Saturday, October 13, 2012

On the issue of transmissibility of Alzheimer disease: A critical review

Review



On the issue of transmissibility of Alzheimer disease: A critical review



November/December 2012


Keywords: Alzheimer, dementia, epidemiology, prion, transmissibility


Authors: Christian Schmidt, André Karch, Carsten Korth and Inga Zerr


Christian Schmidt


Corresponding author: schmidt102@gmail.com


Clinical Dementia Center; Department of Neurology; Georg-August University; Goettingen, Germany


André Karch


Clinical Dementia Center; Department of Neurology; Georg-August University; Goettingen, Germany


Carsten Korth


Department of Neuropathology; Heinrich-Heine University; Duesseldorf, Germany


Inga Zerr


Clinical Dementia Center; Department of Neurology; Georg-August University; Goettingen, Germany



Abstract:



Results from recent experiments with rodents imply that Alzheimer disease might be inducible by seeding Aβ peptides into recipient animals. In respect to this new experimental data, public health aspects as well as epidemiological data have to be reevaluated. In this article, the available experimental and epidemiological data are reviewed.



snip...



In summary, epidemiological evidence is extremely difficult to assess in this context. This is especially true, since case definitions and case detection rates have changed over time. Given the fact that a potential way of transmission is not only unknown but that no way of transmission can be excluded yet, careful assessment is imperative.




Public health implications




In the epidemic of non-communicable diseases AD plays an important role for morbidity and mortality as well as the associated costs. To date, AD is the 6th leading cause of death in the US and the projected costs in the US by 2050 are $1.1 trillion.66




Knowledge about transmissibility is essential in all kinds of epidemics for prevention, diagnosis and treatment. If AD featured transmission patterns comparable with those of prion diseases, iatrogenic induction/transmission would play a major role for public health. Prevention would be first priority and might include measures such as extended sterilization methods for surgical instruments as well as identification of patients potentially posing a risk as well as patients at risk. From a public health perspective also alternate ways of transmission not evaluated yet must be considered. For prevention to work, biomarkers for early disease detection must be validated, independently of the ways of possible induction since the disease itself starts well before clinical onset. As Sigurdsson stated correctly almost 10 years ago, future research on therapies might also be limited as long as there is no convincing evidence against transmissibility of AD.8 This is especially true for vaccination studies and clinical trials using parts of β-amyloid.




Conclusion




In conclusion, with this short review, we want to encourage a broader discussion and modern epidemiological research in this context. Well-designed epidemiologic studies have to be initiated. Methodologically these studies must be constructed to address the epidemiologically challenging aspects of Alzheimer disease such as dissociation between first neuropathological alterations and clinical onset, uncertainties in early diagnosis as well as AD heterogeneity.




This work was supported by a Bundesministerium für Bildung und Forschung grant within the German Network for Degenerative Dementia (KNDD-2, 2012-2015, determinants for disease progression in AD, grant no. 01GI1010C), as well as JPND, EU-FP7 PRIORITY.Authors’ contributions: C.S. was responsible for the initiation of the project, general conception and the composition of the final manuscript. A.K. provided parts of the section on epidemiology. C.K. provided parts of the section on experimental clues regarding AD transmissibility/inducibility. I.Z. was responsible for the initiation of the project, the critical review for contentual errors and writing parts of the conclusion. All authors contributed to the revision of the manuscript. The authors declare no conflicts of interest.









Wednesday, May 16, 2012


Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?


Proposal ID: 29403






Wednesday, May 16, 2012


Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?



Proposal ID: 29403



Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?



Background



Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both disease, and it’s variants, in many cases are merely names of the people that first discovered them. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer than the TSE prion disease. Symptoms are very similar, and pathology is very similar. I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. today, there is enough documented science (some confidential), that shows that indeed Alzheimer’s is transmissible. The risk factor for friendly fire, and or the pass-it-forward mode i.e. Iatrogenic transmission is a real threat, and one that needs to be addressed immediately.



Methods



Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.



Results



The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease. TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. you cannot cook the TSE prion disease out of meat. you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. the TSE prion agent also survives Simulated Wastewater Treatment Processes. IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. you can bury it and it will not go away. TSE prion agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. it’s not your ordinary pathogen you can just cook it out and be done with. that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.



Conclusions



There should be a Global Congressional Science round table event (one of scientist and doctors et al only, NO CORPORATE, POLITICIANS ALLOWED) set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics let science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already. what’s the use of science progressing human life to the century mark, if your brain does not work?








combined cannot exceed 350 Words




shortened to proper word count ;




Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?



Background



Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.



Methods



Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.



Results



I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.



Conclusions



There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.



end...tss




Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?



source references



Ann N Y Acad Sci. 1982;396:131-43.



Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).



Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.



Abstract



Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.










