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From: TSS ()
Subject: Association between Deposition of Beta-Amyloid and Pathological Prion Protein in Sporadic Creutzfeldt-Jakob Disease
Date: March 21, 2008 at 11:00 am PST

Original Paper

Association between Deposition of Beta-Amyloid and Pathological Prion
Protein in Sporadic Creutzfeldt-Jakob Disease

Laura Debatina, Johannes Strefferb, Markus Geissenc, Jakob Matschkec,
Adriano Aguzzia, Markus Glatzela, c

aInstitute of Neuropathology, and
bDivision of Psychiatry Research, University Hospital Zurich, Zurich,
Switzerland;
cInstitute of Neuropathology, University Medical Center Hamburg-Eppendorf,
Hamburg, Germany


Address of Corresponding Author

Neurodegenerative Dis (DOI: 10.1159/000121389)


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Key Words

Sporadic Creutzfeldt-Jakob disease
Alzheimer's disease
Deposition of -amyloid
Prion protein

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Abstract

Background: Alzheimer's disease (AD) and prion diseases such as sporadic
Creutzfeldt-Jakob disease (sCJD) share common features concerning their
molecular pathogenesis and neuropathological presentation and the
coexistence of AD and CJD in patients suggest an association between the
deposition of the proteolytically processed form of the amyloid precursor
protein, -amyloid (A), which deposits in AD, and the abnormal form of the
prion protein, PrPSc, which deposits in sCJD. Methods: We have characterized
sCJD patients (n = 14), AD patients (n = 5) and nondemented controls (n = 5)
with respect to the deposition of PrPSc and A morphologically, biochemically
and genetically and correlated these findings to clinical data. Results:
sCJD-diseased individuals with abundant deposits of A present with a
specific clinicopathological profile, defined by higher age at disease
onset, long disease duration, a genetic profile and only minimal amounts of
PrPSc in the cerebellum. Conclusion: The co-occurrence of pathological
changes typical for sCJD and AD in combination with the inverse association
between accumulation of A and PrPSc in a subgroup of sCJD patients is
indicative of common pathways involved in the generation or clearance of A
and PrPSc in a subgroup of sCJD patients.

Copyright © 2008 S. Karger AG, Basel


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Author Contacts

Markus Glatzel
Institute of Neuropathology, University Medical Center Hamburg-Eppendorf
Martinistrasse 52, DE-20246 Hamburg (Germany)
Tel. +49 40 42 803 2218, Fax +49 40 42 803 4929
E-Mail m.glatzel@uke.uni-hamburg.de

http://content.karger.com/produktedb/produkte.asp?typ=fulltext&file=000121389


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


Diagnosis and Reporting of Creutzfeldt-Jakob Disease

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


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


http://jama.ama-assn.org/cgi/content/extract/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT

JOURNAL OF NEUROLOGY

MARCH 26, 2003

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


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


Human BSE

snip...

These are not relevant to any possible human hazard from BSE nor to the much
more common dementia, Alzheimers.

snip...

http://www.bseinquiry.gov.uk/files/yb/1990/07/09001001.pdf


IN STRICT CONFIDENCE

TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES

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


Subject: Re: Hello Dr. Manuelidis Date: Fri, 22 Dec 2000 17:47:09 -0500
From: laura manuelidis Reply-To:
laura.manuelidis@yale.edu Organization: Yale Medical School To: "Terry S.
Singeltary Sr."

References: <

Dear Terry,

One of our papers (in Alzheimer's Disease Related Disord. 3:100-109, 1989)
in text cites 6 of 46 (13%) of clinical AD as CJD. There may be a later
paper from another lab showing the same higher than expected incidence but I
can't put my hands on it right now. We also have a lot of papers from 1985
on stating that there are likely many silent (non-clinical) CJD infections,
i.e. much greater than the "tip of the iceberg" of long standing end-stage
cases with clinical symptoms. Hope this helps.

best wishes for the new year laura manuelidis

"Terry S. Singeltary Sr." wrote: > > Hello again Dr. Manuelidis, > > could
you please help me locate the 2 studies that were > done on CJD where it
showed that up to 13% of the people > diagnosed as having Alzheimer's
actually had CJD. > trying to find reference... > > thank you, > Terry S.
Singeltary Sr.


==================================
http://neurotalk.psychcentral.com/thread13175.html

http://neurotalk.psychcentral.com/showthread.php?p=156015


TSE UPDATE (SEE LINKS BELOW)

Thursday, March 13, 2008

DOWNER COW BLUES SENATORS WANT CRACKDOWN

http://downercattle.blogspot.com/2008/03/downer-cow-blues-senators-want.html


Thursday, March 6, 2008

House committee subpoenas Hallmark/Westland CEO - i call for an
investigation of the investigators


http://downercattle.blogspot.com/2008/03/house-committee-subpoenas.html

Friday, March 7, 2008

QUESTIONS AND ANSWERS HALLMARK/WESTLAND MEAT PACKING CO.

March 6, 2008

Consumer Concerns

Q. My child/school recently consumed Hallmark/Westland products. What is the
risk to children's health?


SEE FULL TEXT ;


http://downercattle.blogspot.com/2008/03/usda-questions-and-answers.html

March 16, 2008


MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or
Italian L-BASE

http://bse-atypical.blogspot.com/2008/03/mad-cow-disease-terminology-uk-c-bse.html


IN FY 2007 TWO FIELD CASES, ONE VALIDATION CASE, AND TWO RSSS CASES WERE
CONSISTENT WITH NOR-98 SCRAPIE. ...


(BRINGS A TOTAL OF 5 NOR-98 CASES DOCUMENTED IN 2007 IN USA. ...TSS)


http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps

http://nor-98.blogspot.com/


http://scrapie-usa.blogspot.com/


CWD


http://chronic-wasting-disease.blogspot.com/


TME


http://transmissible-mink-encephalopathy.blogspot.com/


TSS





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