LONG TERM EFFECTS OF DBS ON PARKINSON'S DISEASE

Researchers assessed the long term effect of Subthalamic nucleus Deep Brain Stimulation (DBS) on Parkinson's Disease. People with Parkinson's Disease were assessed before DBS and 1, 3, 5 years after DBS had begun.

DBS involves the use of electrodes that are implanted into the brain and connected to a small electrical device called a pulse generator that can be externally programmed. DBS can reduce the need for L-dopa and related drugs, and reduce dyskinesia. For more information go to : http://www.ninds.nih.gov/disorders/deep_brain_stimulation/deep_brain_stimulation.htm 

As a result of DBS the quality of life improved by 58% after 3 years but gradually declined afterwards. Sleep, cognition, and emotion were mostly unchanged. After 5 years, when assessed without medication DBS improved Parkinson's Disease motor symptoms by 35%. However, after 5 years, when assessed with the simultaneous use of medication, motor symptoms were similar to those at the outset. L-dopa intake was reduced from 660mg to 310mg after 5 years. STN DBS can therefore improve Parkinson's Disease and reduce the need for L-dopa but there is a gradual decline and diminished efficacy after five years of use. 

Reference : Chinese Medical Journal [2015] 128 (18) : 2433-2438 (L.L.Jiang, J.L.Liu, X.L. Fu, W.B.Xian, J.Gu, Y.M.Liu, J.Ye, J.Chen, H.Qian, S.H.Xu, Z.Pei, L.Chen) 

Complete abstract : http://www.ncbi.nlm.nih.gov/pubmed/26365958

http://www.viartis.net/parkinsons.disease/news/150919.pdf mail@viartis.net

©2015 Viartis 

Everyday activity more beneficial than occasional strenuous exercise for Parkinson's disease

PR Newswire

ANN ARBOR, Mich., Sept. 17, 2015

ANN ARBOR, Mich., Sept. 17, 2015 /PRNewswire-USNewswire/ -- New University of Michigan research finds people with Parkinson's disease may want to consider attempting to do the dishes, fold the laundry and take strolls around the neighborhood in their quest to control their symptoms.

Parkinson's patients often become sedentary because of motor symptoms such as gait, balance problems or falls, said study principal investigator Nicolaas Bohnen, M.D., Ph.D., director of the U-M Functional Neuroimaging, Cognitive and Mobility Laboratory.

Once patients feel unstable on their feet, they may develop a fear of falling and then get scared to do any activity at all. Bohnen's team investigated whether participation in exercise, like swimming or aerobics, could help alleviate the motor symptoms that made these patients want to stay sedentary in the first place.

"What we found was it's not so much the exercise, but the routine activities from daily living that were protecting motor skills," Bohnen said. "Sitting is bad for anybody, but it's even worse for Parkinson's patients."

The imaging study, now available online in Parkinsonism and Related Disorders, was conducted by U-M faculty who hold appointments in both radiology and neurology.  

Researchers investigated the relationship between the duration of both non-exercise and exercise physical activity and motor symptom severity for 48 Parkinson's disease patients over a 4-week period. They performed PET brain imaging to measure dopamine levels and used a questionnaire to learn about how physically active the patients were, including both exercise and non-exercise activity. They found that non-exercise physical activity was linked to less severe motor symptoms. 

Although loss of dopamine is a key brain change for Parkinson's patients, and has been thought to be the main reason why Parkinson's patients become more sedentary, the researchers found non-exercise physical activity protected motor skills even among patients with differing levels of dopamine.

"This may have a big impact for Parkinson's patients," said co-author Jonathan Snider, M.D., clinical lecturer of neurology at the University of Michigan. "Not only worsening Parkinsonism but also increasingly sedentary behavior may explain more severe motor symptoms in advanced Parkinson's disease."

"I tell my patients to stand up, sit less, and move more," said Bohnen, also professor of radiology and neurology at the University of Michigan, VA Ann Arbor Healthcare System staff physician and investigator in U-M's Udall Center for Excellence in Parkinson's Disease Research. 

Additional authors: Martijn L.T.M. Müller, Ph.D., Vikas Kotagal, M.D., Robert A. Koeppe, Ph.D., Peter J.H. Scott, Ph.D., Kirk A. Frey, M.D., Roger L. Albin, M.D., all of U-M.

