New PD drug study to halt progression

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Today, researchers are evaluating an investigational drug that focuses on the earliest stages of Parkinson’s disease that may potentially offer a new option for recently diagnosed patients.

If you have been recently diagnosed with Parkinson’s disease, you may want to consider a newly opened study. It is evaluating the safety and potential efficacy of an investigational drug that targets alpha-synuclein (α-syn), a molecule associated with Parkinson’s disease. The investigational drug is being studied to see if it may potentially help to slow or reduce disease progression.

For people who:

— Have been diagnosed with Parkinson’s disease in the last 3 years

— Are 40 to 80 years of age

— Have not received levodopa in the last 12 weeks

Learn more! #sponsored #cureclick
Learn why I’m talking about Clinical Trials – we are closer than ever to deciphering this complex disease ..but even if we don’t discover a cure at worst we would have developed new treatments to make living with PD a thing of the past…by becoming as close to normal as possible.
Just in the two decades i have been involved in this field i have seen so many advances and people like you and me can have fruitful productive lives even when afflicted with PD.

today at least 3 new drugs are in the fda approval line due to be released within the next 6months to a year and perhaps sooner. but there are also many more on the works like this new #Parkinsons disease clinical study which is in the process of evaluating an investigational drug to see if it may potentially help slow or reduce disease progression. if you are interested in finding out more or think you like to participate and add your own grain to the cure go to the link below
#cureclick https://curec.lk/2PkJInb

@maria de leon 2018

How To Make The Most Out of Your Neurology/MDS Visit: by Dr. De Leon

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I know many of you have expressed the concern that some of the issues don’t get addressed or addressed in a timely manner when visiting your neurologist or MDS. This especially difficult to deal with since many do not live close to a neurologist and have to travel a way to go see them. So of course you are tired and frustrated of  having to wait both to see a neurologist or movement disorder specialist as well as in pain and discomfort if asked by your doctor to be off your medications for evaluation.

We all have experience the feeling of disgust at ourselves when after leaving the doctor’s office after being there several hours we realized that we forgot to ask or discuss an issue that was utterly important.

A few tips to minimize frustration and maximize our time and neurologists focus on our issues are the following recommendations based on my extensive experience as a Parkinson’s specialist and as a patient.

First, I am sure many of you have experienced the phenomena I like to call the ‘doctor syndrome.’ For some reason, it happens to me all the time and I am certain it happens to you because many of my patients told me that they were worst before coming to see me. I am not sure why that is but my Parkinson’s symptoms are always better when I see my doctor!

Second, especially if it’s the first visit make sure if possible to bring someone with you that can be your ears. Because unless you are savvy in the medical field and medical jargon, after the first few sentences where your doctor tells you the diagnosis I guarantee you will not remember anything else said or explained.

As physicians we usually concentrate on what’s visually in front of us and have to pay close attention to non visible symptoms and rely on you unfortunately too much to let us know how your life is being affected by these invisible otherwise known as non-motor symptoms.

Parkinson’s disease is extremely complex illness and increasingly getting more as we speak even though most neurologists and movement disorder specialist like me typically spend an hour or more per patient it is impossible to cover ALL possible symptoms in detail.

Therefore it is imperative that you prioritize your problems:

  1. Are you there as a new patient and looking for diagnosis and new treatment?
  2.  New patient for second opinion and alter treatment?
  3.  Established patient for management of symptoms?
  4.  Established or new looking for disability?
  5.  Interested in participating in studies or research and what are you willing to do?-e.g. participate in studies with new unknown meds vs. known medications already approved, invasive vs. non-invasive?

All of these will require different focus from your doctor.

I recommend that you limit your discussion to main reason (chief complaint-e.g. new patient looking for diagnosis) you are there and two other symptoms that need immediate addressing!

If you have more pressing issues make an appointment sooner than what they will suggest don’t settle for appointment in 3-6 months if NOT doing well!

