Sunday, September 7, 2014

Twice as many cases of early dementia than was thought Alzheimer’s Society, the London School of Economics and the Institute of Psychiatry

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 ?
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.
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.
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.
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.
Wednesday, May 16, 2012
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
 Wednesday, September 21, 2011
 PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)
Wednesday, January 5, 2011
 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.
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
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 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
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 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
From: Dr J S Metters DCMO
4 November 1992
CJD1/9 0185
Ref: 1M51A
From: Dr. A Wight Date: 5 January 1993
Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray
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]