Funding: This research was funded by the Department of Veterans Affairs (grant I01RX000317), the Michael J. Fox Foundation and the National Institutes of Health (grants P01 NS015655 and RO1 NS070856). Support was also provided by the University of Michigan Udall Center of Excellence for Parkinson's Disease Research (P50 NS091856-01).

Disclosure: The authors declare no conflict of interest relevant to this work.

Reference: "Non-exercise physical activity attenuates motor symptoms in Parkinson disease independent from nigrostriatal degeneration," Parkinsonism and Related Disorders(2015).

http://health.einnews.com/article/286854224/iN9x7IVPN1u6yo0j

Czech scientists invent system to diagnose Parkinson's disease

ČTK |  

17 SEPTEMBER 2015

Brno, Sept 16 (CTK) - Czech researchers from the laboratory of brain diseases analysis of the University of Technology in Brno have developed a computer system to diagnose Parkinson's disease with more than 90-percent certainty, laboratory head Jiri Mekyska told reporters yesterday.

The system is also able to detect the phase of the disease from the very beginning to its severe form on the basis of the analysis of the patients' writing and speech.

The researchers have tested the system for six years on about 100 patients with Parkinson's disease, in cooperation with the St Anne Teaching Hospital in Brno.

Now all doctors who are interested in it can start using the system.

The system is monitoring how the patient is speaking, writing and drawing, in particular the articulation, as well as quickness, strength and possible shaking.

It provides results in figures on the basis of which doctors can determine whether the patient is healthy or suffers from Parkinson's disease and possibly its phase.

The new invention will save time and money, Mekyska said.

"Above all the possibility to estimate the stage of Parkinson's disease is very important now. Though the disease is incurable, doctors have various methods to attenuate its symptoms and slow down its course," Mekyska said.

On top of that, the six-year research has revealed how to improve the patients' speech.

The patients suffering from Parkinson's disease can be treated by repetitive transcranial magnetic stimulation, which uses magnetic pulses instead of electricity to activate parts of the brain.

The latest research has proved on which part of the brain the method should focus to minimise speech problems, Mekyska added.

Parkinson's disease (PD) is a degenerative disorder of the central nervous system mainly affecting the motor system. The most obvious symptoms include shaking, rigidity, slowness of movement and difficulty with walking and gait.

Copyright 2015 by the Czech News Agency (ČTK). All rights reserved.

Copying, dissemination or other publication of this article or parts thereof without the prior written consent of ČTK is expressly forbidden. The Prague Daily Monitor is not responsible for its content.

http://health.einnews.com/article/286846278/rt5Uq5H6YVAwCYBH

Rapamycin prevents Parkinson's in mouse model of incurable neurodegenerative disease

The image on the left shows dysfunctional lysomes clustered outside the nucleus in a mouse model of Parkinson's. The image on the right shows a dramatic reduction of the dysfunctional organelles following treatment with rapamycin.
Image credit: Shankar Chinta, Ph.D., staff scientist, Buck Institute

Published: Thursday 17 September 2015 

Rapamycin, an FDA-approved drug that extends lifespan in several species, prevented Parkinson's disease (PD) in middle-age mice that were genetically fated to develop the incurable neurodegenerative motor disease that affects as many as one million Americans. While the rapamycin did great things for the mice, scientists in the Andersen lab at the Buck Institute also got an unexpected plus from the research - a new understanding of the role parkin plays in cellular dynamics, one that challenges the current dogma in PD research and presents new opportunities for drug discovery. The study is currently online in the Journal of Neuroscience.

"Given its side effects as an immunosuppressant, there are issues with long-term use of rapamycin, but the results of our study suggest that use of derivatives of rapamycin or other agents with similar biological properties may constitute novel therapeutics for the disorder," said senior scientist and Buck faculty Julie Andersen, PhD. "Our discoveries regarding parkin may provide an even more important therapeutic target for PD."

Parkin is a protein encoded by the PARK2 gene in humans. Mutations in PARK2 are most commonly linked to both sporadic and familial forms of PD; they diminish the cell's ability to recycle its internal garbage. PD is characterized by the accumulation of damaged proteins and mitochondria in the area of the brain where the neurotransmitter dopamine is produced.

