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From: TSS ()
Subject: TRANSMISSION OF B-amyloidosis TO PRIMATES strengthens the parallels between Alzheimer's disease and CJD - IN CONFIDENCE
Date: April 25, 2007 at 6:25 pm PST

IN CONFIDENCE

TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES

H F BAKER, R M RIDLEY, L W DUCHEN, T J CROW, C J BRUTON


As part of a larger series of experiments designed to assess the transmissibility of various neurodegenerative disease including the spongiform encephalopathies (eg Creutzfeldt-Jakob disease and BSE we injected several marmosets (Callithrix Jacchus) intracerebrally with brain homogenate from :

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.


DISCLOSURE


This work is currently under preparation for publication BUT IN VIEW OF PUBLIC CONCERN OVER THE TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES (eg BSE) AND THE HIGH INCIDENCE OF ALZHEIMER'S DISEASE IN THE GENERAL POPULATION, IT IS IMPORTANT THAT THESE FINDINGS ARE NOT DISCUSSED OPENLY BEFORE FULL PUBLICATION.

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.


SAFETY

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.


FURTHER EXPERIMENTS

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

http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf

Regarding Alzheimer's disease

(note the substantial increase on a yearly basis)

http://www.bseinquiry.gov.uk/files/yb/1988/07/08014001.pdf


snip...


The pathogenesis of these diseases was compared to Alzheimer's disease at a molecular level...


snip...

http://www.bseinquiry.gov.uk/files/yb/1990/03/12003001.pdf


And NONE of this is relevant to BSE?

There is also the matter whether the spectrum of ''prion disease'' is wider than that recognized at present.


http://www.bseinquiry.gov.uk/files/yb/1990/07/06005001.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
Date: March 20, 2007 at 5:35 pm PST
Alzheimer?s Disease Prevalence Rates Rise to More than Five Million in the United States
Someone develops Alzheimer?s every 72 seconds, according to new Alzheimer?s Association report

http://lists.iatp.org/listarchive/archive.cfm?id=121742


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0701&L=sanet-mg&P=7387

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 a Slow Death

an editorial by Terry S. Singeltary Sr.

HUMAN AND ANIMAL FOOD POISONING WITH MAD COW DISEASEs A SLOW DEATH


WITH all the pet food deaths mounting from tainted pet food, all the suffering not only the animals are going through, but there owners as well, why are owners of these precious animals not crying about the mad cow tainted animal carcasses they poison there animals with everyday, and have been for decades, why not an uproar about that? well, let me tell you why, they don't drop dead immediately, it's a slow death, they simply call it FELINE and or CANINE ALZHEIMER'S DISEASE, DEMENTIA OR MAD CAT/DOG DISEASE i.e. FSE and they refuse to document CSE i.e.Canine Spongiform Encephalopathy, but it's there and there is some strange pathological findings on that topic that was convientantly swept under the rug. Sadly, this happens everyday with humans, once again confidently swept under the rug as Alzheimer's and or dementia i.e. fast Alzheimer's. Who wants to spend money on an autopsy on an old dog or cat? Sadly, it's the same with humans, you get old and demented your either die or your family puts you in an old folks home and forgets about you, then you die, and again, no autopsy in most cases. Imagine 4.5 annually with Alzheimer's, with and estimated 20+ million dieing a slow death by 2050, and in reality it will most likely be much higher than that now that the blood supply has been infiltrated with the TSE agent, and we now know that blood is another route and source for this hideous disease. It's hell getting old now a days.

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.
Our federal Government has failed us at every corner when it comes to food safety. maybe your dog, your cat, your mom, your dad, your aunt, or your uncle, but again, who cares, there old and demented, just put them down, or put them away. It's hell getting old. ...END



http://www.swnebr.net/newspaper/cgi-bin/articles/articlearchiver.pl?160273


FELINE AND CANINE ALZHEIMER'S OR MAD CAT/DOG DISEASE AND PET FOOD ...
...TSS Name: Terry S. Singeltary Sr. Date: Jan 26, 2007 Dear Terry S. Singeltary Sr. ... specifically dry dog food, some of which was reported to have been ...
www.kxmb.com/getArticle.asp?ArticleId=113652 - 107k -

http://www.kxmb.com/getForumPost.asp?ArticleId=113652


FELINE AND CANINE ALZHEIMER'S OR MAD CAT/DOG DISEASE AND PET FOOD ...
...TSS Name: Terry S. Singeltary Sr. Date: Jan 26, 2007 Dear Terry S. Singeltary ... so that the dog food will not mistakenly be mixed into cattle or other ...
www.kxnet.com/t/schools/113652.asp - 107k -



http://www.kxnet.com/getForumPost.asp?ArticleId=113652


Crushed heads (which inevitably involve brain and spinal cord material)
are used to a limited extent but will also form one of the constituent
raw materials of meat and bone meal, which is used extensively in
pet food manufacturer...

http://www.bseinquiry.gov.uk/files/yb/1989/03/17004001.pdf


Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.


http://jama.ama-assn.org/http://www.neurology.org/cgi/eletters/60/2/176#535


BRITISH MEDICAL JOURNAL


BMJ


http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2


BMJ


http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1

Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States


Email Terry S. Singeltary:


flounder@wt.net

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?


http://www.neurology.org/cgi/eletters/60/2/176#535

LANCET INFECTIOUS DISEASE JOURNAL


Volume 3, Number 8 01 August 2003


Newsdesk


Tracking spongiform encephalopathies in North America


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 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.


Singeltary was greatly demoralised at the few attempts to monitor the

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.


Until recently, CWD was thought to be confined to the wild in a small

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.


To date, experimental studies have proven that the CWD agent can be

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.


Part of the problem seems to stem from the US surveillance system. CJD

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.


Although in November last year the US Food and Drug Administration

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.


Getting data on TSEs in the USA from the government is like pulling

teeth, Singeltary argues. You get it when they want you to have it,

and only what they want you to have.


Norman Foster, director of the Cognitive Disorders Clinic at the

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.


CDC spokesman Ermias Belay says that the CDC will not be investigating

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.


http://infection.thelancet.com/journal/journal.isa

Re: Colorado Surveillance Program for Chronic Wasting Disease Transmission to Humans (TWO SUSPECT CASES) (8150 lines)
From: Terry S. Singeltary Sr.
Date: Wed, 4 Apr 2007 16:22:22 -0500


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0704&L=sanet-mg&T=0&P=1165


Re: Suspect BSE in Horse and SCRAPIE transmission to CHIMPS IN CONFIDENCE (2059 lines)
From: Terry S. Singeltary Sr.
Date: Wed, 25 Apr 2007 13:07:35 -0500


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0704&L=sanet-mg&T=0&P=16765

NOR98-LIKE STRAIN OF SCRAPIE FOUND IN WYOMING (1791 lines)
From: Terry S. Singeltary Sr.
Date: Wed, 11 Apr 2007 15:08:15 -0500


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0704&L=sanet-mg&T=0&P=8315

From: "Terry S. Singeltary Sr." <[log in to unmask]>
To: <[log in to unmask]>
Sent: Monday, April 02, 2007 2:37 PM
Subject: Re: FOIA REQUEST FOR ATYPICAL TSE INFORMATION ON VERMONT SHEEP

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0704&L=sanet-mg&T=0&P=816


10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007

Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling’s 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007. Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross-contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI

___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI – 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J – PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A-BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007


http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html


Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518




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