Herbicide Tests and Storage in the U.S.

Be aware that some areas have tested on and around bases.

Agent Orange and other herbicides used in Vietnam were tested or stored elsewhere, including many military bases in the United States. Below is information from the Department of Defense (DoD) on projects to test, dispose of, or store herbicides in the U.S.

http://www.publichealth.va.gov/exposures/agentorange/locations/tests-storage/usa.asp

More detailed Here:

- See more at: http://www.publichealth.va.gov/exposures/agentorange/locations/tests-storage/usa.asp#sthash.WOW19tir.dpuf



EXAMPLE:

New Details On Md. Agent Orange Tests

February 23, 2011 2:45 PM

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Health, Local, News

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Activist Group, Agent Orange, Army, Fort Detrick,Testing

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FREDERICK, Md. (AP) — Military records are shedding new light on Agent Orange testing decades ago at Maryland military installations and raising new concerns about health hazards from the Vietnam War-era chemical defoliant.

Fort Detrick released fresh details Tuesday on outdoor experiments with Agent Orange and similar compounds at the Army installation in Frederick.

The Army says it also tested Agent Orange outdoors at the former Fort Ritchie near Cascade, a disclosure that is expected to further delay redevelopment of the property by its private owner, Corporate Office Properties Trust.

The concerns stem from a dioxin in Agent Orange that has been linked to adverse health effects among service members who were exposed to it when it was used reduce enemy cover in Vietnam in the 1960s and early 70s.

Fort Detrick is trying to counter claims by an activist group that its carelessness with chemicals caused a cancer cluster among neighboring residents. An investigation by state public health officials hasn’t found higher rates of cancer within a mile of Fort Detrick than in the rest of Frederick County.

Fort Detrick officials said their preliminary archive search confirmed that researchers used nearly 17 pounds of Agent Orangeand other chemical defoliants from 1944 to 1968. The tests were done mostly with hand-held sprayers on 6-feet-by-18-feet outdoor plots sheltered by portable windscreens, the report said.

The Army said the compounds were identical to commercially available defoliants that were widely used across the country for farms, lawn care, rights of way and other applications.

The attack on Fort Detrick is led by Randy White, a former televangelist who heads the Kristen Renee Foundation, named for a daughter who grew up near Fort Detrick and died of brain cancer in 2008. Her mother, White’s ex-wife Debra Cross, died of kidney cancer in November.

White said Tuesday that he doesn’t trust the military to make public all its Agent Orange research.

What’s Delaying New Drugs? Part One: The Cost of Traveling to Trials

Picture this: you sign up for a clinical trial testing a new medication, perhaps because you want to help advance Parkinson’s disease (PD) research.

You learn that as part of the trial, you have to spend one weekend a month at a major medical center, which is a three-hour drive away. You are unable to drive so your spouse or care partner has to come with you, missing a day at work. But the study will not cover the out-of-pocket expenses you incur for gas, tolls, or hotel — not to mention that lost day at work.

What do you do? If you are like most of us, you might decline to participate in the study. In a small survey PDF conducted recently among a group of volunteer Research Advocates, one in four respondents told us that they have declined to be a part of a clinical study because it did not offer travel reimbursement.

This poses a challenge for all of us, and for the future of Parkinson’s drugs. If people are not signing up for trials for financial reasons, then those trials will take longer to complete. Longer trials, in turn, result in higher costs for the manufacturers, and most importantly, delays for the people with Parkinson’s who are hoping for new and better treatments.

At PDF, we work to identify the obstacles that are delaying better treatments, and then to implement strategies to overcome them. In this new series, “What’s Delaying New Drugs?” we’ll be sharing with you the obstacles we have identified since we began our research advocacy program almost a decade ago, and then letting you know what we are doing to solve them — and how you can help. Our first topic is the matter of travel reimbursement.

A Complicated Issue

Do the sponsors of drug trials routinely reimburse travel expenses? If so, what type of costs will they typically cover? And if lack of adequate reimbursement is a significant reason for why recruitment takes so long and trials are delayed, what can we do to fix it?

