CJD1/9 0185
Ref: 1M51A
IN STRICT CONFIDENCE
Dr McGovern From: Dr A Wight
Date: 5 January 1993
Copies: Dr Metters
Dr Skinner
Dr Pickles
Dr Morris
Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
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.
93/01.05/4.1
http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
BSE101/1 0136
IN CONFIDENCE
5 NOV 1992
CMO From: Dr J S Metters DCMO 4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
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) the
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 clinical
condition as the "animals were behaving normally when killed'. As the report
emphasises the unanswered question is whether the disease condition would have
revealed itself if the marmosets had lived longer. They are planning funher research
to sec if the conditions, as opposed to the partial pathological process, is transmissible.
What are the implications for public health?
3. . The route of transmission is very specific and in the natural state of things
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 pathological
process. Should therefore brain tissue from such cases be regarded as potentially
infective? Pathologists, morticians, neuro surgeons and those assisting at neuro
surgical procedures and others coming into contact with "raw" human brain tissue
could in theory be at risk. However, on a priori grounds given the highly specific
route of transmission in these experiments that risk must be negligible if the usual
precautions for handling brain tissue are observed.
92/11.4/1-1
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 intra-cerebral
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 marmoset.
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 comfortable
message, but until we know more about the causation of Alzheimer's disease the total
reassurance is not practical.
JS METTERS
Room 509
Richmond House
Pager No: 081-884 3344
Callsign: DOH 832
121/YdeS
92/11.4/1.2
http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
Regarding Alzheimer's disease
(note the substantial increase on a yearly basis)
http://www.bseinquiry.gov.uk/files/yb/1988/07/08014001.pdf
snip...
The pathogenesis of these diseases was compared to Alzheimer's disease at a molecular level...
snip...
http://www.bseinquiry.gov.uk/files/yb/1990/03/12003001.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/yb/1990/07/06005001.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/yb/1990/07/09001001.pdf
TSS
Ref: 1M51A
IN STRICT CONFIDENCE
Dr McGovern From: Dr A Wight
Date: 5 January 1993
Copies: Dr Metters
Dr Skinner
Dr Pickles
Dr Morris
Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
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.
93/01.05/4.1
http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
BSE101/1 0136
IN CONFIDENCE
5 NOV 1992
CMO From: Dr J S Metters DCMO 4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
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) the
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 clinical
condition as the "animals were behaving normally when killed'. As the report
emphasises the unanswered question is whether the disease condition would have
revealed itself if the marmosets had lived longer. They are planning funher research
to sec if the conditions, as opposed to the partial pathological process, is transmissible.
What are the implications for public health?
3. . The route of transmission is very specific and in the natural state of things
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 pathological
process. Should therefore brain tissue from such cases be regarded as potentially
infective? Pathologists, morticians, neuro surgeons and those assisting at neuro
surgical procedures and others coming into contact with "raw" human brain tissue
could in theory be at risk. However, on a priori grounds given the highly specific
route of transmission in these experiments that risk must be negligible if the usual
precautions for handling brain tissue are observed.
92/11.4/1-1
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 intra-cerebral
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 marmoset.
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 comfortable
message, but until we know more about the causation of Alzheimer's disease the total
reassurance is not practical.
JS METTERS
Room 509
Richmond House
Pager No: 081-884 3344
Callsign: DOH 832
121/YdeS
92/11.4/1.2
http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
Regarding Alzheimer's disease
(note the substantial increase on a yearly basis)
http://www.bseinquiry.gov.uk/files/yb/1988/07/08014001.pdf
snip...
The pathogenesis of these diseases was compared to Alzheimer's disease at a molecular level...
snip...
http://www.bseinquiry.gov.uk/files/yb/1990/03/12003001.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/yb/1990/07/06005001.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/yb/1990/07/09001001.pdf
TSS