Also if need a family intervention to discuss prognosis and long-term treatment plan and care, make appointment with you, family and doctor exclusively to discuss these issues. Let the doctor know ahead of time that this is purpose for visit so doctor and staff can be prepared for meeting as far as time so you won’t be rushed and also and most importantly so doctor can formulate plan ahead of time and bring ancillary services if needed such as social services or names of assisted living, nursing home, or rehabilitation places etc.

Third, know your insurance coverage of medications. This will expedite treatment and allow doctors to know which prescriptions to write. Unfortunately, due to recent changes in healthcare and medication coverage (at least in this country) it is becoming increasingly more common for doctors particularly specialists to prescribe medications base on a patient’s formulary rather than what they think should be first choice! Ask for samples, ask for assistant programs, and let them know if meds will require pre-authorization or paper work filled out. If you are new patient or established patient who will be on new drug- it is best to not have that medication sent to mail order pharmacies until required dose achieved and / or know if can tolerate otherwise will get stuck with a bunch of medicine can’t use.

Fourth, always bring a list of your medications better yet the medications themselves which should ALWAYS include name of over the counter medicines even if they are as needed because could possibly interact with new prescription.

Fifth, ask for side effects of new meds, what to expect, how fast will notice improvement, do they need to be titrated and how often? In this should also inquire if meds will affect women issues such as safe if planning to conceive or are breastfeeding, ask especially if risk of melanoma, breast cancer and prostate cancer in family to be referred to specialist for follow-up given that some medicines will increase these risk and others like melanoma simply by having PD make you at higher risk.

Finally, at least in this country know that if you require paperwork filled out there most likely be a fee and a few days to get paper back so plan ahead.

Ask for literature, support groups, as well as ancillary services such as speech therapy if needed.

If you follow these simple rules, I guarantee that you will have a much happier and successful journey with PD as you and your doctor work as a team.

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Dr. M. De Leon is a movement disorder specialist on sabbatical, PPAC member and research advocate for PDF (Parkinson’s Disease Foundation); Texas State Assistant Director for PAN (Parkinson’s Action Network). You can learn more about her work at http://www.facebook.com/defeatparkinsons101 you can also learn more about Parkinson’s disease at www.pdf.org or at www.wemove.org; http://www.aan.org, http://www.defeatparkinsons.blogspot.com All materials here forth are property of Defeatparkinsons. without express written consent, these materials only may be used for viewers personal & non-commercial uses which do not harm the reputation of Defeatparkinsons organization or Dr. M. De Leon provided you do not remove any copyrights. To request permission to reproduce release of any part or whole of content, please contact me at deleonenterprises3@@yahoo.com contributor http://www.assisted-living-directory.com Contributor http://www.lavozbrazoriacounty.com

DAT Scan: Can it Really Tell Me I have PD? : By Dr. De Leon

Dat Scan (Ioflupane I 23 injection also known as phenyltropane) is a radio pharmaceutical agent injected into the veins of a patient known as SPECT nuclear medicine test. When this test was approved in was under the premise that it will be an added tool in the armamentarium of the neurologists/ movement disorder specialist to help decipher difficult cases.

So, the answer to the question…can it tell you have PD? – NO!

The test can’t confirm you have PD! – it can only tell if there is abnormality in the dopamine system which can include any and all of the Parkinson’s plus syndromes including Parkinson’s disease. If abnormal it means there is a problem in the dopamine system period.

Furthermore, like any test is user dependent. My husband who is a neuroradiologist in a small community who has extensive experience in reading PETs for lots of disease and specializes in the brain would not give an accurate reading of a DATSCAN as his colleagues up the road in Houston at the medical center who do hundreds of them.  Since the only PET scans of the brain that have been FDA approved are for diagnosis of dementia- there are standard things that the radiologists look for by guidelines set by the Academy of Radiology who also mandate general training in reading of these tests across the border to all practicing radiologist to maintain their credentials. However, no such mandate has been given in the reading in SPECT or DAT scans  for diagnosis of PD and only those that are in academic centers who have seen hundreds of these studies are actually the only ones qualified to give an expert opinion as to the “quantitative” measure of the uptake in the brain.