The answers vary greatly. In some clinical trials, such as those sponsored by the National Institutes of Health (NIH) in its own facilities in Bethesda, MD, participants can show proof of travel costs, and be reimbursed for some or all out-of-pocket expenses. But in PDF’s survey, an astonishing 58 percent of respondents who traveled to and from a study site over a two-year period reported that they received no form of travel reimbursement. For the 42 percent that did receive reimbursement of some kind, the most common expenses covered were for meals, parking and gas or mileage.

Why don’t all the trial coordinators reimburse legitimate expenses? In some cases, sponsors or scientists may not have funds in their budget to reimburse for travel. In other cases, sponsors say they would like to offer reimbursement, but the boards that oversee the ethics of studies, called Institutional Review Boards (IRBs) may discourage or reject the request to reimburse, on the grounds that reimbursement could be interpreted as a form of coercion. In yet other cases, the coordinators running clinical studies may not be aware that lack of travel reimbursement is the reason people are not signing up. We cannot point the finger at one person or institution for creating this problem; there may in fact be many reasons. And each one may require its own solution.

What Can Be Done?

PDF, through its network of more than 230 PDF Research Advocates, is using several strategies to understand and solve the problem. And you can help.

First, we are collaborating with scientists at four leading institutions in the US to examine transportation reimbursement and other barriers to research. These institutions are all recipients of the first crop of Leadership Awards through the program we call Parkinson’s Advocates in Research (PAIR). A condition of the award, each of which carries a grant of $5,000 to establish a formal collaboration between scientists and patient advocates, is that study sponsors discuss travel reimbursement and other barriers with PDF Research Advocates and subsequently develop solutions.

Second, we will be redoing the original pilot survey on a wider scale, requesting feedback on travel reimbursement from people with Parkinson’s and care partners across the US. If you have participated in a clinical study in which travel reimbursement has been an issue — positive or negative — please share your experiences with us at www.pdf.org/travel14.

Lastly, we are making a special effort to support the work of our Research Advocates who are tackling this issue locally. Below, see examples of their inspiring work.

Conclusions

We all want better treatments for Parkinson’s at a faster pace. And while many factors are delaying new drugs, including transportation costs, there are solutions for each one. Together, we can all make a difference in overcoming those obstacles and come closer to our ultimate goal: a cure for Parkinson’s disease.

How PDF Research Advocates Are Helping to Remove Roadblocks to Drug Development by Transporting Volunteers to Trials

PDF Research Advocate Steve DeWitte of New Preston, CT, told us a few years back, “When I ask people with Parkinson’s why they are not involved in PD studies, many reply, ‘Because I have no transportation.’” His solution was launching the Clinical Trial Transportation Program (CTTP). By partnering with Beth Israel Deaconess Medical Center in Boston, MA, and Columbia University Medical Center in New York, NY, CTTP has helped 37 volunteers to participate in studies by driving them to these two medical centers.

PDF Research Advocate Ken Reck of Chicago, IL, saw the same issue in his community. So he asked Lucy Blasucci, R.N., program coordinator at the PDF Research Center at Rush University Medical Center in IL, if he could serve as a volunteer driver for those unable to get to trials. So far, he has provided transportation for two participants, driving them to Rush twice a month. Ms. Blasucci, said, “Ken realized what’s really important in research — people. You can have all the money in the world, but you can’t do anything without people volunteering for trials. Ken is a prime example of how one individual really can make a difference.”

PDF Research Advocate Carolyn Weaver of Freeland, MI, knew back in 2008 that a clinical trial at the NIH in Maryland needed more volunteers. But instead of asking friends to travel, she thought, “Why not bring the trial to the people?” She invited scientists from the NIH to travel to her home state and recruited 43 people with PD and loved ones to participate. They all completed the clinical study that day! In addition, she provided transportation (a donated bus) for many of those participants, some of whom traveled from as far as 100 miles away.

