptoms.

"As osteopathic physicians, we constantly tell patients that a healthy lifestyle is the best medicine for preventing disease. We also know that many people tune out messages about nutrition and exercise until a health crisis gets their attention," said Jennifer Caudle, DO, assistant professor of family medicine at Rowan University. "I can't think of a single patient who wouldn't take steps to prevent the progression of Alzheimer's if they could directly affect their prognosis."

Today, there is no definitive FDA-approved blood test for Alzheimer's, which affects an estimated 5.3 million Americans. It is among the top 10 causes of death in America.

Dr. Nagele's research has been supported by grants from the Michael J. Fox Foundation and the Osteopathic Heritage Foundation.

http://www.medicalnewstoday.com/releases/301179.php?tw