Alzheimer’s Society, the London School of Economics and the Institute of
Psychiatry
Twice as many cases of early dementia than was thought
Charity calls for more help for younger people with dementia as new figures
disclose twice as many cases as was thought among those aged between 30 and 65
Charity calls for more help for younger people with dementia as new figures
disclose thousands of cases among those aged between 30 and 65
Surveys have found that dementia is the most feared condition among those
aged 55 and over Photo: Alamy
Laura Donnelly By Laura Donnelly, Health Editor
9:00PM BST 06 Sep 2014
More than twice as many people in the UK have dementia before the age of 65
than was previously thought, new figures show.
A report due to be published this week says that 42,000 people are now
estimated to be suffering early onset dementia, including thousands of cases
among those in their 40s, and more than 700 cases among those in their 30s.
The new statistics also show the condition is slightly more common among
men than women.
Experts said doctors too often missed symptoms of dementia in younger
people, assuming they were too young to be suffering from the condition. They
said services and society needed to do more to help those coming to terms with a
diagnosis of dementia.
The figures, due to be published tomorrow, come from a state of the nation
report by the Alzheimer’s Society, the London School of Economics and the
Institute of Psychiatry, which will show the cost of dementia to the NHS and
social services.
Previous estimates had suggested that just 17,000 cases of dementia involve
younger people. But the new figures suggest 42,325 people below the age of 65
are currently suffering from such conditions – representing roughly five per
cent of all cases of dementia. Three quarters of cases are among those aged
between 60 and 65, but cases can occur among those in their 50s, 40s and even in
their 30s.
Jeremy Hughes, chief executive at Alzheimer’s Society said: “For too long
dementia has been perceived as a natural part of ageing which only affects the
oldest of the old in our society.
“Say the word Alzheimer’s and many people picture a frail, elderly person
in a care home. The risk of developing dementia does increase with age, but the
reality is that dementia is caused by diseases of the brain that don’t
discriminate. “
Surveys have found that dementia is the most feared condition among those
aged 55 and over.
Mr Hughes said: “Many people will be coming to terms with the symptoms
while still in work, perhaps looking after children and paying a mortgage. Too
often we hear of people reporting memory loss to their doctor in mid-life, but
being misdiagnosed because they are considered too young to have dementia. “
He said services need to ensure that younger adults were able to access
specialist treatment and support.
The new estimates suggest that of the 42,325 cases of early-onset dementia
in the UK, 21,519 cases are in men while 20,806 are in women. Around 32,000 of
the cases involve those aged 60 to 65, with 7,700 cases among those in their
50s, 2,010 cases among those in their 40s, and 707 cases among those in their
30s, the figures show.
While Alzheimer’s disease is the most common form of dementia among the
elderly, in those under the age of 65, it represents just one in three cases. In
some cases, there is a family history of early-onset Alzheimer’s disease.
Among younger people, the second most common cause is vascular dementia,
which occurs when there are problems in the blood supply to the brain. One in
five cases of dementia in the under 65s are caused by this.
Around one in ten cases of dementia in younger people are alcohol-related,
and 10 per cent are caused by dementia with Lewy bodies, a build up of tiny
protein deposits in the brain .
A further 12 per cent are caused by front-temporal dementia, which is a
more common cause of dementia among those aged between 45 and 65 than among
dementias in older people, and often relates to a family history of the disease.
Rarer forms of dementia – linked to conditions such as Parkinson's disease,
Huntington’s disease and Creutzfeldt-Jakob disease - also explain a higher
proportion of dementias in younger people than they do in the elderly.
The report also forecasts that the number of people with early-onset
dementia is set to rise by 20 per cent over the next four decades, with more
than 50,000 cases expected by 2051.
Susan Hulme, from Camarthenshire, South Wales, was diagnosed with
Alzheimer’s disease last year, at the age of 59. She said she had been
struggling with memory problems for three years, which had been attributed to
stress, or sinus problems.
When she visited her GP last year, and found herself unable to recall the
reason for her visit, she was referred to a memory clinic, who made the
diagnosis, and prescribed medication which can slow its impact.
