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Dr. Joel Binder

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About Dr. Joel Binder

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  1. Of Possible Interest

    Also from The Michael J. Fox Foundation for Parkinson’s Research: Investigating the Role of LRRK2 in Mycobacterial Infection LRRK2 Challenge, 2013 Objective/Rationale: Mutations in the LRRK2 gene are the most common known genetic risk factors for Parkinson's disease. Although we know that these mutations can cause Parkinson's disease, the physiological function of the LRRK2 protein (genes encode proteins) remains a mystery. However, a hint of the LRRK2 function emerged from genetic studies in people with leprosy, a chronic infection caused by Mycobacterium leprae. They found that LRRK2 is associated to susceptibility to infection with M. leprae. The aim of this project is to find out if LRRK2 participates in the immune response to mycobacteria. Project Description: We will use a wide range of cellular and pre-clinical models of mycobacterial infection combined with methods of LRRK2 manipulation such as pharmacological inhibition and gene knockdown/knockout. First, we will evaluate the impact of pharmacological manipulation of LRRK2’s activity and LRRK2 loss of function on the infective process of Mycobacterium tuberculosis in cellular models. Second, we will investigate whether the loss of LRRK2 in knockout models alters the susceptibility to infection by M. tuberculosis. Relevance to Diagnosis/Treatment of Parkinson’s Disease: Understanding the physiological roles of LRRK2 has the potential to shape our view of its role in Parkinson’s disease as well as our approach to targeting LRRK2 as a means to developing a therapy. Anticipated Outcome: At the end of the project, we will know if LRRK2 is involved in the immune response to mycobacteria. RESEARCHERS Maximiliano Gabriel Gutierrez, PhD Location: London, United Kingdom
  2. Of Possible Interest

    OK. Also I am interested in pursuing and researching out any other possible Parkinson's treatments that this Forum's viewers might need further information about and have found beneficial towards alleviating Parkinson's symptoms. This can even include herbal or homeopathic remedies.
  3. Of Possible Interest