If you have received a diagnosis of PD from an expert specialists in movement disorders and are improving or responding to dopamine therapy there is no reason or gain by getting a Dat scan. Likewise, if someone suspects of Parkinsonism due to PSP, MSA etc. no added benefit will be obtained by getting this scan, you might in fact be wasting your money ($2500 to $5000) and time.

This test was only intended to be used as another diagnostic tool to help decipher between dopamine and non dopamine diseases which can mimic PD. Now it is over used unfortunately for the wrong reasons. The FDA only intended to be used to differentiate between essential tremors and PD. In my humble professional opinion, Dat scans are not required for treatment or diagnosis and only place for a Dat scan is in academics for studies or in rare cases where a procedure like DBS or Pallidotomy is being considered and physician is not sure if treating essential tremors vs. PD; which if this is the case, I would be reluctant to have a brain surgical procedure when clinical diagnosis is in question! This invariable will lead to poor outcome… many other treatments can be employed until diagnosis is certain.

Another thing because the trace used to measure dopamine activity is radioactive and expensive is not ordered till the day or night before the test. Thus, if you decide to cancel at the last minute because not feeling well you are causing the facility to lose a lot of money and some facilities may even charge you for it. If you have history of thyroid disease or take thyroid replacement you may not be able to do the test.

So short and long …Doing a DAT SCAN CAN NOT TELL ANYONE THEY HAVE PD – do not be fooled by those that claim otherwise!!! Parkinson’s unfortunately still remains primarily a clinical diagnosis and ONLY way to diagnosed with 100% certainty is brain biopsy or at autopsy. However, there is a caveat, with more studies being done in academic centers understanding and standardization of DAT scan reading is increasing slowly among those involved in the field. at the same time we are slowly gaining knowledge of PD and its varying presentations. Therefore, it is conceivable that in the near future, we might be able to combine the knowledge of two to predict and detect patients who will develop PD.

According to a new study, Danna Jennings, MD, Clinical Research Director at the Institute for Neurodegenerative Disorders in New Haven, and colleagues have attempted to do just this via the Parkinson Associated Risk Syndrome (PARS) study to identify a large-scale cohort of individuals at risk for Parkinson’s disease using olfactory testing and DAT imaging. What they have found is that although no one had PD symptoms at baseline despite abnormal DAT scans or reduced ability to smell ; 46% of individuals with loss of sense of smell combined with a deficit on the DAT scan have shown to develop clinical features of Parkinson’s disease within four years.

“The knowledge that comes from this study will have important implications for the recruitment of individuals for future neuroprotective trials,” stated Dr. Anthony Lang, Director of the Movement Disorders Clinic at Toronto Western Hospital. Remember, in a previous blog “Thinking Outside the Brain for a Parkinson’s Cure,” I commented that often trials fail or are doomed to fail from the start when it comes to finding neuroprotective agents because we often don’t even have the right diagnosis. If we are able to successfully predict who will develop PD from these early markers: 1) we can institute treatment a lot earlier in hopes of retarding or slowing progression and 2) trials may have a greater chance of success than previously; because we may no longer have to wait until a patient’s disease evolves to the motor stage causing obvious manifestations of Parkinson’s disease in order to include in “early –stage” trials which by definition is no longer early since by then these patients have lost at least 50% of their dopamine producing neurons.

Source: Olfactory Testing and DAT Imaging May Lead to Early Detection of Parkinson’s disease. Neurology Reviews. 2014 22(8):18-21.

