15 years ago, I did not find one who would say that Alzheimer's was connected to Mad Cow or Scrapie
Disease. Today, we are seeing research findings that are indicating a relationship. God has blessed His people with light in advance of what science has discovered.
Association between Deposition of Beta-Amyloid and Pathological Prion Protein in Sporadic Creutzfeldt-Jakob Disease
Debatin, L. ; Streffer, J. ; Geissen, M. ; Matschke, J. ; Aguzzi, A. ; Glatzel, M.
Neurodegenerative Dis (DOI:10.1159/000121389)
Published Online: March 18, 2008
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)
goto top of page Key Words
* Sporadic Creutzfeldt-Jakob disease
* Alzheimer's disease
* Deposition of beta-amyloid
* Prion protein
goto top of page 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, beta-amyloid (Abeta), 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 Abeta morphologically, biochemically and genetically and correlated these findings to clinical data. Results: sCJD-diseased individuals with abundant deposits of Abeta 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 Abeta and PrPSc in a subgroup of sCJD patients is indicative of common pathways involved in the generation or clearance of Abeta and PrPSc in a subgroup of sCJD patients.
What has been seen? Look at the conclusion. I have been pointing to the amyloid plaques that are seen in Alzheimer's brains and the deposition of the same type of material in Scrapie and now in some "mad cows". This study has revealed that the Abeta (amyloid plaque), and the PrPSc (prion protien) appear to share a common route of infection. Science is catching up with the light we have been given. Alzheimers is not caused by aluminum. And, sporadic CJD does not just happen. There is nothing in this study to suggest that mad cows or mad sheep cause either sCJD or Alzheimer's, but we are getting very close to knowing through science that this is the case. We know that mad cows infect humans and cause vCJD. We now know that there is a connection between Alzheimer's and sCJD. But, the meat and dairy industry does not want you to know that both Alzheimer's and sCJD are being transmitted to humans via infected animals, both sheep and cows (and probably other animals that may be carriers). Pigs and chickens are fed material that comes from downer cows that cannot be fed to cows and sheep.
It is not a stretch to understand that sporadic CJD is an infection with a cause. What cause? The same as variant CJD, infected meat. When this is understood, the study we have just been reviewing makes it clear that if sCJD is from infected meat, then since both sCJD and Alzheimer's share a "common pathway" for the development of both the amyloid plaque and the prions, we would then have our connection between mad cows or mad sheep and Alzheimer's.
How long before the evidence is clear? I think it already is. The new varieties, strains, of Mad Cow that we are seeing in Europe and the US which produce the amyloid plaques and the fact that these amyloid plaques have been seen in Scrapie sheep is enough evidence for those who are not biased to say there is reason to believe there is a connection. In fact what we will probably find is that Alzheimer's is in fact Scrapie or Mad Cow Disease in humans. Yes, there are different manifestations of the infection, but the cause is the same, infected meat in which cooking does not inhibit the transmission of the disease.