    How and Why a Recent NIH Clinical Trial Can Also Indirectly Support an Infectious Cause For Parkinson’s In January of 2013 the FoxFeed Blog of The Michael J. Fox Foundation for Parkinson’s Research headlined a post Nicotine Patches to Stop…..Parkinson’s Disease? (file:///C:/Users/Joel/Documents/Nicotine Patches to Stop… Parkinson’s disease _ Parkinson'sDisease.html). Epidemiological data (in which patterns in comparative populations are analyzed) has long supported the idea that those who have spent years as smokers don’t get PD as often as non-smokers. The Fox Foundation became interested in learning more about nicotine and PD to the point that it launched a U.S. study to explore the potential therapeutic benefits of the very same nicotine patches that people take to try and quit smoking. https://clinicaltrials.gov/ct2/show/NCT01560754 . In this study, which Fox called the “NIC-PD” trial (Nicotine-Parkinson’s Disease Trial) they planned to enroll 160 PD patients in Germany and the U.S., providing some volunteers with nicotine patches and others with placebo patches, in order to determine if the real patches might have the potential to slow the progression of PD. In the American arm of the study, eighty of these patients would be enrolled at 11 centers in the United States. The best case scenario was that the results would both show that disease progression was slowed, and are convincing enough to encourage a larger follow-up study which could prove to be more definitive. Collaborators in the study were: Michael J. Fox Foundation for Parkinson's Research Parkinson Study Group (PSG) International Parkinson Fonds Germany GmbH German Parkinson Study Group (GPS) German Parkinson Society (DPG) Philipps University Marburg Medical Center Results were expected in early 2017, although no formal data to this point have been published. In the meantime, in 2012, the Journal called Neurology published a U.S. study which concluded that transdermal nicotine could be safely administered to nonsmoking subjects with MCI (mild cognitive impairment) over 6 months with improvement in primary and secondary cognitive measures of attention, memory, and mental processing, but not in ratings of clinician-rated global impression. (The clinical global impression (CGI) rating scales (Guy 1976) are commonly used clinician-rated measures of global symptom severity and treatment response for patients with mental disorders.) These investigators concluded that this initial study provides evidence for nicotine-induced cognitive improvement in subjects with MCI; but that, whether these effects are clinically important will require larger studies. (http://www.neurology.org/content/78/2/91.abstract) However the larger question remained how does nicotine prevent Parkinson’s and theories as dispersed as that nicotine may reduce the level of protein misfolding (prions) and prevent any proteins that have misfolded from accumulating in the cells to a genetic reason soon predictably sprang up. But there was another possibility that clearly went under the radar of these scientists. By the early 20th century pellagra, caused by either the complete lack of or severe deficiency of vitamin B3 spurred research as to just what the chemical structure of vitamin B3 might be. Two forms of this vitamin were uncovered –both of them, so similar to nicotine that UK scientists named them “nicotinic acid” and “nicotinamide”. And in Britain they remain so-named to this day. However regulatory bodies in the US thought it might be better to hide such direct naming, lest people seek to obtain their Vitamin B3 through smoking cigarettes. Therefore in the US, nicotinic acid was renamed niacin, and nicotinamide was retitled “niacinamide”. Such linguistic maneuvering, of course, did not change the fact that both molecules were still closely related to nicotine. The story of nicotinamide’s anti-mycobacterial capacity is unknown to many, because the literature predates the careers of most people currently involved in the treatment of these infections as well as the National Institutes of Health PubMed database. In 1945, the first trials of streptomycin that involved humans were taking place in the United States, and a worldwide search for other effective anti–Mycobacterium tuberculosis therapies was underway. That year, in Paris, Ernst Huant reported a serendipitous discovery regarding the use of nicotinamide for the treatment of patients undergoing radiation therapy for “lung tumors.” He found that nicotinamide therapy, which he had initiated in an attempt to protect patients’ mucous membranes from the effects of radiation, shrunk those lung infiltrates that were caused by M. tuberculosis. This report complemented another report from France by Chorine, who suggested a new role for nicotinamide, distinct from its known vitamin effect, as an anti–M. tuberculosis therapy. McKenzie et al., who apparently were screening compounds without knowledge of either Huant or Chorine’s work, independently confirmed these findings. Two structurally related compounds, pyrazinamide and isoniazid, were found to be effective anti–M. tuberculosis therapies in the period from 1945 through 1951; these discoveries were made, in part, through the use of nicotinamide as a lead compound. Nicotinamide monotherapy resulted in clinical improvement for up to 64% of M. tuberculosis–infected patients described in published reports. However, interest in nicotinamide as a treatment for M. tuberculosis faded rapidly when one of the foremost research groups of the day reported antagonism between nicotinamide and isoniazid, a first line drug against tuberculosis when they were used together as a 2-drug therapeutic regimen. By the 1990s, all of this information had fallen into relative obscurity. In fact, a comprehensive review of nicotinamide’s pharmaceutical effects, published in 1991 (the year of the first reported use of nicotinamide in HIV research), makes no mention of its effects against M. tuberculosis. Therefore, if James Parkinson’s original ideas that Parkinson’s could be a manifestation of tubercular ‘scrophula’ were correct, no other explanation for the Michael J. Fox’s NIH study entitled Disease-modifying Potential of Transdermal NICotine in Early Parkinson's Disease (NIC-PD) need be given. And now you know the rest of the story………………
  4. Of Possible Interest