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Dr. M. De Leon is a movement disorder specialist on sabbatical, PPAC member and research advocate for PDF (Parkinson’s Disease Foundation); Texas State Assistant Director for PAN (Parkinson’s Action Network). You can learn more about her work at http://www.facebook.com/defeatparkinsons101 you can also learn more about Parkinson’s disease at www.pdf.org or at www.wemove.org; http://www.aan.org, http://www.defeatparkinsons.blogspot.com All materials here forth are property of Defeatparkinsons. without express written consent, these materials only may be used for viewers personal & non-commercial uses which do not harm the reputation of Defeatparkinsons organization or Dr. M. De Leon provided you do not remove any copyrights. To request permission to reproduce release of any part or whole of content, please contact me at deleonenterprises3@@yahoo.com contributor http://www.assisted-living-directory.com Contributor http://www.lavozbrazoriacounty.com

 

Dopamine, Chocolate & Art In PD: By Dr. De Leon

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What do these things have in common? Well, everything! They are the heart and soul of what makes us thrive as human beings!

Long before I became I neurologist and Parkinson’s specialist & patient, I was a neurobiology major studying the basis of behavior learning the dopamine structures and pathways. I remember vividly having a discussion, thinking out loud if the chemicals of our brains, in our brains particularly things like dopamine REALLY DID defined us as individuals …giving us our unique personalities and abilities?

Dopamine that magnificent chemical which permeates our brains deep in the basal ganglia controlling everything from precision of movement, to deep feelings of love and everything in between. No wonder dopamine, art and chocolate all play such a vital role in most of our life’s. One author referred to “art  like chocolate for the brain.” This may be spot on since the mere thought of chocolate causes our brains to start producing dopamine.   I feel like I have come full circle… now a Parkinson’s patient …I have become a chocoholic and most definitely have experienced a profound change in personality much to my chagrin! However, a little dopamine and chocolate go a long way to restore my natural perky, adventures self back…maybe why I crave that wonderful substance so much?  Perhaps the Mayans were unto something after all when they named cacao the drink of the “god’s”-it is pure ecstasy, heaven on earth! Dopamine is the feel good chemical of the brain and if it mimics this well there you have it same as taking cocaine…same effect ( except without all the addiction and lethal side effects!)

This may explain why as our Parkinson’s advances a lot of us have a tendency to have an increase in craving for sweets particularly chocolate. But, there must be more to the story since scientist have attempted to find treatment for Parkinson’s using chocolate. The reason behind this is that the mere thinking of eating chocolate and of course consumption of chocolate releases quantities of endogenous dopamine according to research at the Georgia health science university. Intake of chocolate can give us an immediate quick ” fix.” It is no wonder that I and my grandmother and my close friend seem to gravitate towards chocolate as the demands on our body for dopamine increases and as the medications wear off especially when under stress and consumption of dopamine is at an all time high in our systems. Thus,  I firmly believe that some of that so called ” binging” phenomena seen with dopamine medication intake is due to fluctuations in blood stream and brain levels of dopamine …if we were able to maintain steady states the binging would diminish …as I have personally noticed in myself that when I am not as busy to forget to take medicines on time I don’t have the need to take or scrunch for ” chocolaty” treats. This may be an indication for us all to be more vigilant of our medication intake schedules and if we are reaching for supplement to increase the endogenous/ intrinsic production this could be a sign of fluctuations in a non motor system just like having a DYSKENESIAs or dystonia in the motor system.

Furthermore, chocolate has shown to release yet another chemical known as serotonin which is also believed to be involved in patients with Parkinson’s and dysfunction is what leads to depression especially in woman. Serotonin as many of you know is the compound or chemical used to treat depression, this again maybe a physiologic reason why women tend to reach for chocolate as comfort food more than men since it provides a natural antidepressant affect. So, both art and chocolate gives us a sense of pleasure and satisfaction by releasing natural dopamine chemicals in our brains. And as I described at the beginning dopamine is what makes us who we are as individuals by being more prone to be in love more easily than others, pursue pleasures more often than some and even have more developed reward driven centers than others. So, yes, those pesky chemicals in our brain like dopamine can wreak havoc in our world if not balanced throwing our established personalities for a loop making us behave in opposite ways than we once were. This can occur rather frequently after replacement begins by tipping scales over in excess of dopamine and lowering other chemicals in brain like serotonin which were once in perfect harmony. These chemicals REALLY do define us as human beings but more importantly as individuals with certain traits and characteristics that is why some of us are more driven than others, more likely to seek immediate gratification while others not so much. They determine our compulsions and our thrill seeking behavior. Some of us love the rush of adrenaline (use for dopamine precursor of adrenaline) so we look for jobs or hobbies that make us feel good by always having us on the border of excitement.