BSE101/1 0136



IN CONFIDENCE



CMO



From: Dr J S Metters DCMO



4 November 1992



TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES










CJD1/9 0185



Ref: 1M51A



IN STRICT CONFIDENCE



From: Dr. A Wight Date: 5 January 1993


Copies:


Dr Metters


Dr Skinner


Dr Pickles


Dr Morris


Mr Murray



TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES










Wednesday, January 5, 2011



ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions



David W. Colby1,* and Stanley B. Prusiner1,2













Tuesday, October 4, 2011




Molecular Psychiatry



advance online publication 4 October 2011; doi: 10.1038/mp.2011.120



De novo induction of amyloid-ß deposition in vivo



Our results suggest that some of the typical brain abnormalities associated with AD can be induced by a prion-like mechanism of disease transmission through propagation of protein misfolding. These findings may have broad implications for understanding the molecular mechanisms responsible for the initiation of AD, and may contribute to the development of new strategies for disease prevention and intervention. Keywords: amyloid; prion; protein misfolding; disease transmission








see more here ;












Wednesday, September 21, 2011



PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)












snip...end




Thank You for accepting my submission




# 29403, Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ? and the opportunity to present it, at the Alzheimer’s Association International Conference 2012 (AAIC), as a poster presentation. However, with great sadness, I must regretfully decline the invitation due to a medical reasons, and traveling to Canada, of which is not possible. ...



Thank You,



With Kindest Regards,



I am sincerely,



Terry S. Singeltary Sr.



P.O. Box 42



Bacliff, Texas USA 77518



flounder9@verizon.net



From:



Sent: Saturday, April 07, 2012 8:20 PM



To: Terry S. Singeltary Sr.





Subject: RE: re-submission



Dear Terry,



Yes, your proposal was accepted as a poster presentation. Please decline the invitation if appropriate.




Best Regards,



______________________________________




Alzheimer’s Association – National Office


225 North Michigan Avenue – Floor 17


Chicago, Illinois 60601





=============snip...end...source reference...# 29403==========












UPDATE JUNE 28, 2012



Scottish TSE Network November Symposium Announcement Event: 12 November 2012



Chair: Prof Hugh Perry, University of Southampton, Southampton UK



Location: The Roslin Institute Building Auditorium



If you would like to book a place at this event, please let Gila Holliman know.



Cost: £125.




Title: Is Alzheimer’s Disease a transmissible disease?




Speakers:


Session 1:


Prof Bob Will, National CJD Surveillance Unit, Edinburgh UK


Prof James Ironside, National CJD Surveillance Unit, Edinburgh UK


Prof Lary Walker, Emory School of Medicine, Atlanta USA




Session 2:


Prof Mathias Jucker, Hertie Institute for Clinical Brain Research, Stuttgart Germany


Prof William Van Nostrand, Stony Brook University, Stony Brook USA


Dr Claudio Soto, University of Texas Medical School, Houston USA




Session 3:



Dr Fabrizio Tagliavini, Instituto Neurologico Carlo Besta, Milan Italy


Prof Pedro Piccardo, Food and Drug Administration, Washington DC USA


Dr Bruce Chesebro, National Institutes of Health, Missoula USA







see ;




Wednesday, May 16, 2012



Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?



Proposal ID: 29403









14th ICID International Scientific Exchange Brochure -



Final Abstract Number: ISE.114



Session: International Scientific Exchange



Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009



T. Singeltary



Bacliff, TX, USA



Background:



An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.



Methods:



12 years independent research of available data



Results:



I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.



Conclusion:



I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.









Friday, October 05, 2012



Differential Diagnosis of Jakob-Creutzfeldt Disease








Monday, August 20, 2012



CASE REPORTS CREUTZFELDT-JAKOB DISEASE: AN UNDER-RECOGNIZED CAUSE OF DEMENTIA








see the Duke, Pa, Yale, and Mexican study here, showing the misdiagnosis of CJD TSE prion disease as Alzheimers ;








Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis













full text with source references ;









re-Human Prion Diseases in the United States Posted by flounder on 01 Jan 2010 at 18:11 GMT



I kindly disagree with your synopsis for the following reasons ;








Tuesday, November 08, 2011



Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease Surveillance? A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011 Original Paper



Conclusions:These findings raise doubt about the possibility of a reliable CJD surveillance only based on mortality data.









Views & Reviews



Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States



Ermias D. Belay, MD, Ryan A. Maddox, MPH, Pierluigi Gambetti, MD and Lawrence B. Schonberger, MD



+ Author Affiliations



From the Division of Viral and Rickettsial Diseases (Drs. Belay and Schonberger and R.A. Maddox), National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA; and National Prion Disease Pathology Surveillance Center (Dr. Gambetti), Division of Neuropathology, Institute of Pathology, Case Western Reserve University, Cleveland, OH.



Address correspondence and reprint requests to Dr. Ermias D. Belay, 1600 Clifton Road, Mailstop A-39, Atlanta, GA 30333.








