- Note - This extensive, powerful assemblage of science
was first posted on 1-24-3. The
- following data is even more important today. -ed
- To: Terry S. Singletary Sr
- From: Cindy B.
- Date: Friday, Jan 24 2003
- Subj: CJD $ Alzheimer's
- Hi Terry, I read your article on CJD on Rense.com and
was wondering when they are going to alert the population of this and start
testing all animals that are being consumed by humans.
- I have also read other articles that relate Alzheimer's,
ALS, Parkinson's disease among others that have all been linked to BSE/Mad
- Assuming all this is true (which I have no doubt it is),
wouldn't everyone have to get tested to see if they have contracted any
of these or their variants?
- I am really bothered by this whole thing and the lies
that have been perpetuated by their many fronts in our government.
- Also, when they talk about "downers", does
that refer to sick animals? And that even these sick animals are given
as feed to the other animals?
- One last thing, I have information that an individual
has "mad cow" who was in surgery here in our local hospital.
The individual that told me says they are keeping it under tight wraps.
- Thanks for your work and the very informative article,
- Cindy Bouthillier
- Greeley, Colorado
- From: Terry S. Singeltary Sr.
- To: Cindy B
- Subject: Re: CJD $ Alzheimer's
- Date: Fri, 24 Jan 2003
- Hello Cindy,
- Thank you for your kind words. I have posted some data
below on CJD and Alzheimer's that you may find interest in.
- Yes, there are about 200,000 downers annually in the
USA. This involves cattle that go down for one reason or another and that
includes prion/CNS disorder cattle of all sorts and yes, you are feeding
dead doggy and kitty cat (and the chemicals used to euthanize old pets,
dead downer cattle, 'roadkill' which includes scrapie infected sheep and
CWD/mad deer infected deer and elk. It's just and endless cycle of greed.
- I would be interested to know more about the case of
CJD and the hospital/surgical arena. This will be a major vector (of transmission)
- OH...and don't start looking for rapid TSE/prion testing
in sufficient numbers to find TSEs/mad cow in US cattle anytime soon, because
if you don't look...you don't find. Thus, you keep the 'gold card' of 'BSE/TSE
FREE' status in US cattle. Of course, we know different...
- Kind regards, Terry
- Regarding Alzheimer's disease
- (note the substantial increase on a yearly basis)
- The pathogenesis of these diseases was compared to Alzheimer's
disease at a molecular level...
- 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.
- Human BSE
- These are not relevant to any possible human hazard from
BSE nor to the much more common dementia, Alzheimers.
- From: TSS
- Subject: CJD or Alzheimer's, THE PA STUDY...full text
- Date: May 7, 2001 at 10:24 am PST
- Diagnosis of dementia: Clinicopathologic correlations
- Francois Boller, MD, PhD; Oscar L. Lopez, MD; and John
- Article abstract--Based on 54 demented patients consecutively
autopsied at the University of Pittsburgh, we studied the accuracy of clinicians
in predicting the pathologic diagnosis. Thirty-nine patients (72.2%) had
Alzheimer's disease, while 15 (27.7%) had other CNS diseases (four multi-infarct
dementia; three Creutzfeldt-Jakob disease; two thalamic and subcortical
gliosis; three Parkinson's disease; one progressive supranuclear palsy;
one Huntington's disease; and one unclassified). Two neurologists independently
reviewed the clinical records of each patient without knowledge of the
patient's identity or clinical or pathologic diagnoses; each clinician
reached a clinical diagnosis based on criteria derived from those of the
NINCDS/ADRDA. In 34 (63 %) cases both clinicians were correct, in nine
(17%) one was correct, and in 11 (20%) neither was correct. These results
show that in patients with a clinical diagnosis of dementia, the etiology
cannot be accurately predicted during life.
- NEUROLOGY 1989;39:76-79
- Several recent papers and reports have addressed the
problem of improving the clinician's ability to diagnose dementia. Notable
among those reports are the diagnostic criteria for dementia of the American
Psychiatric Association, known as DSM III,1 as well as the clinical and
neuropathologic criteria for the diagnosis of Alzheimer's disease (AD).2,3
Other researchers have published guidelines for the differentiation of
various types of dementia4 and for antemortem predictions about the neuropathologic
findings of demented patients.5
- Most studies on the accuracy of clinical diagnosis in
patients with dementia, especially AD, have used clinicopathologic correlation,6-15
and have found a percentage of accuracy ranging from 43% to 87%. Two recent
reports, however,16,17 have claimed an accuracy of 100%. These two reports
are based on relatively small series and have consisted of very highly
selected patient samples. In our own recent experience, several cases of
dementia have yielded unexpected neuropathologic findings,18 and we hypothesized
that, in larger series, there would be a significant number of discrepancies
between clinical diagnoses and autopsy findings. The present paper reviews
the neuropathologic diagnosis of 54 demented patients who were autopsied
consecutively at the University of Pittsburgh over a 7-year period, and
reports the ability of clinicians to predict autopsy findings.