Although, there have been suggestions of a PD “personality type” (I will not go into detail about all the literature at this time) I truly believe that the “personality type” that is typically described that of rigid, socially awkward, depressive, overly controlling, morally rigid and stoic goes against every person whom I have ever known to have PD young and old, including myself, my grandmother and my best friend. Each one of us had opposite traits than those described in the literature prior to disease. I firmly believe that is the lack of dopamine or rather decline which causes these characteristic behaviors to begin to take place. All 3 of us became extremely depressed and despondent at the very early signs of disease even long before any motor symptoms were present. In talking to many groups during my advocacy work, I have found this to be the case as well for most of them. Since PD premorbid, or preclinical symptoms can present up to 10-15 years prior to motor symptoms occur what retroactive analysis of PD patients in regards to personality is encountering is the pre clinical state and not the normal phase of the individual. No studies have gone back to interview friends and family or coworkers of these patients further in the past while in school or at much younger ages. What this tells me is there is still much we don’t know and understand and endless possibilities for both clinical and scientific research to be done in this arena to attempt to clarify some of these very important questions. Therefore, when dopamine is reintroduced there may be a tendency to over correct and shift balance because we are disrupting normal brain homeostasis pushing dopamine in another direction…..Too much dopamine causing excessive behaviors that were once in check like punding (fascination with meaningless objects and activities), over eating (overindulgence, binge eating) increase in thrill seeking behaviors like hyper sexuality ( having multiple partners, engaging in porn), gambling, impulse buying, reckless driving, hoarding. Perhaps, our minds and bodies are trying to compensate for time lost, feelings, emotions lost-.trying to find a way of making us feel alive again or regain a sense of the way we were but go too far in the other direction because we are not sure how long the feeling will last…like a drug addict trying to maintain a high for as long as possible.

 Interestingly, there seems to be a greater occurrence of these behaviors in Europe followed by the US, then Canada ( not found a basis for this yet but something to think about) The abnormal behaviors are described as “failures to resist or control impulse, drive, or temptation to perform an act that is harmful to a single person or multiple groups including self.” I tried to find a reason for this but was unable to. I suspect that it has to do with numbers of prescriptions and years of usage but I could not get into a back to retrieve information. Perhaps some of you could enlighten me. Both Mirapex and Requip were introduced in the states in the late 1990’s. And NEUPRO was introduced in early 2000’s but only briefly because later taken off market and only returned to market just within last 2 years or so. I know that this has been out in Europe and in Canada a lot longer but longest in Europe and at higher doses than used in the US. These aberrant behaviors are mostly associated with dopamine agonists especially Mirapex (pramipexole), & Requip ( ropinirole) to a less extent NEUPRO (rigotine). actually all behaviors except the sexual and gambling problems occur in women more often then in men. interestingly…I think it has to do with women’s emotional needs to control world and express themselves emotionally- the way female brains are wired different particularly due to certain hormones (cortisol, adrenaline, oxytocin) in  dealing with stress; although present in both men and women they vary in quantities while dealing with stress. So, if we can learn to understand the gender differences in coping with stress, and predisposition to certain types of behaviors and realize that these come on most often at end of dose when wearing off and with long term usage of meds perhaps we can begin to make a difference in quality of life and avoid embarrassing moments or going into debt because can’t control spending or jeopardize relationships due to hyper sexuality and perhaps due learn to use alternative treatments to release endogenous dopamine in conjunction like chocolate intake to maintain steady states.