Rapamycin prevented PD symptoms from occurring in middle-aged mice who had a human mutation in the PARK2 gene. Researchers in the Andersen lab expected this benefit to come via the accepted role of parkin - they thought rapamycin would boost the mutated protein's ability to label certain types of cellular garbage for recycling. Instead they discovered that parkin plays a much broader role in the actual recycling of garbage and the manufacturing of new mitochondria.

"This is a completely new, unrecognized, function for parkin," said Andersen. "Our work shows that parkin plays a much broader role than was originally thought in getting rid of damaged mitochondria and proteins. It's very exciting because it gives us new ways to look at potential therapeutics to boost cellular clean up."

Working in both neuronal stem cell models and mouse tissue, scientists found that rapamycin not only boosted the mutated protein's ability to label cellular garbage, but also affected the process of recycling the garbage itself via up-regulation of a protein known as TFEB which increased the degradation and purging of both damaged proteins and mitochondria via a process known as lysosomal autophagy. Apart from rapamycin's effects, Andersen's team also discovered that parkin is involved in mitochondrial biogenesis - via up-regulation of PGC1alpha, a protein which drives increased mitochondrial synthesis.

"Problems with autophagy, which result in the accumulation of damaged proteins and organelles, have long been linked to PD," said Ana Maria Cuervo, MD, PhD, professor and recipient of the Robert and Renée Belfer Chair for the Study of Neurodegenerative Diseases at Albert Einstein College of Medicine in New York City. "This novel role of parkin in the regulation of the overall process of autophagy gives us new ways to address its dysfunction in PD."

"Researchers are already very interested in parkin as it relates to PD," said Andersen. "I'm hoping that uncovering this novel role for the protein will bring it center stage as an extremely important therapeutic target for the disorder."

Citation: Journal of Neuroscience: Mitochondrial Quality Control via the PGC1alpha-TFEB Signaling Pathway is Compromised by Parkin Q311X Mutation but Independently Restored by Rapamycin. DOI: 10.1523/JNEUROSCI.0109-15.2015
Other Buck Institute researchers involved in the study include Almas Siddiqui, Dipa Bhaumik, Shankar Chinta, Anand Rane, Subramanian Rajagopalan, Christopher A. Lieu, and Gordon J. Lithgow. This work was supported by the National Institutes of Health grant AG025901.
Buck Institute for Research on Aging
http://www.medicalnewstoday.com/releases/299633.php?tw