PDF Research Advocates Marilyn and Jay Phillips of Charleston, SC, thought if travel is so difficult, why not let people participate in trials remotely? They are helping to study the potential role of telehealth, which would allow people to participate in trials using their computers to see and talk to scientists from home. So far, they have helped PDF medical advisor, Christina Vaughan, M.D., of the Medical University of South Carolina, to recruit 17 people to her Parkinson’s telehealth study. As Marilyn said, “Enabling people to volunteer for trials remotely will encourage greater and more diverse enrollment.”

Gaucher Disease Points Way to Possible New Treatment for Parkinson’s

Science News- Jun 11 2014

Researchers may have identified a novel therapeutic approach to Parkinson’s disease (PD) by examining tissue samples from people with a rare genetic disorder known as Gaucher disease (GD) who have an increased risk of PD. Their findings, published in the May 2014 issue of the journal Brain, suggest that a medicine called ambroxol might help treat some forms of PD.

People with Gaucher disease have mutations in both copies of a gene known asGBA. In the disease, the enzyme produced by this gene (glucocerebrosidase), is unable to do its job of clearing out fatty deposits in certain cells and organs. Carriers of Gaucher (people with only one mutated copy of the gene) do not show any symptoms of the disease, but have been shown to have an increased risk of developing PD.

Scientists do not yet understand how mutations in the GBA gene contribute to PD risk. To help answer this question, researchers led by Anthony Schapira, M.D., D.Sc., F.R.C.P., at University College London in the United Kingdom, removed and examined skin cells from five people with Gaucher, four carriers (those with just one mutated copy of GBA) who also had PD, two carriers without PD, and three people without GBA mutations or PD (controls). They then treated the cells with a medicine called ambroxol which is known to boost the activity of the glucocerebrosidase enzyme and observed the effects.

Results

• As expected, in the skin cells of people with Gaucher disease, researchers found that the enzyme glucocerebrosidase was significantly less active than in other groups — in fact, it was reduced by 95 percent compared to healthy controls.  
• The enzyme activity in Gaucher carriers, both with and without PD, was about 60 percent of normal. 
• Cells from people with Gaucher and carriers (people with one or two mutated copies of GBA) showed more signs of stress, which can lead to cell damage or death, than controls. 
• In cells from all groups, the drug ambroxol increased the activity of the enzyme glucocerebrosidase and also increased its production.
• Cells with GBA mutations, which were treated with ambroxol appeared healthier and showed fewer signs of stress.
• In neuronal cells, ambroxol reduced the levels of a certain protein, calledalpha-synuclein, which is known to accumulate in PD.

What Does It Mean?

Better understanding of the biological connection between Gaucher disease and PD may help us to develop new treatment approaches for PD. Findings from the current study suggest that ambroxol, a drug already on the market in Europe should be studied as a treatment for PD, possibly in those who carry mutations in the Gaucher gene (GBA), but hopefully in people with PD generally.

The current study suggests that Gaucher and PD may both be linked to cellular recycling — the ability of cells in the body to recycle waste. In Gaucher disease, when there are mutations in the GBA gene, the cell is unable to properly dispose of fatty deposits. Similarly, in PD, cells may be unable to effectively dispose of troublesome proteins like alpha-synuclein.  

The study shows that ambroxol may possibly “clear the drains.” In this case, the drug does so by increasing the amount of the enzyme glucocerebrosidase, and increasing its activity level. Cells with increased glucocerebrosidase activity looked healthier and were able to better dispose proteins such as alpha-synuclein.

While ambroxol is a medication already on the market for other health conditions, these laboratory studies provided only modest improvements of enzyme activity and will still need to be confirmed. It will be important to further study the cellular effects of GBA mutations and of ambroxol in neuronal and animal models of PD.  