Do not make any changes to your regimens without first discussions with your physicians or health care providers. This piece is intended to arouse stimulation and thought of possible mechanisms of action which could be leading to some of these behaviors and also explore some of the alternative treatments based on literature and basic science. Please feel free to make any comments, very interested to hear your thoughts especially about intake of chocolate and also about when meds were introduced in your countries of origin? Thank you.

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Dr. M. De Leon is a movement disorder specialist on sabbatical, PPAC member and research advocate for PDF (Parkinson’s Disease Foundation); Texas State Assistant Director for PAN (Parkinson’s Action Network). You can learn more about her work at http://www.facebook.com/defeatparkinsons101 you can also learn more about Parkinson’s disease at www.pdf.org or at www.wemove.org; http://www.aan.org, http://www.defeatparkinsons.blogspot.com

All materials here forth are property of Defeatparkinsons. without express written consent, these materials only may be used for viewers personal & non-commercial uses which do not harm the reputation of Defeatparkinsons organization or Dr. M. De Leon provided you do not remove any copyrights. To request permission to reproduce release of any part or whole of content, please contact me at defeatparkinsons101@yahoo.com

Parkinson’s Disease: an Autoimmune DIsease? By Dr. De Leon

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For some time me and others like myself have been toying with the idea could it be possible that Parkinson’s is yet another autoimmune disease like diabetes or thyroid disease or even pernicious anemia? Or even an inflammatory disorders like ulcerative colitis? Perhaps some genetic subtypes can more easily fall into this category than others. For instance, it is interesting that the majority of Parkinson’s Disease (PD) patients have B12 deficiency as a co morbidity. Or that the type of Gaucher patients that are most likely to develop and have an increase risk of developing PD are type I patients – those without central nervous system involvement.

Patients who posses Gaucher and are carriers of a GBA gene mutation have increased risk of developing Parkinson’s disease and parkinsonism. Gaucher patients carry a deficiency of the enzyme glucocerobrosidase.  This enzyme is typically acts on the glycolipid glucocerobroside. So, when the enzyme is defective, glucosylceramide aggregates and accumulates in white cells (which are responsible for mounting immune attack but particularly like to congregate in the macrophages. The macrophages are like “Pac Man” hungry white blood cells gobbling up invading bacteria. They are formed in response to an infection or accumulating damage or dead cells. Thus, they are unable to break down fatty acids and they have abnormal accumulation into the white cells and macrophages which are the ones responsible for being able to mount an appropriate immune response against a foreign attack like bacteria or virus. But, if these cells who are to destroy the offending viruses etc. are unable to take them up because already full with unwanted stored up material then more white cells, T cells and macrophages have to be created jamming up the system and thus indiscriminately attacking normal cells throughout the body and brain. Some evidence of this is present in the preliminary data in a study I am involved at the University Of Texas Houston Center. My friend and colleague has informed me that my blood levels of T cells and other inflammatory and immune markers have been measured and found to be elevated and have improved as my disease has been treated. Data hopefully will be released soon.(this is all preliminary and confidential).

The other subtype of PD which points to an inflammatory and autoimmune component is the LRRK2 gene phenotype. Many of these patients with this type of phenotype have a history of inflammatory bowel disease most often ulcerative colitis. Ulcerative colitis (UC) is another autoimmune disease characterized by T-cells infiltrating the colon. Although Crohn’s disease another inflammatory bowel disease which is much more extensive beyond the colon as compared to UC has also been seen in this group of PD patients, once again making a case for a possibility of our immune system going haywire and attacking the nervous system. In medicine, it is dogma to say that once a patient has one autoimmune disease they are at higher risk for contracting another and we frequently see this in our practices. But, until recently, no one had really dared to contradict the underlying notion that “neurons” were somehow protected from attacks from the immune system. Although, we have clear evidence of instances of where there is an autoimmune reaction in the central and peripheral nervous system after vaccine injections causing “Acute disseminated encephalomyelitis” and also MS but these have only targeted the connections not destroyed or actually damaged actual Neurons! Therefore, if it is true that Parkinson’s neuronal loss is a result of attack of the immune system itself it would revolutionize not only our thinking but our way of preventing and going after treatments for Parkinson’s.