Top 10 Tips for Exercising with Parkinson’s Disease

1. Exercise is medicine, so don’t miss a dose.Exercise has been proven to build a healthier heart, lungs, and muscles, boost metabolism, prevent diabetes, and reduces disability. Research shows that exercise can slow many aspects of the physical decline of PD and new research also suggests that exercise may even be neuroprotective – that is, slowing the progression of PD in the brain.
   1. “…Exercise or other motor enrichment methods might delay the onset of parkinsonian symptoms or slow the degenerative process, but only when there are no substantial breaks in motor activity” (1763). – Motor Enrichment and the Induction of Plasticity Before or After Brain Injury (Kleim et al, 2004)
   2. “Our findings indicate that exercise reduces the behavioral impairments elicited by the dopaminergic neurotoxins as well as the loss of DA neurons” – Triggering endogenous neuroprotective processes through exercise in models of dopamine deficiency (Zigmond et al, 2009)
   3. “What is clear is that exercise can influence the multiple levels of support necessary for maintaining optimal neuronal function, which is unique among proposed interventions for aging.” (Anderson et al, 2010)
2. Be realistic – something is better than nothing.There is no perfect one-size-fits-all exercise for people with Parkinson’s. Don’t wait. Start walking around the block. Or dancing. Find a physical therapist that can design an exercise program that is right for you.
   1. “Considered together. These studies suggest that the type of activity may not be important, but rather that the performance of some sort of physical activity or exercise as opposed to being sedentary is critical.” (Dibble et al, 2008)
   2. It is important to find a physical therapist with expertise in Parkinson’s disease. Ask for a referral or consult a resource like http://www.neuropt.org for a physical therapist who specializes in neurological disorders – or who is board certified as a clinical specialist in neurologic physical therapy – or who typically works with people with PD in their day to day practice. (Ellis, 2010)
3. Have fun.Consistency is critical and if you don’t enjoy it, you won’t stick with it. Do something you like. Dance, yoga, tai chi, cycling and strength exercises have been shown to help with physical and cognitive symptoms of PD. And because Parkinson’s also robs you of energy, try exercising with a group. Research shows that people stick with exercise when there is encouragement and an expectation for you to show up.
   1. People with Parkinson’s disease who participated in 20 lessons of Tango experienced significant improvements in mobility, social support and health related quality of life – Health-related quality of life and alternative forms of exercise in Parkinson disease (Hackney & Earhart, 2009)
   2. “Maintaining a regular schedule of dancing into old age can preserve cognitive, motor and perceptual abilities and prevent them from degradation…beyond its ability to facilitate balance and posture, dance is a prime candidate for the preservation of everyday life competence of elderly individuals” (Kattenstroth et al, 2010)
4. Break a sweat:Movement only becomes exercise when it is done several times per week at an intensity that is high enough to be physically challenging. If you can carry a conversation with someone while exercising, you are not working hard enough. Because Parkinson’s is a disease of slowed movement, exercising at a slow rate may not provide the best results. Research shows that it’s not the exercise, but the level of the intensity of the exercise, that may be the most beneficial.
   1. Following forced, intense exercise, Parkinson’s symptoms improved 35%, whereas persons with Parkinson’s completing voluntary exercise did not exhibit any improvement. Despite only completing lower extremity exercise, the forced exercise group demonstrated improvements in upper extremity coordination as well as improvements in stiffness and speed of movement. These results were maintained 4 weeks after the forced exercise stopped. The control and coordination of grasping forces during the performance of a functional bimanual dexterity task improved significantly for patients in the FE group, whereas no changes in motor performance were observed following VE. Improvements in clinical measures of rigidity and bradykinesia and biomechanical measures of bimanual dexterity were maintained 4 weeks after FE cessation. – Forced, Not Voluntary, Exercise Improves Motor Function in PD Patients (Ridgel et al, 2009)
5. Do three major types of exercise.Do aerobic conditioning or cardiovascular exercise for 30 minutes, three times per week; strength or resistance training for 30 minutes, three times per week and stretching or flexibility exercises daily.
   1. An exercise program consisting of cardiovascular activities, stretching, strengthening, walking and balance training resulted in significant improvements in daily function and quality of life related to mobility. – Efficacy of a Physical Therapy Program in Patients with Parkinson’s Disease: A Randomized Controlled Trial (Ellis et al, 2005).
6. Start today, don’t wait.The sooner after diagnosis you begin exercising, the greater your physical reserve and self-motivation are likely to be. Don’t wait for the disease to progress further or for problems to emerge. Start strong to stay stronger longer.
   1. “…It is so encouraging to learn based on the observations of this study that exercise training can effectively reverse certain behavioral deficits, like impaired movement, imbalance and inconsistent gait pattern that are associated with the Parkinsonian syndrome in spite of the existing severe loss.” – Restorative effect of endurance exercise on behavioral deficits in the chronic mouse model of Parkinson’s disease with severe neurodegeneration (Pathakos, Kurz & Lau, 2009)
7. Find an exercise buddy.Exercise with people at a life station and physical ability similar to your own. Especially for people with young-onset Parkinson’s, exercising with peers may be more enjoyable, more motivating and more appropriate than finding a Parkinson’s-specific exercise group.
   1. “Consider developing an exercise buddy system which matches up [individuals] who are already exercising with patients who are just starting out. Such group support from patients with similar medical problems may help improve short-term adherence.” – Clinical Exercise Physiology (Ehrman, Gordon, Visich & Keteyian, 2009)
   2. “In our experience implementing community exercise programs for people with PD, it is often easier for those with apathy or depression to ‘show up’ at an appointment to exercise compared to exercising independently.” – Exercise Adherence in Persons with PD (Ellis, 2009 – pdonlineresearch.org)
8. Stick with it.If you stop exercising, the positive effects you’ve worked so hard to achieve through exercise will decline and disappear. People with PD who exercise do better than those who don’t.
   1. “Discontinuation of exercise in advance of brain injury may…leave the brain more vulnerable to degeneration.” ). – Motor Enrichment and the Induction of Plasticity Before or After Brain Injury (Kleim et al, 2004)
9. Exercise for your whole being.Exercise isn’t just good for your body. Other issues related to Parkinson’s disease – like depression, sleep and constipation could also be positively affected by exercise and activity.
   1. “…Exercise may be conceptualized as a non-pharmacological equivalent of antidepressant medication, which is presumed to exert its effects by modifying brain chemical systems.” – Exercise for Mood and Anxiety Disorders (Smits & Otto, 2009)
10. Use exercise to take control of your PD.People with Parkinson’s are robbed of so much control in their lives, but exercise is one thing you can control and in the process, create a better quality of life for yourself.
    1. “Exercise can be fun and is good for you. It can give you more 
confidence and more energy. More importantly, exercise is something that you can do to help manage your disease and improve your quality of life.” – Be Active! An Exercise Program for People with Parkinson’s Disease (Ellis, Rork & Dalton et al, 2008

