Alzheimer's and Transmissible Spongiform Encephalopathies

flounder · 03-09-2007, 10:19 PM

Subject: Alzheimer-type neuropathology in a 28-year old patient with iatrogenic CJD after dural grafting
Date: March 9, 2007 at 9:15 am PST

HUMAN-04

Alzheimer-type neuropathology in a 28-year old patient with iatrogenic

Creutzfeldt-Jakob disease after dural grafting

M Preusser1, T Stroebel1, E Gelpi1, 2, M Eiler3, G Broessner4, E Schmutzhard4, 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, Austria

We report the autopsy case of a 28-year old male patient who had received a cadaverous dura

mater graft after a traumatic open skull fracture with tearing of 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 diseaseassociated

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 1. the

iCJD case with the longest incubation time after dural grafting reported so far, 2. the youngest

documented patient with concomitant CJD and Alzheimer-type neuropathology to date, 3. the

first description of Alzheimer type-changes in iCJD, and 4. 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.

249 of 411 pages...tss

http://www.tse-forum.de/tse_forum/de...FINAL_nov2.pdf

TSS

flounder · 03-23-2007, 11:39 AM

Subject: Every 72 seconds someone in America develops Alzheimer's
Date: March 20, 2007 at 5:35 pm PST
Alzheimer's Disease Prevalence Rates Rise to More than Five Million in the United States
Someone develops Alzheimer's every 72 seconds, according to new Alzheimer's Association report

The Alzheimer's Association today reports that in 2007 there are now more than 5 million people in the United States living with Alzheimer's disease. This number includes 4.9 million people over the age of 65 and between 200,000 and 500,000 people under age 65 with early onset Alzheimer's disease and other dementias. This is a 10 percent increase from the previous prevalence nationwide estimate of 4.5 million.

The greatest risk factor for Alzheimer's is increasing age, and with 78 million baby boomers beginning to turn 60 last year, it is estimated that someone in America develops Alzheimer's every 72 seconds; by mid-century someone will develop Alzheimer's every 33 seconds.

These new estimates, as well as other data concerning the disease and its effects, are issued today as hundreds of advocates from across the country gather in the nation's capitol for the Alzheimer's Association's annual Public Policy Forum. The report titled, 2007 Alzheimer's Disease Facts and Figures, is being released at a hearing today chaired by Senator Barbara Mikulski. Senators Barbara Mikulski and Christopher Bond and Representatives Edward Markey and Christopher Smith have introduced bipartisan legislation to address problems identified in the Association's report. The Association's report details the escalation of Alzheimer's disease which now is the seventh leading cause of death in the country and the fifth leading cause of death for those over age 65. It also offers numerous statistics that convey the burden that Alzheimer's imposes on individuals, families, state and federal governments, businesses, and the nation's health care system. For example:

Without a cure or effective treatments to delay the onset or progression of the Alzheimer's, the prevalence could soar to 7.7 million people with the disease by 2030, which is more than the population of 140 of the 236 United Nations countries.
By mid-century, the number of people with Alzheimer's is expected to grow to as many as 16 million, more than the current total population of New York City, Los Angeles, Chicago and Houston combined.
As the prevalence impact of Alzheimer's grows, so does the cost to the nation. The direct and indirect costs of Alzheimer's and other dementias amount to more than $148 billion annually, which is more than the annual sales of any retailer in the world excluding Wal-Mart.
"Alzheimer's Disease Facts and Figures clearly shows the tremendous impact this disease is having on the nation; and with the projected growth of the disease, the collective impact on individuals, families, Medicare, Medicaid, and businesses will be even greater," says Harry Johns, President and CEO of the Alzheimer's Association. "However there is hope. There are currently nine drugs in Phase III clinical trials for Alzheimer's several of which show great promise to slow or stop the progression of the disease. This, combined with advancements in diagnostic tools, has the potential to change the landscape of Alzheimer's."

According to the latest statistics from the Centers for Disease Control and Prevention, from 2000-2004 death rates have declined for most major diseases -- heart disease (-8 percent), breast cancer (-2.6 percent), prostate cancer (-6.3 percent) and stroke (-10.4 percent), while Alzheimer's disease deaths continue to trend upward, increasing 33 percent during that period.