So, recently researchers tested this hypothesis to see if indeed living neurons would display antigens (like bacteria or viruses) which then trigger an immune mediated response to neutralize this force. Drs. Sutzer and Cebrian from Columbia University used in vitro mouse and human neurons from embryonic stem cells. Their studies revealed that under certain circumstances- including those known to occur in PD. These neurons produced a special protein which presented an antigen which was recognized by the T cells and triggered an attack on these neurons. They prove an autoimmune process can happen and neurons can be attacked but is not known if this is the initial or final response or if all Parkinson’s is started this way or only those subtypes I alluded to previously. One thing is for sure future is bright and field is ripe for new and novel treatment options!

For more information on the subject go to:

  http://www.sciencedaily.com/releases/2014/04/140417151227.htm

 

 

 

 

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Dr. M. De Leon is a movement disorder specialist on sabbatical, PPAC member and research advocate for PDF (Parkinson’s Disease Foundation); Texas State Assistant Director for PAN (Parkinson’s Action Network). You can learn more about her work at http://www.facebook.com/defeatparkinsons101 you can also learn more about Parkinson’s disease at www.pdf.org or at www.wemove.org; http://www.aan.org, http://www.defeatparkinsons.blogspot.com

All materials here forth are property of Defeatparkinsons. without express written consent, these materials only may be used for viewers personal & non-commercial uses which do not harm the reputation of Defeatparkinsons organization or Dr. M. De Leon provided you do not remove any copyrights. To request permission to reproduce release of any part or whole of content, please contact me at defeatparkinsons101@yahoo.com

Thinking Outside the Brain for a Parkinson’s Cure : By Dr. De Leon

Thinking Outside the Brain for a Parkinson's Cure : By Dr. De Leon

I don’t think inside the box, I don’t think OUTSIDE the box, I don’t EVEN KNOW where the box is!”- unknown

The other day while I was giving a talk about how to diagnose PD, I was giving my usual spill about ” in the hands of a specialist like myself- accuracy is 95%,” when someone in the audience asked me a very thought provoking question. So, how early can you diagnose with such certainty? Therein lies the BIG Problem in why we need biomarkers and be able to think outside of our current diagnostic criteria!

In reality, I told her it is still very accurate above 90% for someone that has a lot of experience -that’s where art meets medicine …you get your “intuition” about things based on past knowledge and experience and are able to predict with fair accuracy and since at this point there is NO difference in treatment really between one type of Parkinson syndrome or another it does not much matter at the beginning…However, where it becomes a problem is being able to predict outcome and assign patients to studies because you have to follow strict criteria and even if you just KNOW that someone has Parkinson’s or an atypical variant you have to back it up…and as you all know EVERYONE is different so it may take some one ten years to develop all 4 cardinal symptoms of Parkinson’s while someone else only 2. So, it is hard to at present time to make a lot of head way in the discovery of new medications that might be beneficial to slow or stop the progression of early stage of Parkinson’s because unfortunately there is still a lot of variability in early diagnostic accuracy depending on the field. Even among neurologist not Parkinson’s specialist, a published study indicated that for PD patients who had symptoms less than 5 years, they were wrong 50% of the time. These patients turned up to have another reason for their Parkinsonism which translates to automatic failure of any drug being studied since 50% of the patients in any given trial of early PD may not even respond because they don’t have the right diagnosis!

So, I realized that in order for us to start thinking OUTSIDE the BOX we need to FIRST get a CLUE of where the BOX is – what Parkinson’s looks like- acts like, presents like so THAT EVERYONE IS on the same page and able to diagnose with same degree of accuracy!!! This needs of course to go back to medical school, residency and communities and we all as PD advocates can play a role in educating health staff and other health professionals about Parkinson’s. The better we are at recognizing early symptoms the better chance we have for participating in neuro-protective trials as well as be able to determine biomarkers early on.