    Hi Linda: Thank you for your inserts. Yes, sadly it’s a different world and I know just what you are talking about…..and yes the cancer study is one that I have been researching. Actually as mentioned, the anti-mycobacterials mentioned in this thread have been used in both people with Parkinson’s and Lyme’s, Lyme associated diseases, or just Parkinson’s disease. So this discussion is not really limited to Parkinson’s and Lyme-associated diseases. Interestingly, studies such as Fung’s showed that when patients suffering from Parkinson’s disease were treated with rifampin and isoniazid, two first line TB drugs, their condition was observed to improve [1]. Mital, Sarkari and Singh [2] published two cases of T.B. meningitis with Parkinsonism in which Parkinson’s symptoms almost completely disappeared during anti-TB therapy. In their first case, a 19-year-old farmer, seen six weeks after hospitalization, went from full-blown Parkinson’s towards a tremendous improvement in both his gait and tremors when put on antibiotics designed to combat tuberculosis. He was then lost to further follow-up. A second case they presented, involved a 25-year-old female, completely lost her tremors, parkinsonian facies and rigidity, again on anti-TB drugs. Mital, Sarkari and Singh’s conclusion: Not only did these cases illustrate that Parkinson’s could come from CNS tuberculosis, but this conclusion was reinforced by the fact that Parkinsonism almost completely disappeared through the use of anti-TB drugs. Concurrently, Kurasawa, Ikeda, and Inoue [3], puzzled by a lung mass in a 71-year-old Parkinsonian man’s chest, thought it to be malignant. But when it proved mycobacterial instead and the patient was put on two first-line drugs for tuberculosis, the patient lost his Parkinson’s –and two years later remained without it. A study by Otaki, at Ichikawa and Oizumi [4] at the Kirume University in Japan showed similar marked improvement in a 79-year old man placed on anti-tuberculous treatment after his upper right lung collapsed from the disease. Fuente-Aguado and Bordon [5], working out of the Infectious Disease Unit of Hospital Xeral in Bigo, Spain, treated a case of parkinsonism associated with tuberculous meningoencephalitis with TB medications. Seven days after starting tuberculous therapy, signs of Parkinsonism disappeared entirely, accompanied by overall improvement in the patient’s clinical picture. Fuente-Aguado and Bordon’s conclusion: The extinction of Parkinsonism after tubercular therapy supported tuberculosis as a cause of Parkinsonism. Solanki and Kothari [6] reported two cases of full-blown Parkinsonism developing in a 30-year-old housewife and a 32-year-old male laborer, both of whom were being treated for CNS tuberculosis and both of whom lost their Parkinson’s with continued anti-tubercular medicines. 1. Fung VS and Thompson PD. “Rigidity and spasticity”. In Tolosa E, Jankovic. Parkinson’s disease and movement disorders”. Hagerstown, MD: Lippincott Williams & Wilkins (2007): 504–513. 2. Mital OP., et al. “Parkinsonian symptoms in TBM. (a case report)”. Journal of the Association of Physicians of India 22:8 (1974): 629-631. 3. Kurasawa T, Ikeda T, Inoue T, et al. Pulmonary infection with Mycobacterium kansasii presenting as solitary nodule shadow in the left anterior basal segment. Nihon Kyobu Shikkan Gakkai Zasshi. 1997 Feb;35(2):215-9. 4. Otaki M., et al. “A case of endobronchial tuberculosis complicated with atelectasis of right upper lobe”. Kekkaku 69:7 (1994): 491-495. 5. Fuente-Aguado J de la and Bordon J. “Parkinson in an HIV infected patient with hypodense cerebral lesion”. Tubercle and Lung Disease 77:2 (1996): 191-192. 6. Solanki SV and Kothari VR. “Parkinsonian Syndrome”. Journal of the Indian Medical Association 68:12 (1977): 255-257.
  5. Of Possible Interest

