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From: TSS ()
Subject: Re: Alzheimer’s may 'seed' itself like mad cow disease
Date: September 26, 2006 at 7:37 am PST

In Reply to: Re: Alzheimer’s may 'seed' itself like mad cow disease posted by TSS on September 21, 2006 at 1:22 pm:

1: Ann N Y Acad Sci. 1982;396:131-43. Links
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).
Brown P,
Salazar AM,
Gibbs CJ Jr,
Gajdusek DC.
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.

1: Neurology. 1990 Feb;40(2):226-8.

Coexistence of Creutzfeldt-Jakob disease and Alzheimer's disease in the same patient.
Brown P,
Jannotta F,
Gibbs CJ Jr,
Baron H,
Guiroy DC,
Gajdusek DC.
Laboratory of CNS Studies, NINDS, National Institutes of Health, Bethesda, MD 20892.

We report the case of a 73-year-old patient in whom a diagnosis of Creutzfeldt-Jakob disease, suggested by the clinical course, was verified by the neuropathologic finding of widespread spongiform change and astrogliosis, the presence of proteinase-resistant protein in brain extracts, and the experimental transmission of spongiform encephalopathy to primates inoculated with brain tissue. However, neuropathologic examination also revealed a profusion of senile and neuritic plaques and neurofibrillary tangles that reacted with antibody to the amyloid beta-protein characteristic of Alzheimer's disease, but not with antibody to the scrapie amyloid protein characteristic of Creutzfeldt-Jakob disease.

1: Prog Clin Biol Res. 1989;317:549-57. Links

Neuroaxonal dystrophy: an ultrastructural link between subacute spongiform virus encephalopathies and Alzheimer's disease.
Liberski PP,
Yanagihara R,
Gibbs CJ Jr,
Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892.


Two patients with transmissible virus dementias were not diagnosed clinically
or neuropathologically as having CJD, but rather as having Alzheimer’s
disease (62). In both cases the disease was familial: in one (Fig. 21) there
were six close family members with the disease in two generations; in the other
both the patient’s father and sister had died of presenile dementia. The
diseases as transmitted to primates were clinically and pathologically typical
subacute spongiform virus encephalopathies, and did not have pathological
features of Alzheimer’s disease in man. More than 30 additional specimens of
brain tissue from non-familial Alzheimer’s disease have been inoculated into
TVD-susceptible primates without producing disease. Therefore, although we
338 Physiology or Medicine 1976
cannot claim to have transmitted the classical sporadic Alzheimer’s disease to
primates, we are confronted with the anomaly that the familial form of
Alzheimer’s disease has, in these two instances, transmitted as though it were
The above findings have added impetus to our already extensive studies of
Huntington’s chorea, Alzheimer’s and Pick’s diseases, parkinsonism-dementia,
senile dementia, and even “dementia praecox", the organic brain disease
associated with late uncontrolled schizophrenia.

Figure 21a. Y family. Brain tissue obtained from patient A. Y. at biopsy induced subacute
spongiform encephalopathy in a squirrel monkey 24 months after intracerebral inoculation.
The patient, a 48-year old woman who died after a 68 month course of progressive dementia,
quite similar in clinical aspects to the progressive dementia from which her father
and brother had died at 54 and 56 years of age, respectively, was diagnosed clinically and
neuropathologically as suffering from Alzheimer’s disease. Her sister is at present incapacitated
by a similar progressive dementia of 4 years’ duration. Although the transmitted
disease in the squirrel monkey was characterized by severe status spongiosis, none was seen
in the patient. although amyloid plaques and neurofibrillary tangles were frequent.




Nobel Lecture, December 13, 1976


National Institutes of Health, Bethesda, Maryland, U.S.A.


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