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From: TSS ()
Subject: Alzheimer's cases will quadruple to 1.7 MILLION in 40 years
Date: June 10, 2007 at 3:16 pm PST

Alzheimer's cases will quadruple to 1.7m in 40 years
By DANIEL MARTIn - More by this author »

Last updated at 21:40pm on 10th June 2007

The number of people in Britain with Alzheimer's will more than quadruple in the next 40 years, experts warned yesterday.

By 2050 there will be 1.7million with the disease, half of whom will need high-level care.

At present there are 700,000 with dementia in Britain, around half of whom have Alzheimer's. Around 60,000 die of dementia every year.

Experts warned of a "global epidemic" of Alzheimer's, with the estimated 26 million worldwide living with the condition growing to more than 106 million by 2020.

The U.S. research was presented at an international conference on the prevention of dementia being held in Washington.

"We face a looming global epidemic of Alzheimer's disease as the world's population ages," said lead author Professor Ron Brookmeyer, from the Bloomberg School of Public Health in Maryland.

"By 2050, one in 85 persons worldwide will have Alzheimer's disease.

"If we can make even modest advances in preventing the disease or delaying its progression, we could have a huge global public health impact."

The biggest rise in cases will come in Asia, where 48 per cent of sufferers currently live.

The total there will grow from 12.6million last year to 62.8 million in 2050 (59 per cent of the world's cases), the study said.

The predictions came as other experts unveiled a test that can predict a person's risk of getting dementia in the next six years.

It combines medical history, cognitive function and a physical examination and is 87 per cent accurate, according to experts at San Francisco VA Medical Centre in California.

Neil Hunt, chief executive of the UK's Alzheimer's Society, said tools to predict dementia were important but warned: "Any risk model should be used alongside guidance on how people can reduce their chances of developing dementia."

He said the Maryland research painted a stark picture and added: "We cannot afford to ignore the challenge of the disease.

"The Alzheimer's Society's recent Dementia UK report put the cost of the condition to this country at £17 billion a year.

"A national dementia strategy must consider the global scale of Alzheimer's disease and other types of dementia."

Alzheimer's and Transmissible Spongiform Encephalopathies ???

Alzheimer-type neuropathology 28 year old patient with idCJD
Sun Feb 19, 2006 11:14

Alzheimer-type neuropathology in a 28 year old patient with iatrogenic Creutzfeldt-Jakob disease after dural grafting
M Preusser1, T Ströbel1, E Gelpi1,2, M Eiler3, G Broessner4, E Schmutzhard4 and H Budka1,2
1 Institute of Neurology, Medical University Vienna, Austria
2 Austrian Reference Centre for Human Prion Diseases (OERPE), General Hospital Vienna, Austria
3 Department of Neurology, LKH Rankweil, Austria
4 Department of Neurology, Medical University Innsbruck, Innsbruck, Austria

Correspondence to:
Dr H Budka
Institute of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 4J, 1097 Vienna, Austria;

We report the case of a 28 year old man who had received a cadaverous dura mater graft after a traumatic open skull fracture with tearing of the dura at the age of 5 years. A clinical suspicion of Creutzfeldt-Jakob disease (CJD) was confirmed by a brain biopsy 5 months prior to death and by autopsy, thus warranting the diagnosis of iatrogenic CJD (iCJD) according to WHO criteria. Immunohistochemistry showed widespread cortical depositions of disease associated prion protein (PrPsc) in a synaptic pattern, and western blot analysis identified PrPsc of type 2A according to Parchi et al. Surprisingly, we found Alzheimer-type senile plaques and cerebral amyloid angiopathy in widespread areas of the brain. Plaque-type and vascular amyloid was immunohistochemically identified as deposits of beta-A4 peptide. CERAD criteria for diagnosis of definite Alzheimer’s disease (AD) were met in the absence of neurofibrillar tangles or alpha-synuclein immunoreactive inclusions. There was no family history of AD, CJD, or any other neurological disease, and genetic analysis showed no disease specific mutations of the prion protein, presenilin 1 and 2, or amyloid precursor protein genes. This case represents (a) the iCJD case with the longest incubation time after dural grafting reported so far, (b) the youngest documented patient with concomitant CJD and Alzheimer-type neuropathology to date, (c) the first description of Alzheimer-type changes in iCJD, and (d) the second case of iCJD in Austria. Despite the young patient age, the Alzheimer-type changes may be an incidental finding, possibly related to the childhood trauma.