    Hi Linda: Yes, I fully share your sentiments. The article you've linked to from the Czech Republic is excellent, and I thank you for posting it for us to read. Not to go too far off topic, but when I was considering Long Island breast cancer, I found it hard to swallow electromagnetic waves, etc and instead found a possible link to water contaminated with one of the pathogens listed in this article, Mycobacterium avium.....as the history of Eastern Long Island is rife with poultry and especially large farms with Long Island ducks and the waste they necessarily produce. And yet a closer scrutiny of the extent to which this pathogen was being tested for in drinking water, even to this day, was quite disappointing. Look, whether we like it or not we are part of an ecology consisting of many, many species: humans, animals, pets, insects, poultry etc which are also susceptible to these particular organisms, which are extremely difficult to diagnose. (To this day, there is no definitive cure for M. avium). And since they literally can attack all tissue and organ systems in the body, they can manifest in much more then one way in our body, including its central nervous system. James Parkinson was quite aware of a possible connection between Parkinson's disease and the Mycobacteria. It was one of the major reasons he wrote his Essay, and now I notice that some of the anti-mycobacterial drugs are used by Lyme experts to combat not only Lyme but its related tick-borne pathogens (babesia-bartonella-ehrlichia). Rifampacin and pyrazinamide are being used.............Rifampacin in combination with other antibiotics in particular. Yet Rifampacin, is a first line anti-mycobacterial, as is pyrazinamide. We know this from Dr. Horowitz's fine book and we also know it from the work of Dr. Ken Singleton (http://www.lymebook.com/antibiotic-treatment-for-babesia-bartonella-ehrlichia-co-infections). Also there are those cases, already cited, that led to the abatement of Parkinson's symptoms with anti-mycobacterial drugs (presently off patent), although I notice that most of those studies were done abroad and not in the United States. Yes.In lieu of Dr. Mac Donald's excellent presentation, the link to which you have shared, we know that present Lyme assays in America are far, far from bullet-proof. So it is puzzling why the CDC would not want to modify what is already in place. And unfortunately, I can not disagree with you about that our government seems to be deeply under influence of special interest groups, including the CDC and the NIH, even in such important/once important areas as the Zika virus and AIDS. But can we change this? I'm not so sure. So for now its best that we just simply try to help one another as best we can. Best regards
  6. Of Possible Interest