http://www.davisphinneyfoundation.org/living-pd/10tools/

Parkinson's Imaging Agent Descheduled

Sue Hughes

September 15, 2015

The imaging agent, ioflupane I 123 (DaTscan; GE Healthcare), has been removed from the schedules of the US Controlled Substances Act, meaning that it will be more widely available for use in the diagnosis of Parkinson's disease and associated conditions.

Ioflupane I 123 is a US Food and Drug Administration–approved imaging agent that allows an assessment of the integrity of the striatal dopaminergic system via the dopamine transporter to help physicians determine whether patients have essential tremor or a parkinsonian syndrome movement disorder, such as Parkinson's disease.

Since approval in 2011, it has been listed by the Drug Enforcement Administration (DEA) as a Schedule II controlled substance, which has restricted the drug's use to only those healthcare professionals and imaging facilities registered with the DEA and able to comply with all of the requirements for the appropriate prescribing, storage, use, and disposal of Schedule II controlled substances.  

But the DEA has now descheduled ioflupane I 123, lifting these restrictions, making it easier for imaging specialists to order and administer it in their facilities.

DaTscan is a radioactive drug injected into the bloodstream to help image areas of the brain using single-photon emission computed tomography (SPECT). SPECT with DaTscan, along with other medical tests, aids in diagnosis of a Parkinsonian syndrome or essential tremor. Parkinsonian syndromes include Parkinson's disease, multiple system atrophy, and progressive supranuclear palsy.

DaTscan was not designed to differentiate among these different forms of parkinsonian syndrome, the company release notes. Its effectiveness as a screening or confirmatory test and for monitoring disease progression or response to therapy has also not been established.

Quoted in a GE Healthcare press release, Ted Thompson, JD, chief executive officer of the Parkinson's Action Network, said, "The Parkinson's Action Network applauds the DEA for descheduling the active ingredient in DaTscan and allowing many more people to have access to this important diagnostic tool. Having this tool available for people with suspected Parkinsonian syndromes and essential tremor may help them to receive appropriate diagnosis and treatment sooner."

http://www.medscape.com/viewarticle/851027?src=wnl_edit_tpal

Saskatchewan scientists work with Harvard on new Parkinson's research

THE CANADIAN PRESS  09.14.2015

SASKATOON - Researchers at the University of Saskatchewan are teaming up with colleagues at Harvard Medical School in Boston to use stem cells to treat Parkinson’s disease.

Parkinson's disease attacks the cells in the brain that create dopamine, a chemical that carries action signals through your brain.

Dr. Ivar Mendez of the Saskatchewan Brain Repair Program at the Saskatoon university says when this happens, it causes the loss of function, but new research is hoping to restore those.

The process involves taking stem cells from a patient's skin or blood, and converting them into a brain stem cell which is rich in dopamine neurons.

Once they are injected into the brain, the dopamine is released and the broken links begin to be repaired.

Currently, a dopamine chemical is injected into the body with heavy immune suppression so the body will accept the chemical. In the new method, because a person's own cells are used, the theory is their body will accept the treatment more easily.

