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From: TSS ()
IN CONFIDENCE TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES H F BAKER, R M RIDLEY, L W DUCHEN, T J CROW, C J BRUTON 1) a 56 year old patient with severe Alzheimer's disease - B - amyloid plaques and conogophilic angiopathy (CAA) and neurofibrillary tangles; and 2) a 62 year old patient with Gerstmann-Straussler disease, a spongiform encephalopathy with PrP Plaques and, in this case, B-amyloid plaques and CAA. These monkeys were killed more than 6 years after inoculation and their brains were found to contain moderate numbers of B-amyloid plaques and CAA but NO neurofibrillary tangles NO PrP. The brains of more than 12 monkeys killed at an older age did not contain these changes. B-amyloid was not found in the brains of monkeys injected with brain material which did not contain B-amyloid. These results suggest that B-amyloidosis is a transmissible process resembling the transmissibility of PrP amyloidosis in transmissible dementia and strengthens the parallels between Alzheimer's disease and Creutzfeldt-Jakob disease. It should be stressed, however, that we are not claiming to have transmitted Alzheimer's disease because 1) the animals were behaving normally when killed and 2) no neurofibrillary tangles were seen. We have argued previously that transmission of spongiform encephalopathy, particularly from the genetic cases (GSS and some CJD), does not imply that the donor cases themselves acquired the disease by infection. We would apply the same arguments in this case, particularly in view of the genetic basis of some cases of Alzheimer's disease and the extensive epidemiological data which does not link Alzheimer's disease to infection. Furthermore, BEFORE DISCLOSURE, IT IS IMPORTANT THAT INTERESTED PARTIES BE PROPERLY APPRAISED OF THE DATA AND THERE IMPLICATIONS. Previous attempts to transmit Alzheimer's disease to rodents and large primates have been unsuccessful. It is our belief that post-mortem tissue from these animals still exists and we are anxious that research workers (in the USA) SHOULD NOT RE-EXAMINE this material until our data are published. At this point we would like to stress again the lack of evidence relating Alzheimer's disease to exposure to brain tissue through neurosurgery or occupation. NEVERTHELESS it is appropriate that proper bodies should consider whether the results of our experiments have any implications for human health. The interpretation we have made that B-amyloidosis as a self-peretuating process has important implications for understanding the process of neurodegeneration, which are best studied at the level of protein chemistry. However, we can see arguments for some transmission experiments including: 1) serial passage of B-amyloidosis in order to strengthen the evidence of transmissibility; 2) transmission from other cases of Alzheimer's disease in order to establish the generality of this effect; 3) transmission to primates which are allowed to run their full course, ie to see whether the full syndrome of Alzheimer's disease develops including neurofibrillary tangle formation, astrocytosis, neuronal loss and concomitant cognitive decline. (We are already expert in the neuropsychological assessment of marmosets). It should be remembered that, at the present time, only the amyloidosis have been found to be transmissible such that Alzheimer's disease PER SE has not been transmitted; 4) comparison of transmission from cases which contain only CAA and those which contain only B-amyloid plaques. These two forms of amyloid differ very slightly and it is not known whether this difference is preserved on transmission; 5) establishment of the time course of the development of B-amyloidosis. The present experiment suggests that the time course is somewhere between 1-5 years; 6) transmission using larger quantities of purified preparations of B-amyloid. This may reduce the transmission time considerably; 7) transmission using animals of different initial ages to investigate the relationship between transmission time and chronological age, eg transmission into mature animals may decrease transmission time through an interaction between the pathological process and senescence; 8) manipulation of transmission time by treatments which may speed up plaque formation, eg by increasing the production of amyloid precursor protein, or which may slow down plaque formation and protect from disease progression. The proposal is to inoculate about 25 marmosets in the first instance and to replace them in a 'rolling' experiment as they die or are killed according to the experimental design. The marmosets will be kept in the MRC Marmoset Colony in Cambridge. Additional facilities and personnel are not required over and above that awarded to Dr. Ridley in an MRC Programma Grant. A preliminary report of our findings will be presented by Professor L W Duchan at the January 1993 meeting of the British Neuropathological Society. http://www.bseinquiry.gov.uk/ TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES Regarding Alzheimer's disease http://www.bseinquiry.gov.uk/files/yb/1990/03/12003001.pdf Alzheimer's and Transmissible Spongiform Encephalopathies TERRY S. SINGELTARY SR. http://neurotalk.psychcentral.com/showthread.php?t=13175 Subject: Every 72 seconds someone in America develops Alzheimer?s http://lists.iatp.org/listarchive/archive.cfm?id=121742 http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&P=8554 Article Posted: 04/15/2007 9:16:48 PM HUMAN AND ANIMAL FOOD POISONING WITH MAD COW DISEASEs A SLOW DEATH NOW, for the ones that don't believe me, well mad cow has been in the USA for decades undetected officially, but the late Richard Marsh documented way back, again, swept under the rug. Then in 2003 in December, the first case of BSE was finally documented, by accident. Then you had the next two cases that were documented in Texas and Alabama, but it took an act of Congress, literally, to get those finally documented, and when they were finally documented, they were atypical BSE or Bovine Amyloid Spongiform Encephalopathy (BASE), which when transmitted to humans is not vCJD or nvCJD, but SPORADIC CJD. Now you might ask yourself what about that mad cow feed ban of August 4, 1997, the year my mother died from the Heidenhain Variant of Creutzfeldt Jakob Disease (confirmed), well that ruminant to ruminant was merely a regulation on paper that nobody enforced. Just last month there was 10+ PLUS MILLION POUNDS OF BANNED BLOOD TAINTED MBM DISPERSED INTO COMMERCE, and there is no way the FDA will ever recover it. It will be fed out again. 2006 was a banner year for FDA mad cow protein fed out into commerce. Looks like 2007 will be also. http://www.swnebr.net/newspaper/cgi-bin/articles/articlearchiver.pl?160273 FELINE AND CANINE ALZHEIMER'S OR MAD CAT/DOG DISEASE AND PET FOOD ... http://www.kxmb.com/getForumPost.asp?ArticleId=113652 FELINE AND CANINE ALZHEIMER'S OR MAD CAT/DOG DISEASE AND PET FOOD ... http://www.bseinquiry.gov.uk/files/yb/1989/03/17004001.pdf Singeltary, Sr et al. JAMA.2001; 285: 733-734. Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 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? LANCET INFECTIOUS DISEASE JOURNAL 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. largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD) the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation. occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source. region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle. transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive. is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk. issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE. teeth, Singeltary argues. You get it when they want you to have it, and only what they want you to have. University of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings; adding that, the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure. The USA should develop a system modelled on that established in the UK, he points out. Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunters two of whom were friends who died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans; adding that [only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further. Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison. the [Samii] cases because there is no evidence that the men ate CWD-infected meat. He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited. Re: Colorado Surveillance Program for Chronic Wasting Disease Transmission to Humans (TWO SUSPECT CASES) (8150 lines) NOR98-LIKE STRAIN OF SCRAPIE FOUND IN WYOMING (1791 lines) From: "Terry S. Singeltary Sr." <[log in to unmask]> http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0704&L=sanet-mg&T=0&P=816 Date: March 21, 2007 at 2:27 pm PST ___________________________________ END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
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