"We must make the fight against Alzheimer's a national priority before it's too late. The absence of effective disease modifying drugs, coupled with an aging population, makes Alzheimer's the health care crisis of the 21st century," Johns said.

Medicare currently spends nearly three times as much for people with Alzheimer's and other dementias than for the average Medicare beneficiary. Medicare costs are projected to double from $91 billion in 2005 to more than $189 billion by 2015, more than the current gross national product of 86 percent of the world's countries. In 2005, state and federal Medicaid spending for nursing home and home care for people with Alzheimer's and other dementias was estimated at $21 billion; that number is projected to increase to $27 billion by 2015.

The new report also highlights the impact that Alzheimer's has on states with more than 6 in 10 (62%) having double digit growth in prevalence by the end of the decade. In addition, Alaska (+47%), Colorado (+47%), Utah (+45%), Wyoming (+43%), Nevada (+38%), Idaho (+37%), Oregon (+33%), and Washington (+33%) will experience increases ranging from one-third to one-half. The states with the largest numbers of deaths due to Alzheimer's disease in 2003 were (1) California, (2) Florida, (3) Texas, (4) Pennsylvania, and (5) Ohio.

The Alzheimer's Association is the first and largest voluntary health organization dedicated to finding prevention methods, treatments and an eventual cure for Alzheimer's. For more than 25 years, the Association has provided reliable information and care consultation; created services for families; increased funding for dementia research; and influenced public policy changes.

Contact: Call our media line at 312.335.4078

Download Report: 2007 Alzheimer's Disease Facts and Figures (28 pages)

Quote Sheet (2 pages)

http://www.alz.org/national/document...quotesheet.pdf

Fact sheet (2 pages)

http://www.alz.org/national/document...Ffactsheet.pdf

http://www.alz.org/news_and_events_rates_rise.asp

Every 72 seconds

someone in America

develops Alzheimer's.

http://www.alz.org/national/document...AndFigures.pdf

More Evidence Mad Cow Same
As CJD And Alzheimer's
1-24-3

IN STRICT CONFIDENCE

TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES

http://www.bseinquiry.gov.uk/files/y...1/05004001.pdf

full text ;
http://www.rense.com/general34/cjmd.htm

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
12-27-03

Regarding Alzheimer's disease

(note the substantial increase on a yearly basis)

http://www.bseinquiry.gov.uk/files/y...7/08014001.pdf

snip...

The pathogenesis of these diseases was compared to Alzheimer's disease at a molecular level...

snip...

http://www.bseinquiry.gov.uk/files/y...3/12003001.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/y...7/06005001.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/y...7/09001001.pdf

================================================== ===

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

snip...

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: <39B5561A.87B84A28@wt.net> <39B64574.A4835745@yale.edu>
<39B680D8.3872535B@wt.net> <39B66EF1.4CE25685@yale.edu>
<39BBB812.425109F@wt.net> <39BE84CB.D7C0C16B@yale.edu>
<3A3BA197.7F60D376@wt.net>

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.

4.5 MILLION DEMENTED ALZHEIMER'S PATIENTS, HOW MANY ARE CJD/TSEs ???

HOW CAN ONE-IN-A-MILLION BE ACCURATE WHEN CJD IS NOT REPORTABLE,

AND WHEN THE ELDERLY DO NOT GET AUTOPSIED??????

TSS

http://www.rense.com/general46/proofa.html

Alzheimer's and Transmissible Spongiform Encephalopathies

snip...

Subject: Alzheimer-type neuropathology in a 28-year old patient with iatrogenic CJD after dural grafting
Date: March 9, 2007 at 9:15 am PST

HUMAN-04

Alzheimer-type neuropathology in a 28-year old patient with iatrogenic

Creutzfeldt-Jakob disease after dural grafting

M Preusser1, T Stroebel1, E Gelpi1, 2, M Eiler3, G Broessner4, E Schmutzhard4, 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, Austria

We report the autopsy case of a 28-year old male patient who had received a cadaverous dura

mater graft after a traumatic open skull fracture with tearing of 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 diseaseassociated

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 1. the

iCJD case with the longest incubation time after dural grafting reported so far, 2. the youngest

documented patient with concomitant CJD and Alzheimer-type neuropathology to date, 3. the

first description of Alzheimer type-changes in iCJD, and 4. 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.