    Hi Linda: I am sorry to hear that your symptoms of fatigue and cognition have not lessened. You have also mentioned that you have a cerebral “meningioma”. How much of your present symptoms can be attributed to the agents you are now taking I cannot ascertain and it would be very useful if you would now mention all prescription, herbal medicines and other over-the counter medications that you are taking to cope with your conditions. Also, I have seen the presentations of MacDonald and Shapi. Very solid. I agree with much (but not all) in their respective talks. While on that subject, as previously mentioned please get not only the latest serology for Borrelia but also all other tick related disease. And yes, Shapi is suggesting the blood panel tested include mycoplasma, so include that as well. I imagine that the MRI they are giving you is simply to detect change in interval growth of your brain meningioma. Of course the radiologist’s conclusion in the original MRI which showed the meningioma would be valuable to know in so far as I would like to know whether he even considered a granulomatous meningioma in his radiologic differential. Also the location of the meningioma is important as to various symptoms that could be attributed to that location, such as Parkinsonian symptoms. It is doubtful that Lyme caused this particular space occupying meningioma in the brain. It might be good to ask the MRI techs and radiologist if they have considered a granulomatous meningioma in their differential such as from sarcoidosis or tuberculosis. MRI has limitations and will not get an actual organism identification as would a spinal tap or the even more invasive skinny needle biopsy (which I would not at this point suggest). The differential diagnosis for a meningioma is just below: Other primary brain tumours. Metastases from lymphoma and adenocarcinoma. Inflammatory disorders - eg, sarcoidosis. Infections - eg, tuberculosis. (tuberculoma) The good news is that ninety percent of meningiomas are classified as benign meningiomas. However there is, as mentioned, a differential diagnosis which must always be considered. Essentially, meningiomas are space occupying lesions. Although claimed “uncommon” by some, intracranial tuberculomas present in a similar way to meningiomas and can account for 0.5-30.5% of all intracranial lesions (Tiwari et al., 1989). In the study linked to below they have been treated successfully with a floxacins such as Levofloxacin (where it showed up as active against the disease in a culture and sensitivity) in conjunction with the standard anti-TB medicines rifampicin, ethambutol and pyrazinamide. In that study tuberculoma of the brain and not meningioma was confirmed based on histology of the excision biopsy and cerebrospinal fluid (CSF) culture (from a spinal tap) results: Mycobacterium tuberculosis resistant to isoniazid (INH) with sensitivity to other standard drugs, including fluoroquinolones, was cultured from the CSF. (https://www.ncbi.nlm.nih.gov/pubmed/21659503) There was a time (not long ago) when a “therapeutic trial” was suggested in major medical school textbooks such as Cecil and Loeb and Harrison’s for a variety of reasons and conditions. After all, it is less invasive then going after a lesion surgically. If a granulomatous lesion in the brain such as a tuberculoma of the brain or elsewhere was suspected, then such a therapeutic trial would be given and then checked radiologically, at intervals, for the recession of the lesion. Today, due to the malpractice atmosphere in the United States, that possibility is no longer feasible, and that is the reason why Dr. Horowitz must get a signed release from his patients before pursuing the use of anti-mycobacterial antibiotics for resistant Lyme and its related conditions. Probably any physician treating you, whether for Lyme-related disorders or other lesions will get an informed consent release from you as well. Dr. Horowitz, as mentioned, initially was drawn use of anti-mycobacterials original designed for TB because of Dr. Zhang’s study which showed Pyrazinamide to be effective against Lyme “persisters”. As you had mentioned Bartonella, which you aptly described as the one that leaves straight red lines sometimes on the skin that look like scratches but that aren't........I notice that some favor Levoquin and Rifampicin in its treatment and some (such as Dr. Horowitz) favor Zithromax (Azithromycin) and rifampicin. I would go with the Azithromycin and rifampicin (in addition to the pyrazinamide and myambutol mentioned above). The idea of pulsed therapy, mentioned by both Mac Donald and Horowitz seems to be a good idea, as in taking these antibiotics every other day. And as with all medicines, the higher the dose of the antibiotics used the greater the toxicity, so low doses should be maintained. Liver enzymes do have to be checked before starting drugs like rifampicin and pyrazinamide and then every few months (especially at the beginning of treatment) to make sure that they stay stable and do not increase. And from a gastrointestinal tract point of view, probably Nexium 20mg daily or ranitidine 150mg every 12 hours should be taken to calm the stomach and prevent gastric erosion. If it works and you feel better (symptoms resolve) they might be able to slowly wean you off your other meds. That would be ideal. I know that it might sound strange to you at this point, but it is my firm belief that the less medicines the better......unless the organism/organisms behind the disease are so virulent or persistent as to call for more. As always you must discuss things over with your doctor, who will make the final decision. Should that decision be affirmative I will come across with a proposed low dose schedule of treatment. Be well
  7. Of Possible Interest

    Good morning Linda: I do not come here to promote my brand on the World Wide Internet and the references given here to you are from other doctors and researchers. You can add to my experience besides my research activities that I am a Physician with extensive clinical experience as a diagnostician in general medicine, and with a particular interest (yet not a specialty) in infectious diseases…..and that will have to do. Although I did view some of the Mattman video I was unable to find and frankly did not have the time to view the Shapi video to this point. I can understand your hesitation as per that review you cited regarding seeing Dr. Horowitz, and I also know that you would prefer to go to Johns Hopkins. However I have also read some reviews touting his Lyme treatment which again includes medicines commonly used to treat TB (rifampin, pyrazinamide, etc). If you can find somebody at Hopkins that is open to trying Horowitz’s methods then by all means go to him or her. Dr. Ying Zhang might know of who fits this description. Horowitz, as I mentioned, from time to time does use Dapsone (another anti-mycobacterial, but this time for Leprosy) and although I am sure it works, its potential side-effects are rather frightening. By the same token he states that Dapsone does not necessarily have to be used. In the meantime, just as important is that you have your doctor refer you to an Infectious Disease specialist and that that specialist perform not only the latest serology for Lyme and Lyme related diseases but blood stains and cultures for a wide range of bacteria, including regular blood cultures, blood cultures for tubercular AFB (acid-fast bacilli) and blood cultures for anaerobes. This can be repeated in urine samples and if there is discolored phlegm, specimens of that as well. At the same time, cytology for the remote possibility of malignancy should be also done. An x-ray of the chest should be available and if it shows anything there should be an MRI with contrast follow-up. If there are any enlarged lymph nodes, either axillary (in the armpits) or on the neck these should be biopsied as should any mass that is found anywhere in the body. Again all of the diagnostic probes mentioned above should be used for any enlarged lymph node or mass as well as. And if the Infectious Disease specialist deems it advantageous than the more recent PCRs can be sought on all specimens sent in. A TB skin test should be performed and read in a timely manner. Depending on the severity of central nervous system symptoms and your general clinical situation (extreme lethargy, etc), a spinal tap might even be considered after doing an MRI with contrast of the brain. A tap, of course is a more invasive procedure and must be done in the hospital yet at times, providing all of the tests mentioned above are performed, it can yield invaluable information. I think you will agree that it is time, if not past time, for you to find out why you are feeling the way you are feeling. Dr. B.
  8. Of Possible Interest