CJD1/9 0185

Ref: 1M51A


Dr McGovern From: Dr A Wight

Date: 5 January 1993

Copies: Dr Metters

Dr Skinner

Dr Pickles

Dr Morris

Mr Murray


1. CMO will wish to be aware that a meeting was held at DH yesterday,
4 January, to discuss the above findings. It was chaired by Professor
Murray (Chairman of the MRC Co-ordinating Committee on Research in
the Spongiform Encephalopathies in Man), and attended by relevant
experts in the fields of Neurology, Neuropathology, molecular biology,
amyloid biochemistry, and the spongiform encephalopathies, and by
representatives of the MRC and AFRC.

2. Briefly, the meeting agreed that:

i) Dr Ridley et als findings of experimental induction of p amyloid
in primates were valid, interesting and a significant advance in the
understanding of neurodegeneradve disorders;

ii) there were no immediate implications for the public health, and no
further safeguards were thought to be necessary at present; and

iii) additional research was desirable, both epidemiological and at the
molecular level. Possible avenues are being followed up by DH
and the MRC, but the details will require further discussion.


BSE101/1 0136


5 NOV 1992

CMO From: Dr J S Metters DCMO 4 November 1992


1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have
recognised the public sensitivity of these findings and intend to report
them in their
proper context. This hopefully will avoid misunderstanding and possible
distortion by
the media to portray the results as having more greater significance than
the findings
so far justify.

2. Using a highly unusual route of transmission (intra-cerebral injection)
researchers have demonstrated the transmission of a pathological process
from two
cases one of severe Alzheimer's disease the other of Gerstmann-Straussler
disease to
marmosets. However they have not demonstrated the transmission of either
condition as the "animals were behaving normally when killed'. As the report
emphasises the unanswered question is whether the disease condition would
revealed itself if the marmosets had lived longer. They are planning funher
to sec if the conditions, as opposed to the partial pathological process, is

What are the implications for public health?

3. . The route of transmission is very specific and in the natural state of
highly unusual. However it could be argued that the results reveal a
potential risk,
in that brain tissue from these two patients has been shown to transmit a
process. Should therefore brain tissue from such cases be regarded as
infective? Pathologists, morticians, neuro surgeons and those assisting at
surgical procedures and others coming into contact with "raw" human brain
could in theory be at risk. However, on a priori grounds given the highly
route of transmission in these experiments that risk must be negligible if
the usual
precautions for handling brain tissue are observed.


BSE101/1 0137

4. The other dimension to consider is the public reaction. To some extent
the GSS
case demonstrates little more than the transmission of BSE to a pig by
injection. If other prion diseases can be transmitted in this way it is
little surprise that
some pathological findings observed m GSS were also transmissible to a
But the transmission of features of Alzheimer's pathology is a different
matter, given
the much greater frequency of this disease and raises the unanswered
question whether
some cases are the result of a transmissible prion. The only tenable public
line will
be that "more research is required" before that hypothesis could be
evaluated. The
possibility on a transmissible prion remains open. In the meantime MRC needs
carefully to consider the range and sequence of studies needed to follow
through from
the preliminary observations in these two cases. Not a particularly
message, but until we know more about the causation of Alzheimer's disease
the total
reassurance is not practical.

Room 509
Richmond House
Pager No: 081-884 3344
Callsign: DOH 832



also, see the increase of Alzheimer's from 1981 to 1986

Proof Mad Cow Is The Same
As Alzheimer's And CJD ???

How Many Of Them Are Really Mad Cow/vCJD/TSEs ???

How Can Government Claims Of Just 'One In A Million' Be Accurate
When CJD Is Not A Reportable Disease? And When The Elderly Do
Not Get Routinely Autopsied??

By Terry Singletary, Sr

Note - This extensive, powerful assemblage of science was first posted on
1-24-3. The
following data is even more important today. -ed


Regarding Alzheimer's disease

(note the substantial increase on a yearly basistss)


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 Moossy, MD

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




Subject: Re: Hello Dr. Manuelidis Date: Fri, 22 Dec 2000 17:47:09 -0500
From: laura manuelidis Reply-To: 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.





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.

Dear Mr. Ed:

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.


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