249 of 411 pages...tss

http://www.tse-forum.de/tse_forum/de...FINAL_nov2.pdf

full text ;

http://neurotalk.psychcentral.com/sh...ad.php?p=78281

FELINE ALZHEIMER'S OR MAD CAT DISEASE I.E. FSE ???

http://lists.ifas.ufl.edu/cgi-bin/wa...-mg&T=0&P=8385

From: terry <[log in to unmask]>
Subject: Re: FELINE ALZHEIMER'S OR MAD CAT DISEASE I.E. FSE ???
In-Reply-To: <[log in to unmask]>
Content-Type: text/plain; charset="Windows-1252"

I have 2 questions for you, terry singeltary. Do you agree with colm kelleher where he states there may be a relationship between vCJD and alzeheimer's in that alzheimers may be misdiagnosed. And is it true that BSE cannot be destroyed by heat or chemical so that any instrument that touches it must be thrown out.
Sent wirelessly via BlackBerry from T-Mobile.

http://lists.ifas.ufl.edu/cgi-bin/wa...-mg&T=0&P=8525

Sender: Sustainable Agriculture Network Discussion Group
<[log in to unmask]>
From: "Terry S. Singeltary Sr." <[log in to unmask]>
Subject: Re: FELINE ALZHEIMER'S OR MAD CAT DISEASE I.E. FSE ???
Comments: To: [log in to unmask]
Content-type: text/plain; charset=Windows-1252

i have written about this many times and spoke with colm on several
occasions when he was writing his book.....

> Do you agree with colm kelleher where he states there may be a
relationship

> between vCJD and alzeheimer's in that alzheimers may be misdiagnosed

NOT JUST vCJD but all human TSE, especially sporadic CJD, there are studies
showing
''CJD'' as being misdiagnosed as Alzheimer's (see below).

AND personally i think there is a potential that Alzheimers may be low
level TSE.

may be something else too, i mean, just what is Alzheimer's???

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
12-27-03

snip...end

http://lists.ifas.ufl.edu/cgi-bin/wa...-mg&T=0&P=8673

TSS

wasabi · 04-11-2007, 01:10 PM

Here is some information relevant to transmissible spongiform encephalopathies - "A Case for the Role of Copper Deficiency in 'Mad-Cow' Disease and Human Creutzfeldt-Jakob Disease"

http://www.copper.org/innovations/2001/12/mad-cow.html

I think that another possible cause for Alzheimer's that needs further investigation is Lyme disease:

"In 1995 Dr. Mattman obtained positive cultures for Bb from 43 of 47 persons with chronic illness. Only 1 of 23 control patients had a positive Bb culture. Dr. Mattman has subsequently recovered Bb spirochetes form 8 out of 8 cases of Parkinson’s Disease, 41 cases of multiple sclerosis, 21 cases of amyotrophic lateral sclerosis and all tested cases of Alzheimer’s Disease."

http://www.digitalnaturopath.com/cond/C351537.html

This group found no association between Lyme and Alzheimer's:

http://www3.niaid.nih.gov/research/t...antibiotic.htm

This group did find an association between Lyme and Alzheimer's:

http://www.canlyme.com/alzjournal6.html

wasabi · 04-11-2007, 06:55 PM

http://infoventures.com/emf/topics/bu42ni05.html

Damaging the blood brain barrier would allow pathogens such as bacteria, viruses and prions easier access to the brain.

"The brain is protected by tight junctions between adjacent cells of capillary walls, the so-called blood-brain barrier, which, like a border patrol, lets nutrients pass through from the blood to the brain, but keeps toxic substances out. Since 1988, researchers in the laboratory of a Swedish neurosurgeon, Leif Salford, have been running variations on this simple experiment: they expose young laboratory rats to either a cell phone or other source of microwave radiation, and later they sacrifice the animals and look for albumin in their brain tissue. Albumin is a protein that is a normal component of blood but that does not normally cross the blood-brain barrier. The presence of albumin in brain tissue is always a sign that blood vessels have been damaged and that the brain has lost some of its protection.