    Dear Linda: Thank you for your kind words and informative posts. I am only here to help. No more no less. I have no other purpose. And if I didn't think I could help, I would not be here as I have many other projects pending. I understand that Johns Hopkins and Ying Zhang, MD, PhD is convenient to you, but be advised that long before I got wind of Dr. Horowitz's thoughts, which was basically only with your pushing and prompting, I was on the same track as what he is doing. How do I know that Ying Zhang is not the right man? Because I was in E-mail contact with him basically espousing what Dr. Horowitz is really getting at even before I knew the name Horowitz. And Zhang was rejecting my ideas after first sending me the E-mail: "Thank you for your mail. I would be interested. Please let me know what topic you have in mind and I'll see how we can collaborate. Best wishes" Well that never happened. Do not make the mistake therefore of thinking that Zhang and Horowitz are in the same league, because they are not. Horowitz has gone far beyond Zhang, and if he were reading this thread, he probably would understand everything that has been put down here. I know you have read some good reviews and some not so good. But the man has a large burden to lift with many, many patients -not all of which are forgiving should he not give the hour or two explanation that some patients demand. Also, all medicines have side effects. If you take too much Tylenol you can slip into liver failure. That can keep somebody stressed for a long, long time. Basically, and to put it in the simplest terms I know, just like we are subject to getting sick from microorganisms, so is the Ixodes tick. And once that organism is exposed to a virulent enough strain of a germ, when it bites it will transmit that germ to whomever it bites. I am also pointing out that the HHS Tick-Borne Disease (TBD) Working Group had better broaden their approach when it comes to tick-borne disease......although whether they do that or not is still in question. It can be proven in the laboratory, but only with sophisticated tests. And in order to order those tests one must approach things with an open mind - not always the case today. Something that might help them is a glance at studies like this. Egyed L, Makrai L. Cultivable internal bacterial flora of ticks isolated in Hungary. Exp Appl Acarol. 2014 May; 63(1):107-22. https://www.ncbi.nlm.nih.gov/pubmed/24366635 About half way down this abstract you will see this statement: “The results show, that members of some genera are able to replicate inside the ticks (Mycobacterium, Bacillus) which can increase their potential risk. Isolated bacteria/tick ratio continuously grew from larvae to adults, indicating that larvae probably are hatched sterile, but later bacterial uptake from the environment and from the hosts increases bacterial contamination.” There is more to be sure. But I will save it for later. Just as a preview when Burgdorfer, Hayes and Barbour did there second report on the Ixodes Dammini spirochete for the Journal of Bacteriology in June of 1983 they noticed a phage (viruses that live in bacteria) in this spirochete. This, they realized could very well have caused the pathogenicity of the spirochete, but the larger question was ....how did it get there? Phages or Bacteriophages can be transferred by one germ to another and often are. So was this a case of phage transfer from one germ to the Ixodes Dammini spirochete without which the spirochete would have been benign? Possible, very possible. And the nature of the phage offered clues as to just what this other germ might be. But that is for another time. It is interesting to note that at one point I found myself in a phone conversation with Lida Mattman PhD, prompted by some Lyme advocates. Lida had a great and long-standing interest in Lyme disease. Lida was also at one point a Nobel Nominee, but for this phone conversation she was just "Dr. Mattman". I had always admired this lady greatly and soon saw the key to her greatness. Over the phone she was picking my brain for any and all thoughts I held regarding Lyme disease and the phage which made it virulent. Yet, like many scientists I held back in favor of collaboration with an NDA (Non-Disclosure Agreement). So Lida as with Dr. Zhang unfortunately never collaborated. But now you have a much clearer vision of what my thoughts really were. Dr. B By the way, please do go ahead and take that latest Lyme disease assay, you mentioned, just to be sure that it is negative. Thank you.
  9. Of Possible Interest