Reference: McNeill A, Magalhaes J, Shen C, Chau K-Y, Hughes D, Mehta A, Foltynie T, Cooper JM, Abramov AY, Gegg M, Schapira AHV (2014) Ambroxol improves lysosomal biochemistry in glucocerebrosidase mutation-linked Parkinson disease cells. Brain 137:1481–1495.  DOI: 10.1093/brain/awu020  http://dx.doi.org/10.1093/brain/awu020

Genetic Variations Related to Gastrointestinal System Linked to Parkinson’s

- Jun 17 2014

A new study bolsters the theory that Parkinson’s disease (PD) may begin in the digestive system.  In research published in the May 17 online edition of Movement Disorders, scientists report that variations in the genes for certain intestinal proteins responsible for keeping the gut healthy may be associated with an increased risk of PD.

The human intestines are lined with trillions of microorganisms, some helpful and others harmful. Several lines of evidence point to a role for the digestive tract early in PD. For example, clumps of alpha-synuclein – the hallmark of PD in the brain – have been found in nerve cells of the colon in people who later developed PD. In addition, constipation is a common early symptom of PD, as are inflammation of the gut and an overgrowth of certain bacteria in the small intestine. 

Researchers led by Samuel M. Goldman, M.D., M.P.H., at the San Francisco Veterans Affairs Medical Center, wanted to understand whether genetics can explain why some people develop PD and others may not. Following up on the gut-PD link, they asked whether variations in the genes encoding key proteins in the intestines may be correlated with increased or decreased risk for PD. These gut proteins are called peptidoglycans and help the body’s immune system recognize and respond to bacteria.  But the components of these proteins can vary slightly from person to person.  

To test whether variations in the genes for the peptidoglycans proteins were associated with PD risk, the researchers analyzed DNA in blood samples collected from 518 people with PD and 543 healthy individuals. Participants were drawn from two earlier studies.

Results

• Common variants in three of four genes encoding peptidoglycan proteins were associated with an altered risk of PD – both decreased and increased risk.
• The results were similar in two distinct populations of people with PD.

What Does It Mean?

This study is the first to link genetic variations in bacteria-responsive gut proteins called peptidoglycans to Parkinson’s disease. In light of other associations between the gut and PD, the authors suggest that peptidoglycan proteins may play a role in causing the disease by influencing a person’s immune response to bacteria in the gut. Because this epidemiological study did not actually demonstrate that these genetic variations actually precipitated PD, further research is needed to discover the mechanisms by which these proteins are linked to PD. Nevertheless, this study helps define a new direction for scientists to pursue an understanding and potential treatment to Parkinson’s disease.

Reference: Goldman SM, Kamel F, Ross GW, Jewell SA, Marras C, Hoppin JA, Umbach DM, Bhudhikanok GS, Meng C, Korell M, Comyns K, Hauser RA, Jankovic J, Factor SA, Bressman S, Lyons KE, Sandler DP, Langston JW, Tanner CM (2014) Peptidoglycan recognition protein genes and risk of Parkinson's disease. Mov Disord. Ahead of Print DOI:10.1002/mds.25895http://dx.doi.org/10.1002/mds.25895 

SMOKING, THE SENSE OF SMELL AND PARKINSON’S DISEASE

Smoking, the Sense of Smell and PARKINSON’S DISEASE

Advice to the general population is that smoking is bad for your health…. very bad, indeed.  But there has been information to the contrary for people with PARKINSON’S DISEASE…some 60 studies report that smokers have a lower risk of developing PARKINSON’S DISEASE.  So, then, what are people with PARKINSON’S supposed to believe?

Smoking, for the general population, is known to lead to lung cancer, Chronic Obstructive Pulmonary Disease (COPD) and ultimately death.  Smoking goes straight through the olfactory system, bypassing any intermediate functions that could serve as a filter, carrying any and all environmental toxins from tobacco or smoke straight to the lungs and the brain.  It is well known that one of the early pre-motor symptoms of PARKINSON’S DISEASE is the loss of sense of smell.  Could smoking possibly be implicated in this?  Could smoking also be an environmental factor implicated in reducing the loss of dopamine producing neurons in the brain?  Can the effects of smoking and early non-motor symptoms help explain the relationship between genetics and environmental factors leading to either neuroprotection or the development and progression of PARKINSON’S DISEASE?

