Tuesday, March 19, 2013

Alzheimer's Association 2013 Alzheimer's Disease Facts and Figures

Today, an American develops Alzheimer's disease every 68 seconds. In 2050, an American will develop the disease every 33 seconds.





An estimated 5.2 million Americans of all ages have Alzheimer's disease in 2013. This includes an estimated 5 million people age 65 and older and approximately 200,000 individuals younger than age 65 who have younger-onset Alzheimer's.





The number of Americans with Alzheimer's disease and other dementias will grow as the U.S. population age 65 and older continues to increase. By 2025, the number of people age 65 and older with Alzheimer's disease is estimated to reach 7.1 million—a 40 percent increase from the 5 million age 65 and older currently affected. By 2050, the number of people age 65 and older with Alzheimer's disease may nearly triple, from 5 million to a projected 13.8 million, barring the development of medical breakthroughs to prevent, slow or stop the disease.





Mortality





Alzheimer's disease is the 6th leading cause of death in the United States overall and the 5th leading cause of death for those aged 65 and older. It is the only cause of death among the top 10 in America without a way to prevent it, cure it or even slow its progression. Deaths from Alzheimer's increased 68 percent between 2000 and 2010, while deaths from other major diseases, including the number one cause of death (heart disease), decreased.





While ambiguity about the underlying cause of death can make it difficult to determine how many people die from Alzheimer's, there are no survivors. If you do not die from Alzheimer's disease, you die with it. One in every three seniors dies with Alzheimer's or another dementia.





Impact on Caregivers





In 2012, 15.4 million family and friends provided 17.5 billion hours of unpaid care to those with Alzheimer's and other dementias — care valued at $216.4 billion, which is more than eight times the total sales of McDonald's in 2011. Eighty percent of care provided in the community is provided by unpaid caregivers.





Nearly 15 percent of caregivers are long-distance caregivers, living an hour or more away from their loved ones. Out-of-pocket expenses for long-distance caregivers are nearly twice as much as local caregivers.





More than 60 percent of Alzheimer's and dementia caregivers rate the emotional stress of caregiving as high or very high; more than one-third report symptoms of depression. Due to the physical and emotional toll of caregiving, Alzheimer's and dementia caregivers had $9.1 billion in additional health care costs of their own in 2012.





Cost to the nation





In 2013, the direct costs of caring for those with Alzheimer's to American society will total an estimated $203 billion, including $142 billion in costs to Medicare and Medicaid. Total payments for health care, long-term care and hospice for people with Alzheimer's and other dementias are projected to increase from $203 billion in 2013 to $1.2 trillion in 2050 (in current dollars). This dramatic rise includes a 500% increase in combined Medicare and Medicaid spending.





Nearly 30 percent of people with Alzheimer's and other dementias are on both Medicare and Medicaid, compared to 11 percent of individuals without these conditions.





The average per-person Medicare costs for those with Alzheimer's and other dementias are three times higher than for those without these conditions; the average per-person Medicaid spending for seniors with Alzheimer's and other dementias is 19 times higher than average per-person Medicaid spending for all other seniors.





Alzheimer's disease facts in each state





The 2013 Alzheimer's Disease Facts and Figures report contains data on the impact of this disease in every state across the nation. Click below to see the effect that Alzheimer's is having in your state.

















very sad, and very disturbing figures...tss







2013 Alzheimer’s disease facts and figures Includes a Special Report on long-distance caregivers












Transmission of Prions and Alzheimer’s disease Abeta Amyloid


Claudio Soto, PhD


Mitchell Center for Alzheimer’s disease and Related Brain Disorders, Dept of Neurology


University of Texas Medical School at Houston










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 ;














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




SEE FULL TEXT AND SOURCE REFERENCES ;




Wednesday, May 16, 2012


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


Proposal ID: 29403








Wednesday, September 21, 2011


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








Sunday, February 10, 2013


Parkinson's Disease and Alpha Synuclein: Is Parkinson's Disease a Prion-Like Disorder?










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.











CJD1/9 0185 Ref: 1M51A


IN STRICT CONFIDENCE


Dr McGovern 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



1. CMO will wish to be aware that a meeting was held at DH yesterday, 4 January, to discuss the above findings. It was chaired by Professor Murray (Chairman of the MRC Co-ordinating Committee on Research in the Spongiform Encephalopathies in Man), and attended by relevant experts in the fields of Neurology, Neuropathology, molecular biology, amyloid biochemistry, and the spongiform encephalopathies, and by representatives of the MRC and AFRC. 2. Briefly, the meeting agreed that:


i) Dr Ridley et als findings of experimental induction of p amyloid in primates were valid, interesting and a significant advance in the understanding of neurodegenerative disorders;


ii) there were no immediate implications for the public health, and no further safeguards were thought to be necessary at present; and


iii) additional research was desirable, both epidemiological and at the molecular level. Possible avenues are being followed up by DH and the MRC, but the details will require further discussion. 93/01.05/4.1









BSE101/1 0136


IN CONFIDENCE


5 NOV 1992 CMO From: Dr J S Metters DCMO 4 November 1992



TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES



1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognized the public sensitivity of these findings and intend to report them in their proper context. This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.