Here is what these researchers have found, consistently for 18 years: Microwave radiation, at doses equal to a cell phone’s emissions, causes albumin to be found in brain tissue. A one-time exposure to an ordinary cell phone for just two minutes causes albumin to leak into the brain. In one set of experiments, reducing the exposure level by a factor of 1,000 actually increased the damage to the blood-brain barrier, showing that this is not a dose-response effect and that reducing the power will not make wireless technology safer."

http://www.mindfully.org/Technology/...ment1jan06.htm

flounder · 04-30-2007, 12:58 PM

Press Release 07-048
Alzheimer's, Parkinson's, Type 2 Diabetes Similar at Molecular Level

Protein analysis may offer new therapeutic route

April 30, 2007

Alzheimer's disease, Parkinson's disease, type 2 diabetes, the human version
of mad cow disease, and other degenerative diseases are more closely related
at the molecular level than scientists realized, a team reports this week in
an advanced online publication of the journal Nature.

While still preliminary, the research, could help scientists develop tools
for diagnosing such diseases, and potentially for treating them through
"structure-based drug design," said David Eisenberg, a UCLA chemist and
molecular biologist who is part of the research team.

The researchers studied the harmful rope-like structures known as amyloid
fibrils--linked protein molecules that form in the brain. The fibrils
contain a stack of water-tight "molecular zippers."

"With each disease, a different protein transforms into amyloid fibrils, but
all of these diseases are similar at the molecular level," Eisenberg said.

If the molecular zipper is universal in amyloid fibrils, as Eisenberg
believes, is it possible to pry open the zipper or prevent its formation?

Eisenberg's research team used X-ray analysis and a sophisticated computer
algorithm to study proteins known to be associated with human diseases. When
the computer said a protein will form an amyloid fibril, it almost always
did. And one team member is experimenting with various compounds to break up
the fibrils.

"Structural analysis of micro-crystals of proteins is an example of how
basic research can have a profound impact on our understanding of health,
biotechnology and other practical issues," said Parag Chitnis, program
director in National Science Foundation's (NSF) Division of Molecular and
Cellular Biosciences.

NSF, the Howard Hughes Medical Institute and the National Institutes of
Health supported the research.

See the UCLA news release at http://www.newsroom.ucla.edu/.

-NSF-

Media Contacts
Cheryl Dybas, NSF (703) 292-7734 cdybas@nsf.gov
Stuart Wolpert, UCLA (310) 206-0511 swolpert@support.ucla.edu

http://www.nsf.gov/news/news_summ.js...=NSF&from=news

TSS

----- Original Message -----
From: "Terry S. Singeltary Sr." <flounder9@VERIZON.NET>
To: <BSE-L@aegee.org>
Sent: Wednesday, April 25, 2007 8:48 PM
Subject: TRANSMISSION OF B-amyloidosis TO PRIMATES strengthens the parallels
between Alzheimer's disease and CJD - IN CONFIDENCE

Subject: TRANSMISSION OF B-amyloidosis TO PRIMATES strengthens the parallels
between Alzheimer's disease and CJD - IN CONFIDENCE
Date: April 25, 2007 at 6:25 pm PST

IN CONFIDENCE

TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES

H F BAKER, R M RIDLEY, L W DUCHEN, T J CROW, C J BRUTON

As part of a larger series of experiments designed to assess the
transmissibility of various neurodegenerative disease including the
spongiform encephalopathies (eg Creutzfeldt-Jakob disease and BSE we
injected several marmosets (Callithrix Jacchus) intracerebrally with brain
homogenate from :

1) a 56 year old patient with severe Alzheimer's disease - B - amyloid
plaques and conogophilic angiopathy (CAA) and neurofibrillary tangles; and

2) a 62 year old patient with Gerstmann-Straussler disease, a spongiform
encephalopathy with PrP Plaques and, in this case, B-amyloid plaques and
CAA.

These monkeys were killed more than 6 years after inoculation and their
brains were found to contain moderate numbers of B-amyloid plaques and CAA
but NO neurofibrillary tangles NO PrP. The brains of more than 12 monkeys
killed at an older age did not contain these changes. B-amyloid was not
found in the brains of monkeys injected with brain material which did not
contain B-amyloid. These results suggest that B-amyloidosis is a
transmissible process resembling the transmissibility of PrP amyloidosis in
transmissible dementia and strengthens the parallels between Alzheimer's
disease and Creutzfeldt-Jakob disease.