A group of researchers at Pennsylvania State University, Milton S. Hershey Medical Center headed by Xuemei Huang, M.D., Ph.D. developed a study to improve understanding of whether or how smoking affects olfaction in PARKINSON’S DISEASE and how the involvement with olfaction contributes to the development of PD.  They planned their study to. “test the hypothesis that smoking is associated with better olfaction in PARKINSON’S DISEASE.”

Seventy-six people with PARKINSON’S and seventy non- PARKINSON’S control subjects were recruited.  Of the PARKINSON’S subjects, there were 22 with a history of smoking and 54 who had never smoked.  In the control group, 17 were smokers and 53 were non-smokers. The histories of the smoking habits of all subjects were carefully noted.  Only one PARKINSON subject and three of the control subjects were current, active smokers.  While all the smokers had begun smoking in their mid to late teens, by their mid thirties they had stopped smoking.  All subjects were assessed by the mini-mental state examination (MMSE) and the University of Pennsylvania Smell Identification Test (UPSIT).  Non-motor symptoms were also carefully evaluated.

In the PARKINSON’S subject, age of onset was found to be at least 4 years later among the smokers than the nonsmokers.  Control subjects had better results overall for UPSIT smell tests than the PARKINSON’S subjects, however the smoker PARKINSON’S subjects scored better than the nonsmokers.  Smell scores among the PARKINSON’S subjects declined in relationship to age, but decline among the control subjects were not significant.  Women tended to have much better sense of smell than male subjects in the control group, but this was not seen in the PARKINSON’S group.  There was no correlation between the number of cigarettes smoked, the number of years smoked, or the years since the cessation of smoking and the scores of the UPSIT in the PARKINSON’S group, nor was there a correlation between the UPSIT scores and the age of onset or duration of the disease. This study also did not find a relationship between smoking and other non-motor symptoms, such as constipation, etc.

This research has shown some interesting results…that sense of smell in smokers is usually considered to be impaired was not found among the controls, and interestingly, the sense of smell among smokers in the PARKINSON’S group was better than that of the non-smokers.  More interesting, that a history of smoking appears to confer a neuroprotective effect and delays the onset of the disease but that smoking after diagnosis or the use of nicotine patches does not offer the same protection. The results of this study suggest that the protection offered from smoking or nicotine may be a gradual process that occurs over many years before the onset of the motor symptoms.

The authors of this study do show a protective correlation between smoking and the onset of PARKINSON’S DISEASE; however they are aware that there may be other factors, such as personality traits, head trauma, or the use of other medications that may play a role in these results.  Other studies will be needed to verify these results, but this study has made a genuine contribution to understanding the relationship between smoking and PARKINSON’S DISEASE.

Lucasson, E>B>; Sterling, N.W.;Lee, E-Y; Chen, H; Lewis, M.M.; Kong, L; Huang, X.; History of Smoking and Olfaction in Parkinson’s disease.  Early View. Mov. Disord.  doi 10.1002/mds.25912

PPMI Shows Protein Levels Lower in Spinal Fluid of People with Parkinson’s

FoxFeed Blog

PPMI Shows Protein Levels Lower in Spinal Fluid of People with Parkinson’s

Posted by  Maggie McGuire, June 24, 2014

Principal investigator of the Parkinson’s Progression Markers Initiative (PPMI), Ken Marek, MD, presented the latest findings from the landmark biomarkers study — sponsored by The Michael J. Fox Foundation — at the 18th International Congress of Parkinson's Disease and Movement Disorders in Stockholm, Sweden earlier this month.

Among findings from the baseline analysis is that participants with Parkinson’s show lower levels of the protein tau in spinal fluid than do control participants. This finding is particularly interesting because people with Alzheimer’s disease show elevated levels of tau.