Mendez began transplanting cells that produce the neurotransmitter dopamine into patients in the late 1990s while he was at Dalhousie University. All 10 patients implanted with these cells improved significantly.

Dr. Ole Isacson of Harvard says if they are successful in this research project, the cells being injected will help restore some function in patients within the first nine months of treatment.

Clinical trials are expected to start within two to three years.

http://health.einnews.com/article/286359029/98IZfjpZ1cIA4yqP

Parkinson's choir may help 'masked face syndrome' Singing appears to help people with movement disorder regain facial expression

                   Click on to watch:  http://www.cbc.ca/1.3227909

CBC News Posted: Sep 14, 2015 4:54 PM ET

Parkinson's choir may help 'masked face syndrome'

A choir of Canadians with Parkinson's disease is helping researchers test how well the performers regain facial movement to express emotions.

Tremors and difficulty walking are often the most noticeable symptoms of Parkinson's disease, which affects about one in 500 people in Canada. Those with the disease may also have limited facial movement, which hampers the ability to express themselves.

For people with Parkinson's who have "masked face syndrome," it can be difficult for others to decipher how they're feeling. That's because we unknowingly mimic or mirror each other during interaction to connect.

"Within a hundred milliseconds of seeing someone else smile or frown, we are smiling or frowning," said Frank Russo, a psychology professor at Ryerson University in Toronto. "We're mirroring what the other person is doing. And that's one of the things that is absent in Parkinson's. It's the absence of mirroring that is leading to some of the deficit in understanding other people's emotions."

Bonnie Le Lyons-Cohen, right, sings in a choir whose members all have Parkinson's disease. She says the experience has helped her confidence. (CBC)

Having a static face can leave people with Parkinson's seem cold and aloof as they also show deficits in understanding other people's emotions. The patient can then become emotionally disconnected from others.

Studying the 28 members of the Parkinson's choirhas bolstered Russo's thinking that singing, facial expressions and social communications are interconnected.

So far Russo has found that mirroring effect or mimicry was restored among choir participants who sang for 13 weeks.  

"We are facilitating exercise of the facial muscles and the vocal muscles. It's through this experience expressing ourselves in emotional communication that we are better able to understand other people's emotions."

The Toronto researchers say their project is the first to look at emotional mimicry in the context of singing. Other Parkinson's choirs exist for a different focus, such as restoring breath support.

Singer Bonnie Le Lyons-Cohen, 58, said participating in the choir has been a life-changing experience. Previously she tended to look down and freeze.

"It's made a big difference, first of all my confidence," she said. "Now I look up and I sing. If people aren't understanding me I just project my voice a little bit louder."

Lyons-Cohen said she's regained the ability to modulate her voice while enjoying hanging out with other members of the choir. 

The project ended last week but choir members hope to keep it going.

http://health.einnews.com/article/286300814/KPXDPpHSn5w6K5kT

UNC researcher's mission? To treat Parkinson's disease with your own white blood cells

While Michael Fox, left, may be among the more famous Parkinson's disease patients, 

it's ailment impacts 7 million to 10 million worldwide. There is no cure.

 Sept.14, 2015

The emails pour into Elena Batrakova’s computer daily.

Batrakova, a researcher at UNC-Chapel Hill’s Eshelman School of Pharmacy's Center for Nanotechnology in Drug Development, didn’t have a personal stake in Parkinson’s disease, a degenerative neurological disorder. There’s no father, brother, child suffering from the ailment, which can impact everything from motor skills to mental clarity. There's no childhood friend-turned-patient to inspire the mission.

But the emails, hopeful messages from patients and their relatives, give her that personal connection.

 “You feel that you’re doing something that is very important,” she says, pausing. “I just think that it’s a dream of maybe every investigator to see at least one person whom you can help by your work. So I’m just really eager and hopeful that one day I could look in the eyes of this person and he’ll tell me he is thankful because it’s working.”

Batrakova is hopeful about a technique that could achieve the very thing those Parkinson’s patients are desperate for: A treatment.

“We are not inventing new drugs,” she explains. “We are taking old, good drugs, which cannot be delivered because of the blood brain barrier … and we formulate them into drug delivery systems.”