    Thank you for that, Peace. I believe that this thread is just where it should be and that it will prove, in the end, to be relevant to its opening topic. Linda there is a book called How Can I Get Better?: An Action Plan for Treating Resistant Lyme & Chronic Disease published by St. Martin’s press on February 14, 2017 by Richard Horowitz, MD, who treats Lyme and related organism routinely. The treatment for every Lyme related microorganism you've mentioned is addressed in his book. Once you have read through this (It is on Google books) I will try to explain why what he says could possibly open-up new horizons to Lyme sufferers (or Lyme/Parkinson sufferers). Glancing through it, I saw that he even has one case of a female Lyme victim with Parkinsonian symptoms in there not unlike yours. Please read that section carefully. He mentions pretty extensively on the use of the following medicines that are first-line antimycobacterial agents which include Pyrazinamide, Rifampin, INH and even at times myambutol all for TB. In addition he talks about the use of Dapsone (which can be a highly toxic drug and is used for Leprosy). I am not a fan of Dapsone, but he has had good results with it. Nevertheless,he mentions that many Lyme sufferers show significant improvement with just Pyrazinamide, Rifampin, etc without the Dapsone. Why are these drugs being used? First of all they have proved successful. Secondly, he claims that in combination with other drugs they take care of Lyme's "persister" microbes. Personally I think there is more involved, but that is for tomorrow's research. Horowitz's work was in part stimulated by Ying Zhang, MD, PhD, a researcher at Johns Hopkins, who at one time was claiming good results with Lyme patients using Pyrazinamide, again to get at Lyme organisms that persisted. As for the reference I cited on Pub Med, you can also see that same reference plus another one in J. Kazda et al (eds.) The Ecology of Mycobacteria: Impact on Animals and Human’s Health. Springer Science & Business Media. June 10, 2010 522 pp. Page 214. There two Ixodes ticks are cited which yielded mycobacteria, both in the reference I gave you plus another one: [Beerwerth W, Eysing B, Kessel U (1979) Zentralbl. Bakteriol. [Orig A] 244:50-57.] [Blagodarnyi I, Makarevich NM, Blekman IM [1971] Probl. Tuberk. 49:74-76] https://books.google.com/books?id=d_xinfzC9o0C&pg=PA214&lpg=PA214&dq=ticks+infected+with+mycobacteria&source=bl&ots=iUd46CgpbD&sig=VqkIWZOplR_6i7m3Oc33L8M0L3U&hl=en&sa=X&ved=0ahUKEwjQ2PSmgs_WAhVLOiYKHbTlDtYQ6AEIPDAE#v=onepage&q=ticks%20infected%20with%20mycobacteria&f=false
  10. Of Possible Interest