It should be stressed, however, that we are not claiming to have transmitted
Alzheimer's disease because

1) the animals were behaving normally when killed and

2) no neurofibrillary tangles were seen.

We have argued previously that transmission of spongiform encephalopathy,
particularly from the genetic cases (GSS and some CJD), does not imply that
the donor cases themselves acquired the disease by infection. We would apply
the same arguments in this case, particularly in view of the genetic basis
of some cases of Alzheimer's disease and the extensive epidemiological data
which does not link Alzheimer's disease to infection.

DISCLOSURE

This work is currently under preparation for publication BUT IN VIEW OF
PUBLIC CONCERN OVER THE TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES (eg BSE)
AND THE HIGH INCIDENCE OF ALZHEIMER'S DISEASE IN THE GENERAL POPULATION, IT
IS IMPORTANT THAT THESE FINDINGS ARE NOT DISCUSSED OPENLY BEFORE FULL
PUBLICATION.

Furthermore, BEFORE DISCLOSURE, IT IS IMPORTANT THAT INTERESTED PARTIES BE
PROPERLY APPRAISED OF THE DATA AND THERE IMPLICATIONS.

Previous attempts to transmit Alzheimer's disease to rodents and large
primates have been unsuccessful. It is our belief that post-mortem tissue
from these animals still exists and we are anxious that research workers (in
the USA) SHOULD NOT RE-EXAMINE this material until our data are published.

SAFETY

At this point we would like to stress again the lack of evidence relating
Alzheimer's disease to exposure to brain tissue through neurosurgery or
occupation. NEVERTHELESS it is appropriate that proper bodies should
consider whether the results of our experiments have any implications for
human health.

FURTHER EXPERIMENTS

The interpretation we have made that B-amyloidosis as a self-peretuating
process has important implications for understanding the process of
neurodegeneration, which are best studied at the level of protein chemistry.
However, we can see arguments for some transmission experiments including:

1) serial passage of B-amyloidosis in order to strengthen the evidence of
transmissibility;

2) transmission from other cases of Alzheimer's disease in order to
establish the generality of this effect;

3) transmission to primates which are allowed to run their full course, ie
to see whether the full syndrome of Alzheimer's disease develops including
neurofibrillary tangle formation, astrocytosis, neuronal loss and
concomitant cognitive decline. (We are already expert in the
neuropsychological assessment of marmosets). It should be remembered that,
at the present time, only the amyloidosis have been found to be
transmissible such that Alzheimer's disease PER SE has not been transmitted;

4) comparison of transmission from cases which contain only CAA and those
which contain only B-amyloid plaques. These two forms of amyloid differ very
slightly and it is not known whether this difference is preserved on
transmission;

5) establishment of the time course of the development of B-amyloidosis. The
present experiment suggests that the time course is somewhere between 1-5
years;

6) transmission using larger quantities of purified preparations of
B-amyloid. This may reduce the transmission time considerably;

7) transmission using animals of different initial ages to investigate the
relationship between transmission time and chronological age, eg
transmission into mature animals may decrease transmission time through an
interaction between the pathological process and senescence;

8) manipulation of transmission time by treatments which may speed up plaque
formation, eg by increasing the production of amyloid precursor protein, or
which may slow down plaque formation and protect from disease progression.

The proposal is to inoculate about 25 marmosets in the first instance and to
replace them in a 'rolling' experiment as they die or are killed according
to the experimental design. The marmosets will be kept in the MRC Marmoset
Colony in Cambridge. Additional facilities and personnel are not required
over and above that awarded to Dr. Ridley in an MRC Programma Grant.

A preliminary report of our findings will be presented by Professor L W
Duchan at the January 1993 meeting of the British Neuropathological Society.

http://www.bseinquiry.gov.uk/

TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES

http://www.bseinquiry.gov.uk/files/y...1/05004001.pdf

Regarding Alzheimer's disease

(note the substantial increase on a yearly basis)

http://www.bseinquiry.gov.uk/files/y...7/08014001.pdf

snip...