The blood brain barrier is exactly what it sounds like – a barrier that protects your brain and, in doing so, acts as a wall. But there’s one particle that can get through – macrophages, white blood cells. When inflammation occurs, they’re signaled and respond.

 “So I realized, why don’t we use macrophages as a drug delivery system?” she says. “It’s a very potent, powerful, nature-prepared mechanism.”

And, when genetically modified to produce anti-inflammation proteins and neuron growth factors, they could – or so the theory goes – repair nerve cells. As cell death causes Parkinson's symptoms, the applications for diseases sufferers could be huge.

“Basically, you have a Trojan horse that goes across the blood brain barrier to the inflammation site, and it’s bringing something very powerful,” she says.

The macrophages can then be injected intravenously into the patient, where they will be able to teach neurons to make the protein for themselves by delivering their own version of an instruction manual: DNA.

It’s complicated – and not just the science. A long regulatory process stands between the science and its use in actual patients. Currently, the team, armed with a $50,000 grant from the N.C. Biotechnology Center, is about to go into preclinical testing, researching how to use the intravenous method in genetically engineered mice.

Even if everything goes perfectly, it will be years before she can respond to those emails with real trial data.

http://www.bizjournals.com/triangle/blog/techflash/2015/09/unc-researchers-mission-to-treat-parkinsons.html

Hallucinations and delusions: Surprisingly common occurrence in Parkinson's disease

Mon Sep 14, 2015.

(BPT) - For the approximately one million Americans living with Parkinson’s disease, the visible motor (movement-related) symptoms associated with the condition are all too familiar. These include tremors, stiff muscles, limited movement and problems standing. However, there is a common non-motor aspect of advanced Parkinson’s disease that isn’t as widely understood or recognized by patients, caregivers, or doctors.

Common symptoms of this condition include hallucinations and delusions. Hallucinations are when a person sees or hears things that are not real. For example, a common hallucination is seeing a person or animal in the room that does not actually exist. Delusions are false and irrational beliefs, and in this case, often involve suspicions of spousal infidelity or other paranoid themes.

The condition is known among the medical community as Parkinson’s disease psychosis, or “PDP.” You may be surprised to learn that PDP affects more than half of all Parkinson’s patients at some point over the course of their disease. Current scientific research indicates that the hallucinations and delusions associated with PDP can result from the progression of the underlying Parkinson’s disease itself.

Understandably, the appearance of hallucinations or delusions can have a negative impact on quality of life for those living with Parkinson’s disease. PDP is also associated with increased distress and burden for caregivers, which can lead to nursing home placement. An especially unfortunate reality of PDP is that many Parkinson’s patients feel embarrassed to report symptoms to their doctors because of the stigma associated with mental disorders. In fact, a surprisingly small amount, only 10-20 percent, report their symptoms spontaneously.

“We are finding that with advancing Parkinson’s disease, complex challenges such as PDP often arise,” said Dr. Michael S. Okun, National Medical Director of the National Parkinson Foundation. “In the case of PDP, the strain on the caregiver can be substantial. As such, it is important to report any symptoms when they start, with a goal of effectively managing the condition and avoiding unnecessary nursing home placement.”

Interestingly, cases that are correctly diagnosed may not be simple to treat. Parkinson’s medications may exacerbate PDP symptoms. Often doctors adjust Parkinson’s medications to treat the psychosis, but in doing so, there is the potential to further compromise the patient’s motor skills. Given the treatment challenges, it is important that patients, their caregivers, and doctors regularly speak about potential symptoms. Open communication may help lead to an earlier diagnosis and an appropriate treatment plan.

To properly understand PDP, the first step is to recognize that it is a commonly associated aspect of Parkinson’s disease and not something to be ashamed or embarrassed about. Obtaining information is essential and people experiencing PDP and their caregivers are not without options.

CareMAP is an online resource created by the National Parkinson Foundation (NPF) that offers families the resources and support they need to provide the best care for advanced stage Parkinson’s disease. The site offers videos, articles, community resources and guides. Visit CareMAP at caremap.parkinson.org to learn more or call the NPF Helpline at 1-800-4PD-INFO (473-4636). The Helpline specialists can answer questions in English and Spanish.

http://health.einnews.com/article/286112650/RB7b30lhEtbBzomz