- Material and methods. We independently reviewed the pathologic
data and clinical records of 54 consecutive patients who had had an autopsy
at the University of Pittsburgh (Presbyterian University Hospital [PUH]
and the Pittsburgh (University Drive) Veterans Administration Medical Center
[VAMC]), between 1980 and 1987.
- The 54 cases included all those where dementia was diagnosed
clinically but for which an obvious etiology, such as neoplasm, trauma,
major vascular lesions, or clinically evident infection had not been found.
The brains, evaluated by the Division of Neuropathology of the University
of Pittsburgh, were obtained from patients cared for in different settings
at their time of death.
- On the basis of the amount of information available in
each case, we divided the patients into three groups. Group 1 included
12 subjects who had been followed for a minimum of 1 year by the Alzheimer
Disease Research Center (ADRC) of the University of Pittsburgh. ADRC evaluations
include several visits and neurologic and neuropsychological testing as
well as repeated laboratory tests, EEG, and CT.19,20
- Group 2 included 28 patients who had been seen in the
Neurology Service of PUH, of the VAMC, or in geriatric or psychiatric facilities
of the University of Pittsburgh or at Western Psychiatric Institute and
Clinic. All patients were personally evaluated by a neurologist and received
a work-up to elucidate the etiology of their dementia.
- Group 3 included 14 patients seen in other institutions;
in most cases, they had also been seen by a neurologist and had had laboratory
studies that included CT of the head. In three of the 14 cases, however,
the information could be gathered only from the clinical summary found
in the autopsy records.
- Many of these subjects were referred for autopsy to the
ADRC because of a public education campaign that encourages families to
seek an autopsy for their relatives with dementia.
- Pathologic data. All brains were removed by a neuropathologist
as the first procedure of the autopsy at postmortem intervals of between
4 and 12 hours. The unfixed brain was weighed and the brainstem and cerebellum
were separated by intercollicular section. The cerebral hemispheres were
sectioned at 1-cm intervals and placed on a glass surface cooled by ice
to prevent adhesion of the tissue to the cutting surface. The brainstem
and cerebellum were sectioned in the transverse plane at 6-mm intervals.
Brain sections were fixed in 10% buffered formalin. Selected tissue blocks
for light microscopy were obtained from sections corresponding as exactly
as possible to a set of predetermined areas used for processing brains
for the ADRC protocol; additional details of the neuropathologic protocol
have been previously published.18,21 Following standard tissue processing
and paraffin embedding, 8-um-thick sections stained with hematoxylin and
eosin and with the Bielschowsky ammoniacal silver nitrate impregnation
were evaluted. Additional stains were used when indicated by the survey
stains, including the Bielschowsky silver technique as previously reported.21
- Clinical data. The medical history, as well as the results
of examinations and laboratory tests, were obtained from the medical records
libraries of the institutions where the patient had been followed and had
died. We supplemented these data, when appropriate, with a personal or
telephone interview with the relatives.
- One neurologist (O.L.L.) recorded the information to
be evaluated on two forms. The first form included sex, age, handedness,
age at onset, age at death, course and duration of the disease, education,
family history, EEG, CT, NMR, medical history, and physical examinationas
well as examination of blood and CSF for factors that could affect memory
and other cognitive functions. The form also listed the results of neuropsychological
assessment, and the characteristics and course of psychiatric and neurologic
symptoms. The form provided details on the presence, nature, and course
of cognitive deficits and neurologic signs. The second form was a 26-item
checklist derived from the NINCDS-ADRDA Work Group Criteria for probable
Alzheimer's disease.2 The forms did not include the patient's identity,
the institution where they had been evaluated, the clinical diagnosis,
or the pathologic findings.
- Each form was reviewed independently by two other neurologists
(F.B. and J.M.), who were asked to provide a clinical diagnosis. In cases
of probable or possible AD, the two neurologists followed the diagnostic
criteria of the NINCDS/ ADRDA work group.2
- The results were tabulated on a summary sheet filled
out after the two neurologists had provided their diagnosis on each case.
The sheet included the diagnosis reached by the two neurologists and the
diagnosis resulting from the autopsy.