“We can't explain it at the moment. It is leading to much discussion, and additional research is needed to understand what we are seeing," Dr. Marek told Medscape. "We are hoping to develop an array of biomarkers that will be of value to track the disease, and to identify subsets of patients that may respond to specific therapeutics."

The PPMI findings were selected for a Blue Ribbon Award at the congress, the professional meeting of the International Parkinson and Movement Disorder Society. The meeting concludes with a Blue Ribbon Highlights session of the best research presented during the proceedings.

Study Shows Promise for LRRK2 Inhibitor Approach

FoxFeed Blog

Posted by  Maggie McGuire, June 13, 2014

A recently published study funded by The Michael J. Fox Foundation and using MJFF research tools showed two avenues through which inhibiting the function of the protein LRRK2 may help treat Parkinson’s. The paper from the laboratory led by Andrew West, PhD, from the University of Alabama at Birmingham, appears in the Proceedings of the National Academy of Sciences.

Mutations in the LRRK2 gene are the greatest known genetic cause of PD, accounting for one to two percent of all cases of PD and more in certain ethnic populations. Mutations appear to heighten activity of the LRRK2 protein. Therefore, development of LRRK2 inhibitors is a priority of the Foundation.

“LRRK2 is one of our most promising areas of research toward a therapy to stop or slow the progression of Parkinson’s, and MJFF has established a roadmap to learn more about this target and build the infrastructure to accelerate discovery and drug development,” said Marco Baptista, PhD, MJFF associate director of research programs.

Part of the Foundation’s LRRK2 roadmap is the creation of research tools such as pre-clinical models and antibodies important to hasten the development of future therapeutics. The LRRK2 knockout pre-clinical model is bred without the LRRK2 gene, which can mimic the effects of a LRRK2 inhibitor drug.

Dr. West and his team studied both the LRRK2 knockout model and a wild-type model (typical form) when they introduced an excess of the protein alpha-synuclein. Parkinson’s is marked by clumps of alpha-synuclein in brain cells, which leads to cell death. The scientists compared the effects of too much alpha-synuclein in a LRRK2 knockout and a control model.

They found cell loss from the excess alpha-synuclein in the wild-type model but not in the LRRK2 knockout, meaning inhibiting LRRK2 could protect from neurodegeneration.

Using new antibodies developed by MJFF, Dr. West also found that LRRK2 was highly expressed in cells that responded to injury, leading to another hypothesis that inhibiting LRRK2 may help alleviate a specific type of inflammation. To test this hypothesis, they also introduced an inflammatory agent into both models and found, again, that the wild-type model experienced cell loss while the LRRK2 knockout did not.

Often tests of LRRK2 inhibitors use models with LRRK2 gene mutations. Since this study compared only knockout and wild-type models, its findings suggest LRRK2 inhibition may also benefit people who have PD but no LRRK2 mutations (the majority of PD patients).

“This broadens the window of those who might be helped by this therapeutic approach beyond only those with a LRRK2 mutation,” said Dr. West. “Seeing protection in this study gave us the green light to attempt and copy the symptomatic results pharmacologically, to help find a drug that we can bring to clinical trial.”

He is working on testing LRRK2 inhibitors, through separate projects with the Alabama Drug Discovery Alliance and with Pfizer. MJFF is funding the collaborative project with Pfizer.

Learn more about LRRK2.

TAGS: Pre-clinical Models, Pathophysiology, LRRK2, Alabama, Neuroprotective/Regenerative,Research News, Alpha-Synuclein, Inflammation, Genetics, Funding Priority Area, Research Tool,Research Grants

Boosting self-repair may preserve brain in Alzheimer's, Parkinson's

In Alzheimer's, Parkinson's, variant Creutzfeldt-Jakob and other brain-wasting prion diseases, cells in the brain gradually deteriorate, begin to function abnormally, and die. However, some parts of the brain have the capacity to self-repair and make new brain cells. A new study suggests there could be a way to harness this and perhaps preserve brain function in neurodegenerative diseases.