2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed'. As the report emphasizes the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible. What are the implications for public health?



3. The route of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.



92/11.4/1-1 BSE101/1 0137



4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required" before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.



JS METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 121/YdeS 92/11.4/1.2








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














Friday, September 3, 2010


Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids, Prionpathy, Prionopathy, TSE















SCENARIO 3: ‘THE THIN STEMMED GLASS’



... a TSE is found that is linked to Alzheimer’s disease.










Thursday, January 17, 2013


TSE guidance, surgical, dental, blood risk factors, Part 4 Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings (updated January 2013)










Monday, January 14, 2013


Gambetti et al USA Prion Unit change another highly suspect USA mad cow victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes along with this BSe










Monday, December 31, 2012


Creutzfeldt Jakob Disease and Human TSE Prion Disease in Washington State, 2006–2011-2012












Saturday, December 29, 2012


MAD COW USA HUMAN TSE PRION DISEASE DECEMBER 29 2012 CJD CASE LAB REPORT












Tuesday, December 25, 2012


CREUTZFELDT JAKOB TSE PRION DISEASE HUMANS END OF YEAR REVIEW DECEMBER 25, 2012












Friday, November 23, 2012


sporadic Creutzfeldt-Jakob Disease update As at 5th November 2012 UK, USA, AND CANADA











Letters


JAMA. 2001;285(6):733-734. doi: 10.1001/jama.285.6.733




Diagnosis and Reporting of Creutzfeldt-Jakob Disease




Terry S. Singeltary, Sr Bacliff, Tex


Since this article does not have an abstract, we have provided the first 150 words of the full text.




KEYWORDS: creutzfeldt-jakob disease, diagnosis.




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.




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












Published March 26, 2003



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


Terry S. Singeltary, retired (medically)




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?




Published March 26, 2003












THE PATHOLOGICAL PROTEIN



BY Philip Yam Yam Philip Yam News Editor Scientific American www.sciam.com



Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.



CHAPTER 14



Laying Odds



Are prion diseases more prevalent than we thought?



Researchers and government officials badly underestimated the threat that mad cow disease posed when it first appeared in Britain. They didn't think bovine spongiform encephalopathy was a zoonosis-an animal disease that can sicken people. The 1996 news that BSE could infect humans with a new form of Creutzfeldt-Jakob disease stunned the world. It also got some biomedical researchers wondering whether sporadic CJD may really be a manifestation of a zoonotic sickness. Might it be caused by the ingestion of prions, as variant CJD is?



Revisiting Sporadic CJD



It's not hard to get Terry Singeltary going. "I have my conspiracy theories," admitted the 49-year-old Texan.1 Singeltary is probably the nation's most relentless consumer advocate when it comes to issues in prion diseases. He has helped families learn about the sickness and coordinated efforts with support groups such as CJD Voice and the CJD Foundation. He has also connected with others who are critical of the American way of handling the threat of prion diseases. Such critics include Consumers Union's Michael Hansen, journalist John Stauber, and Thomas Pringle, who used to run the voluminous www.madcow. org Web site. These three lend their expertise to newspaper and magazine stories about prion diseases, and they usually argue that prions represent more of a threat than people realize, and that the government has responded poorly to the dangers because it is more concerned about protecting the beef industry than people's health.



Singeltary has similar inclinations. ...




snip...




THE PATHOLOGICAL PROTEIN


Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9




June 2003 BY Philip Yam




CHAPTER 14 LAYING ODDS




Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.

































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***












Thursday, February 14, 2013


The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and TSE prion disease











Tuesday, March 5, 2013


Use of Materials Derived From Cattle in Human Food and Cosmetics; Reopening of the Comment Period FDA-2004-N-0188-0051 (TSS SUBMISSION)


FDA believes current regulation protects the public from BSE but reopens comment period due to new studies











Tuesday, March 05, 2013


A closer look at prion strains Characterization and important implications Prion


7:2, 99–108; March/April 2013; © 2013 Landes Bioscience












with kindest regards, terry



MOM RIP 12/14/97 confirmed Heidenhain Variant Creutzfeldt Jakob Disease and her MOM and Brother died with Alzheimer’s...I can’t wait to see what happens...not.



layperson





Terry S. Singeltary Sr.


P.O. Box 42


Bacliff, Texas USA 77518




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