Ms Hulme, a former civil servant, said: “In a way it felt like a relief to
get the diagnosis, because I knew something was wrong for several years, I had
been really struggling with my memory, and with a kind of fuzzy feeling that was
worst in the mornings – but it was a real shock that it was Alzheimer’s disease,
I thought that was something that only came with old age.”
She had already taken voluntary redundancy, after suffering what she had
thought was stress.
Telling people about her diagnosis was one of the most difficult parts of
coming to terms with the condition, she said, calling for more funding of
services for younger people, to provide support.
“I don’t think most people realise this is something that could happen at
this age. Telling my partner and my children was one of the most difficult
things to do,” she said.
Saturday, May 25, 2013
Brain homogenates from human tauopathies induce tau inclusions in mouse
brain
Sunday, February 10, 2013
Parkinson's Disease and Alpha Synuclein: Is Parkinson's Disease a
Prion-Like Disorder?
Wednesday, May 16, 2012
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease
have both been around a long time, and was discovered in or around the same time
frame, early 1900’s. Both diseases are incurable and debilitating brain disease,
that are in the end, 100% fatal, with the incubation/clinical period of the
Alzheimer’s disease being longer (most of the time) than the TSE prion disease.
Symptoms are very similar, and pathology is very similar.
Methods
Through years of research, as a layperson, of peer review journals,
transmission studies, and observations of loved ones and friends that have died
from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant
Creutzfelt Jakob Disease CJD.
Results
I propose that Alzheimer’s is a TSE disease of low dose, slow, and long
incubation disease, and that Alzheimer’s is Transmissible, and is a threat to
the public via the many Iatrogenic routes and sources. It was said long ago that
the only thing that disputes this, is Alzheimer’s disease transmissibility, or
the lack of. The likelihood of many victims of Alzheimer’s disease from the many
different Iatrogenic routes and modes of transmission as with the TSE prion
disease.
Conclusions
There should be a Global Congressional Science round table event set up
immediately to address these concerns from the many potential routes and sources
of the TSE prion disease, including Alzheimer’s disease, and a emergency global
doctrine put into effect to help combat the spread of Alzheimer’s disease via
the medical, surgical, dental, tissue, and blood arena’s. All human and animal
TSE prion disease, including Alzheimer’s should be made reportable in every
state, and Internationally, WITH NO age restrictions. Until a proven method of
decontamination and autoclaving is proven, and put forth in use universally, in
all hospitals and medical, surgical arena’s, or the TSE prion agent will
continue to spread. IF we wait until science and corporate politicians wait
until politics lets science _prove_ this once and for all, and set forth
regulations there from, we will all be exposed to the TSE Prion agents, if that
has not happened already.
end...tss
SEE FULL TEXT AND SOURCE REFERENCES ;
Wednesday, May 16, 2012
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Proposal ID: 29403 http://betaamyloidcjd.blogspot.com/2012/05/alzheimers-disease-and-transmissible.html
Wednesday, September 21, 2011
PrioNet Canada researchers in Vancouver confirm prion-like properties in
Amyotrophic Lateral Sclerosis (ALS)
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions
David W. Colby1,* and Stanley B. Prusiner1,2
Friday, September 3, 2010
Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids,
Prionpathy, Prionopathy, TSE
Ann N Y Acad Sci. 1982;396:131-43.
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob
disease).
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
Abstract
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.
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 neurodegenerative 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
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
recognized 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 emphasizes the unanswered question is
whether the disease condition would have revealed itself if the marmosets had
lived longer. They are planning further research to see 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 in 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
BSE101/1 0136
IN CONFIDENCE
CMO
From: Dr J S Metters DCMO
4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
CJD1/9 0185
Ref: 1M51A
IN STRICT CONFIDENCE
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
Tuesday, July 1, 2014
Distinct synthetic Aβ prion strains producing different amyloid deposits in
bigenic mice
Tuesday, November 26, 2013
Transmission of multiple system atrophy prions to transgenic mice
Tuesday, December 17, 2013
Alzheimer's Disease U.K. diagnosed by region in each of the last five years
[179852]
TSS
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