The pathogenesis of these diseases was compared to Alzheimer's disease at a
molecular level...

snip...

http://www.bseinquiry.gov.uk/files/y...3/12003001.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/y...7/06005001.pdf

TSS

wasabi · 05-09-2007, 04:41 PM

Great information. Thanks.

Also, did you read my post linking to "A Connection between Simian Virus 40 and Alzheimer's?" on my thread "Helpful Information about Alzheimer's" ?

flounder · 06-16-2007, 12:17 PM

Published online before print June 15, 2007
Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0609621104

Neuroscience

Cellular prion protein regulates -secretase cleavage of the Alzheimer's amyloid precursor protein

( lipid raft | proteolysis | scrapie | glycosaminoglycan )

Edward T. Parkin *, Nicole T. Watt *, Ishrut Hussain , Elizabeth A. Eckman ¶, Christopher B. Eckman ¶, Jean C. Manson ||, Herbert N. Baybutt ||, Anthony J. Turner *, and Nigel M. Hooper ***
*Proteolysis Research Group, Institute of Molecular and Cellular Biology, Faculty of Biological Sciences, and Leeds Institute of Genetics, Health and Therapeutics, University of Leeds, Leeds LS2 9JT, United Kingdom; Neurodegeneration Research, Neurology and Gastrointestinal Centre of Excellence for Drug Discovery, GlaxoSmithKline Research and Development Limited, Third Avenue, Harlow, Essex CM19 5AW, United Kingdom; ¶Mayo Clinic, Jacksonville, FL 32224; and ||Roslin Institute, Neuropathogenesis Unit, Edinburgh EH9 3JF, United Kingdom

Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved May 10, 2007 (received for review October 30, 2006)

Proteolytic processing of the amyloid precursor protein (APP) by -secretase, -site APP cleaving enzyme (BACE1), is the initial step in the production of the amyloid (A) peptide, which is involved in the pathogenesis of Alzheimer's disease. The normal cellular function of the prion protein (PrPC), the causative agent of the transmissible spongiform encephalopathies such as Creutzfeldt-Jakob disease in humans, remains enigmatic. Because both APP and PrPC are subject to proteolytic processing by the same zinc metalloproteases, we tested the involvement of PrPC in the proteolytic processing of APP. Cellular overexpression of PrPC inhibited the -secretase cleavage of APP and reduced A formation. Conversely, depletion of PrPC in mouse N2a cells by siRNA led to an increase in A peptides secreted into the medium. In the brains of PrP knockout mice and in the brains from two strains of scrapie-infected mice, A levels were significantly increased. Two mutants of PrP, PG14 and A116V, that are associated with familial human prion diseases failed to inhibit the -secretase cleavage of APP. Using constructs of PrP, we show that this regulatory effect of PrPC on the -secretase cleavage of APP required the localization of PrPC to cholesterol-rich lipid rafts and was mediated by the N-terminal polybasic region of PrPC via interaction with glycosaminoglycans. In conclusion, this is a mechanism by which the cellular production of the neurotoxic A is regulated by PrPC and may have implications for both Alzheimer's and prion diseases.

--------------------------------------------------------------------------------

Author contributions: E.T.P., J.C.M., and N.M.H. designed research; E.T.P., N.T.W., I.H., E.A.E., C.B.E., and H.N.B. performed research; E.T.P., N.T.W., E.A.E., C.B.E., and N.M.H. analyzed data; I.H., E.A.E., and C.B.E. contributed new reagents/analytic tools; and E.T.P., J.C.M., A.J.T., and N.M.H. wrote the paper.

The authors declare no conflict of interest.

Present address: Department of Biological Sciences, Lancaster University, Lancaster LA1 4YQ, United Kingdom.

**To whom correspondence should be addressed.

Nigel M. Hooper, E-mail: n.m.hooper@leeds.ac.uk

www.pnas.org/cgi/doi/10.1073/pnas.0609621104

http://www.pnas.org/cgi/content/abst...9621104v1?etoc

Human and Animal Food Poisoning with Mad Cow a Slow Death

http://www.slowfoodforum.org/showthread.php?p=4042

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
12-27-03

http://www.rense.com/general46/proofa.html

More Evidence Mad Cow Same
As CJD And Alzheimer's
1-24-3

http://www.rense.com/general34/cjmd.htm

TSS