    Frankly, at this point I share in your confusion. Obviously you are getting at the manifestations of a disease which you have in mind which includes both Parkinson’s manifestations and tick- related disease for which you have been seeking an answer. Some of these answers (prion disease, mycoplasma) at the moment I find irrelevant. However giving bits and pieces of the clinical (and perhaps laboratory) manifestations of a disease is not the best way to go about answering things. What is needed here is a complete clinical history, including symptomatology from the very beginning, and all relevant laboratory, serological and radiological evidence to substantiate whatever diagnoses have been handed out. For example to this point I can ascertain that Lyme disease assays have been negative, but has there been any direct proof of borrelia, babesia, and/or bartonella? Also, all that is in the popular Western notion of what constitutes tick-borne disease is not complete as can be seen here: https://www.ncbi.nlm.nih.gov/pubmed/?term=Blagodarya%2C+blekhman+the+role+of+ticks+in+the+transimission+of+tuberculosis+mycobacteria+Veterinaria+1971 As for macrolide antibiotics, an example is azithromycin (Zithromax) used in both Lyme’s disease and in the treatment of some of the non-Lyme’s organisms mentioned. But azithromycin also has anti-mycobacterial activity and is a first line treatment for Mycobacterium avium or fowl tuberculosis. Hope this helps.
  11. Of Possible Interest

    Regarding the prion theory, and theory is just what it is, you might want to take a look at this: http://www.slate.com/articles/news_and_politics/hey_wait_a_minute/1997/10/nobel_gas.html Of course where there is serious infection which goes under the radar of our present diagnostic capabilities, there is going to be misfolding of proteins. But the larger question is whether such proteins magically become infectious or are merely a by-product of underlying disease. I will go with the latter. And as for mycoplasma, your understanding is 100% correct and therein lies the rub. They are pathogens with no cell wall. They are also easily erased with macrolide antibiotics. There are much more serious and credible pathogens whose preferred form is cell-wall-deficient (CWD) and according to Mattman, mycoplasma can easily be mistaken for cell-wall-deficient mycobacteria like tuberculosis, a much more devastating microorganism. Best regards and have a great day.
  12. Of Possible Interest

    And thank you for sharing as well Linda. I do not subscribe to the Prion theory of proteins turning infectious by misfolding. Nor do I put too much stock in those who say mycoplasma is behind various disorders. However I do like to read the Bible. Be well.
  13. Of Possible Interest

    Hi Linda: I am a PhD. I realize that 99% of the time hypotheses are rejected, but I think this one might just be the 1% that cannot be. All I can say is that there is much to be said regarding a chronic infectious etiology for Parkinson's, the main question being which chronic infectious disease? The argument for this is clearly laid out in studies such as the recent review article What James Parkinson Really Thought was Behind Parkinson’s Disease which can be found at https://scientiaricerca.com/cons-articles.php as well as studies like Anthony Fink's at UC Santa Cruz. Also in July, 2017 Emery et al came out with a study done at the University of Bristol in the UK which might seem unrelated since it deals with Alzheimer's but really is not. Often tissue samples of Alzheimer's disease mimic those found in Parkinson's, and clinically patients with Alzheimer's often share symptoms with those of Parkinson's. Emery's study showed a 5 to 10 fold increase in microbes in the Alzheimer's brain which are related to the same order and family (Actinomycetales; actinobacteria) that Berstad and Berstad recently subscribed to as the most likely cause of Parkinson's. By 1911, Alzheimer himself realized that one infectious process in the brain could manifest it as two different diseases, and there are those that feel that Parkinson's is a manifestation of the same disease process which merely concentrates its attack on the substantia nigra and surrounding tissue areas. There is an interesting video on the subject of chronic infectious disease and Parkinson's which you can view by going to https://vimeopro.com/user60766261/richard-melvin-an-artists-journey-into-parkinsons/video/203722203The Michael J. Fox Foundation has also in the past shown interest in research related to the mycobacteria in the Actinomycetales as well (https://www.michaeljfox.org/foundation/grant-detail.php?grant_id=1310) although I am not certain what the outcome of this trial was. Hope this sheds some light on the issue.
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