Writing in the journal Brain, study leader Dr. Diego Gomez-Nicola and colleagues from the Centre   for Biological Sciences at the University of Southampton in the UK describe how previous studies have already revealed that even in neurodegenerative diseases there is evidence that the brain carries on attempting to repair itself.

One area of the brain that shows evidence of self-repair or neurogenesis is the dentate gyrus, which forms part of the hippocampus, which controls learning and memory.

Studying the brains of mice with a prion disease, the team found evidence of increased self-repair in the dentate gyrus that partially compensated for the loss of brain cells caused by the disease.

Their detailed investigation helped them identify how the new brain cell populations were generated over time, and how they integrated with existing brain circuits.

They found that as long as the self-repair occurred in the early or middle stages of the brain-wasting disease, new brain cells integrated into existing circuits in a way that preserved some brain function - but this failed when the disease was advanced.

Postmortem samples also suggest evidence of self-repair in diseased human brain

The team says they also found evidence to suggest increased self-repair in postmortem brain samples of patients who had variant Creutzfeldt-Jakob disease and Alzheimer's disease when they died.

The authors conclude that the brain has some ability to orchestrate self-repair and suggest there is a time-limited window of opportunity for potential treatments to boost this mechanism and preserve brain function in patients with neurodegenerative diseases.

Some parts of the brain have the capacity to self-repair and make new brain cells.

Dr. Gomez-Nicola says the study opens new avenues "to identify what specific signals are used to promote this increased neurogenic response, with views focused in targeting neurogenesis as a therapeutic approach to promote the regeneration of lost neurons."

As they strike primarily in mid- to late-life, neurodegenerative diseases become increasingly more common in aging populations. For instance, in the US, where estimates suggest by 2030 around 20% of the population will be over the age of 65, some 5 million Americans are living with Alzheimer's disease and another 1 million have Parkinson's. Finding treatments and cures for neurodegenerative diseases has never been more urgent.

Funds from the European Union Seventh Framework Programme and the Medical Research Council helped finance the study.

In October 2013, Medical News Today learned how researchers found a new target for drugs against brain cell death. Writing in Science Translational Medicine, they report how they blocked a major pathway leading to brain cell death in mice using an orally administered drug-like compound.

Written by Catharine Paddock PhD

Programs that may help those in need financial medication assistance

I have not used the following services, so I can not recommend one service over another. That is up to you to decide. I am not responsible in anyway.

You should check it out  and come to a decision yourself. I am just assisting by listing a few sites that I found on the internet that may help those needing assistant to get their medicine free or at a reduced cost.

http://www.needymeds.org/inclusions/newuser.htm

http://freemedicineprogram.org/requirements.html

http://www.simplefill.com

http://rxassist.org

https://www.pparx.org

I wish I could wave a magic wand and help. It is heart breaking knowing that some people have to choose between medicine and food. I hope the above programs can be of help to you.

WHAT CAUSES PARKINSON'S DISEASE?

While the exact cause of Parkinson's disease is unknown, research points to a combination of genetic and environmental factors. Some cases may be caused more by genetic factors and others due more to environment, with many somewhere in between.

Researchers have identified certain genes that may play a role in Parkinson’s disease, but studies are still ongoing to understand exactly how mutations in these genes are associated with Parkinson’s. Some of these mutations may cause the disease, but other mutations in Parkinson’s genes may raise the likelihood of onset but would need a separate factor — such as an environmental exposure or another genetic mutation — to ultimately bring on the disease.

While researchers have not identified a cause yet, studies have highlighted some factors that are associated with either greater or lesser risk of Parkinson's disease. Risk factors that have been identified include:

Advancing age

                                     
Family history

Male gender

Exposure to toxins, such as herbicides and pesticides

Head injury:: Boxing

While such studies do not definitively link these factors with Parkinson's disease, they highlight areas where further research may guide us to better understand risk and develop treatment strategies.