26 March 2003



Terry S. Singeltary, retired (medically) CJD WATCH



I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?









Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA



Diagnosis and Reporting of Creutzfeldt-Jakob Disease



To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.



Terry S. Singeltary, Sr Bacliff, Tex



1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL TEXT










The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI



Tracking spongiform encephalopathies in North America



Original



Xavier Bosch



“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt—Jakob ...














2 January 2000



British Medical Journal



U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well










15 November 1999



British Medical Journal



vCJD in the USA * BSE in U.S.











Saturday, January 2, 2010



Human Prion Diseases in the United States January 1, 2010 ***FINAL***









Monday, March 29, 2010



CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER URGENT, PLEASE NOTE ;



>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<




Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas.




She left 6 Kids and a Husband.The Purpose of this web is to give information in Spanish to the Hispanic community, and to all the community who want's information about this terrible disease.- Physician Discharge Summary, Parkland Hospital, Dallas Texas Admit Date: 12/29/2009 Discharge Date: 1/20/2010 Attending Provider: Greenberg, Benjamin Morris; General Neurology Team: General Neurology Team Linda was a Hispanic female with no past medical history presents with 14 months of incresing/progressive altered mental status, generalized weakness, inability to walk, loss of appetite, inability to speak, tremor and bowel/blader incontinence. She was, in her usual state of health up until February, 2009, when her husbans notes that she began forgetting things like names and short term memories. He also noticed mild/vague personality changes such as increased aggression. In March, she was involved in a hit and run MVA,although she was not injured. The police tracked her down and ticketed her. At that time, her son deployed to Iraq with the Army and her husband assumed her mentation changes were due to stress over these two events. Also in March, she began to have weakness in her legs, making it difficult to walk. Over the next few months, her mentation and personality changes worsened, getting to a point where she could no longer recognized her children. She was eating less and less. She was losing more weight. In the last 2-3 months, she reached the point where she could not walk without an assist, then 1 month ago, she stopped talking, only making grunting/aggressive sounds when anyone came near her. She also became both bowel and bladder incontinent, having to wear diapers. Her '"tremor'" and body jerks worsened and her hands assumed a sort of permanent grip position, leading her family to put tennis balls in her hands to protect her fingers. The husband says that they have lived in Nebraska for the past 21 years. They had seen a doctor there during the summer time who prescribed her Seroquel and Lexapro, Thinking these were sx of a mood disorder. However, the medications did not help and she continued to deteriorate clinically. Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. The husband says that he does not know any fellow workers with a similar illness. He also says that she did not have any preceeding illness or travel.









Friday, August 24, 2012



Iatrogenic prion diseases in humans: an update








Thursday, April 12, 2012



Health professions and risk of sporadic Creutzfeldt–Jakob disease, 1965 to 2010



Eurosurveillance, Volume 17, Issue 15, 12 April 2012



Research articles



snip...



In 2009, a pathologist with sporadic Creutzfeldt–Jakob Disease (sCJD) was reported to the Spanish registry. This case prompted a request for information on health-related occupation in sCJD cases from countries participating in the European Creutzfeldt Jakob Disease Surveillance network (EuroCJD). Responses from registries in 21 countries revealed that of 8,321 registered cases, 65 physicians or dentists, two of whom were pathologists, and another 137 healthcare workers had been identified with sCJD. Five countries reported 15 physicians and 68 other health professionals among 2,968 controls or non-cases, suggesting no relative excess of sCJD among healthcare professionals. A literature review revealed: (i) 12 case or small case-series reports of 66 health professionals with sCJD, and (ii) five analytical studies on health-related occupation and sCJD, where statistically significant findings were solely observed for persons working at physicians' offices (odds ratio: 4.6 (95 CI: 1.2–17.6)). We conclude that a wide spectrum of medical specialities and health professions are represented in sCJD cases and that the data analysed do not support any overall increased occupational risk for health professionals. Nevertheless, there may be a specific risk in some professions associated with direct contact with high human-infectivity tissue.



snip...








Friday, August 10, 2012



Incidents of Potential iatrogenic Creutzfeldt-Jakob disease (CJD) biannual update (July 2012)








Wednesday, January 5, 2011



ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011



Prions



David W. Colby1,* and Stanley B. Prusiner1,2







Monday, March 26, 2012



CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE



OR-09 15:10 - 15:25



CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE







======================



*** Saturday, October 6, 2012


*** TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2011 Annual Report








======================



MOM DOD 12/14/97 hvCJD confirmed, Uncle Bo DOD today 10/13/12 RIP with severe and rapid last two weeks Alzheimer’s, he was fishing off pier two weeks ago, hospice 3 days ago, to DOD TODAY (no brain autopsy)?, Mema passed with moderate to slow dementia type Alzheimer’s, wonder what kind of dementia I will get ?



======================










TSS


RIP UNCLE BO (E.S. FREDERICK) DOD OCTOBER 13, 2012