A lot of money and research is being channeled to the finding of these biomarkers in the recent years. According to research initiated by the MJFOX foundation, we may have insight into possible new biomarkers coming from the retina, colon, or skin which could lead to not early detection but a cure for PD.

For a number of years, neuroscientist have known that alpha-synuclein the abnormal protein seen in Parkinson’s is also found outside of the central nervous system. This protein is a major constituent of Lewy body disease another Parkinson’s like disease. However, alpha-synuclein which is located largely at the ends of neurons plays a part in both familial and sporadic Parkinson’s disease as well.

Through the usage of very powerful machines and equipment known as optical coherence tomography (OCT) which takes high resolution pictures of the retina, scientists and doctors have found that PD patients have thinner retinas compared to healthy individuals.
At this point, they are not sure if there is enough evidence to use as a biomarker because they are not certain how specific it is to Parkinson’s since it also has been seen in Alzheimer’s patients who had Parkinson’s as a co-morbidity.
Alpha-synuclein is normally present in several types of retinal cells…so the possibility of serving as a biomarker exists either by accumulation or (absence) at this time no cells have been found in PD patients.

Another place that accumulates alpha-synuclein outside the brain is the colon. Published studies have revealed that immunostaining for Alpha-synuclein in living Parkinson’s individuals results in a positive outcome in 69-100% of the time but not seen in MSA ( multi -system atrophy) patients. Another study showed that these findings preceded the clinical motor symptoms. So far, results which are small have been mixed. They are easy to attain because of flexible sigmoidoscopy can access distal colon easily plus screening is required of all over 50 years of age. However, not all pd people showed pathology. Some explanations have been given which include variation of tissue involvement, change in pathology over time and perhaps unsuitability of this being used as a biomarker.

The third place where scientists are looking for a possible biomarker outside the central nervous system which is also full of alpha -synuclein is the skin. One reason, people are interested in this area is because of the new wave of knowledge and thinking about the etiology of Parkinson’s. Since, we now know that there is a prodrome period of non- motor & autonomic symptoms that precede the development of the motor symptoms, researchers believe that perhaps alpha-synuclein pathology starts outside the brain and migraines to the brainstem.
Also, studies have suggested that peripheral nervous system is equally involved in Parkinson’s. Evidence of this was suggested in an issue of Brain in 2008 where Parkinson’s patients were found to have cutaneous denervation resulting in higher threshold for heat and touch but decrease for pain.

Because the skin is not only easily accessible but also has a plethora of autonomic involvement, and many autonomic nerves making it a great candidate for study.
A study in the Journal of Neuropathology & Experimental Neurology proposed that the skin may be a beneficial site for diagnostic predictability since 70% of PD cases and 40% of PD with dementia revealed positive alpha-synuclein immunoreactivity while absent in other Parkinson plus syndromes like MSA ( multisystem atrophy) , PSP( Progressive supranuclear palsy), & CBGD (Cortico-basal-ganglia-degeneration). The results are very promising but still need to be validated and compared longitudinally and with autopsy confirmed cases of PD.

Out of all these the most promising is the skin biopsies as a possible biomarker..easy and readily accessible and this far able to differentiate between Parkinson’s and other Parkinson’s plus syndromes.
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For more information on the topic: MJFOX research on biomarkers
Haugh, Zac., Movement Disorder Focus: Alpha-synuclein :Thinking Outside the Brain. Practical Neurology. Vol. 13, No.2, March 2014

Dr. M. De Leon is a movement disorder specialist on sabbatical, PPAC member and research advocate for PDF (Parkinson’s Disease Foundation); Texas State Assistant Director for PAN (Parkinson’s Action Network). You can learn more about her work at http://www.facebook.com/defeatparkinsons101 you can also learn more about Parkinson’s disease at www.pdf.org or at www.wemove.org; http://www.aan.org, http://www.defeatparkinsons.blogspot.com

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