- Table 1. Pathologic diagnosis in 54 patients with dementia
- N %
- Alzheimer's disease alone 34 62.9
- Alzheimer's disease and 2 3.7 Parkinsons's disease
- Alzheimer's disease with 2 3.7 multi-infarct dementia
- Alzheimer's disease with amyotrophic lateral sclerosis
- Total Alzheimers disease 39 72.2
- Multi-infarct dementia 4 7.4
- Multi-infarct dementa 1 1.8 with Parkinson's disease
- Parkinson's disease 2 3.7
- Progressive subcortical gliosis 2 3.7
- Creutzfeldt-Jakob disease 3 5.5
- Progressive supranuclear palsy 1 1.8
- Huntington's disease 1 1.8
- Unclassified 1 1.8
- Total other disease 15 27.7
- Total all cases 54
- Table 2. Clinical diagnosis
- Clinical diagnosis Clinician #1 --- #2
- Probable AD 29 21
- Probable AD and MID 3 0
- Probable AD and thyroid disease 1 2
- Probable AD and PD 3 1
- Probable AD and ALS 1 0
- Probable AD and 0 1 olivopontocerebellar degeneration
- Total probable AD 37 25 (68.5%) (46.2%)
- Possible AD 3 2
- Possible AD and MID 2 2
- Possible AD and alcoholism 0 1
- Possible AD and depression 1 0
- Possible and thyroid disease 0 3
- Possible AD and traumatic 1 2 encephalopathy
- Possible AD and PD 3 6
- Total Possible AD 10 16 (18.5%) (29.6%)
- Atypical AD 0 1
- Atuypical AD and MID 0 1
- MID 2 4
- MID and PD 3 0
- Dementia syndrome of depression 0 1
- HD 1 1
- Wernicke-Korsakoff syndrome 1 0
- Dementia of unknown etiology 0 5
- Total 54 54
- Results. The subjects included 26 women and 28 men who
ranged in age from 30 to 91 years (mean, 72.2; SD, 10.7).
- Autopsy findings. Table 1 shows that 39 (72.2%) of the
54 cases fulfilled histologic criteria for AD, with or without other histopathologic
findings. The remaining 15 cases (27.7%) showed changes corresponding to
other neurodegenerative disorders, cerebrovascular disease, or Creutzfeldt-Jakob
disease (CJD). Seven cases met the histopathologic criteria for multi-infarct
de-mentia (MID). Five cases (9.2%) showed changes associated with Parkinson's
- Twenty-two of the 39 AD patients (56%) were age 65 or
greater at the time of the onset of the disease. Seven of the 15 patients
in the group with other diseases (47%) were age 65 or older at the time
of disease onset.
- Clinical diagnosis. There was a general adherence to
the criteria specified by McKhann et al.2 However, the two clinicians in
this study considered the diagnosis of probable AD when the probability
of AD was strong even if a patient had another disease potentially associated
with dementia that might or might not have made some contribution to the
patient's clinical state (table 2).
- Accuracy of the clinical diagnosis (table 3). Group 1
(N = 12). There were six men and six women. Ten cases (83.3%) met the histologic
criteria for AD. In nine cases (75.0%), the diagnosis of both clinicians
agreed with the pathologic findings; in the other case (8.3%), one clinical
diagnosis agreed with the histologic findings. The remaining two cases
(16.6%) had histopathologic diagnoses of CJD and progressive supranuclear
palsy (PSP), respectively. Both cases were incorrectly diagnosed by both
- Group 2 (N = 28). There were 11 women and 17 men. Eighteen
cases (64.2%) had the histopathologic features for AD with or without additional
findings. Sixteen of these cases (57.1%) were correctly diagnosed by both
clinicians, one case by one of them, and both incorrectly diagnosed one
case. The remaining ten cases (35.7%) included two with CJD; two with subcortical
gliosis (SG); two with PD, one of which was associated with MID; one case
of Huntington's disease (HD); two cases with MID; and one unclassifed.
Only one, the HD case (3.5%), was correctly diagnosed by both observers,
and four cases (14.2%), two MID and two PD, one associated with MID, were
correctly diagnosed by one clinician.
- Group 3 (N = 14). In this group there were nine women
and five men. Eleven cases (78.5%) met the histopathologic criteria for
AD with or without additional findings. Eight of these cases (57.1%) were
correctly diagnosed by both clinicians, two cases by one of them, while
both were incorrect in one case. Of the remaining three cases (21.4%),
only one was correctly diagnosed (7.1%) by one clinician. Both missed the
two other cases of MID.
- There was no statistically significant difference in
diagnostic agreement across patient groups in which the amount of clinical
information was different (X2 = 1.19; p > 0.05).
- Table 3. Accuracy of the clinical diagnosis by two clinicians
- Both One Neither Correct Correct Correct
- Group 1 (N = 12) 9 1 2(16.6%)
- Group 2 (N = 28) 17 5 6(21.4%)
- Group 3 (N = 14) 8 3 3(21.4%)
- Table 4. Previously reported studies of clinicopathologic
correlation in demented patients*
- Agreement %
- Number of cases AD
- Retrospective studies
- Todorov et al, 1975(7) 776 43
- Perl et al, 1984(9) 26 81
- Wade et al, 1987(12) 65 85
- Alafuzoff et al, 1987(13) 55 63
- Kokmen at al, 1987(14) 32 72
- Joachim et al, 1987(15) 150 87