Wednesday, January 18, 2012

Government seeking $1T campaign against Alzheimer's

January 17, 2012 12:57 PM
Gov't wants Alzheimer's treatment that works by 2025

By CBS News Staff

(CBS/AP) By 2025, Scientists need to develop an effective treatment for Alzheimer's disease, says the U.S. Government. The Obama administration announced today a plan for the government to step in and help find a way to treat and prevent the deadly neurological disease.

PICTURES: Alzheimer's disease: 7 things that raise your risk

The announcement of the nation's first National Alzheimer's Plan is not a moment too soon. An estimated 5.4 million Americans currently have the disease, but research suggests that by 2050, that number may nearly triple to 16 million Americans living with the disease - costing $1 trillion in medical and nursing home expenditures.

The government is setting what it calls an ambitious goal for progress in tackling the disease. The plan doesn't provide details of how to fund the necessary research to meet that target date. Today's treatments only temporarily ease some dementia symptoms, and work to find better ones has been frustratingly slow.
A committee of Alzheimer's experts begins a two-day meeting Tuesday to help advise the government on how to finalize the plan.

Families have been "reminding us of the enormity of our task, perhaps most important the meaningfulness of it," said the committee's chair, Dr. Ron Petersen, an Alzheimer's specialist at the Mayo Clinic.

But hanging over the meeting is the reality of a budget crunch. It's not clear how much money the federal government will be able to devote to Alzheimer's, and states have seen their Alzheimer's budgets cut.

"We're not going to fix this without substantial resources," said David Hoffman of the New York State Department of Health, who oversees that state's Alzheimer's programs. "In New York, we're hanging on by our nails."

Alzheimer's disease is the sixth leading cause of death in the U.S., according to the CDC's latest report, taking more than 83,000 lives this past year.
The national plan is supposed to tackle both the medical and social aspects of dementia, and advocacy groups had urged that it set a deadline for progress.

One of the draft's goals it to improve the timely diagnosis for the disease. A recent report found as many as half of today's Alzheimer's sufferers haven't been formally diagnosed, in part because of stigma and the belief that nothing can be done. Symptomatic treatment aside, a diagnosis lets families plan, and catching the disease earlier would be crucial if scientists ever find ways to slow the disease's progress.

Another goal of the plan is to improve support and training for families so they know what resources are available for patients and what to expect as dementia worsens. A caregiver-training program in New York has shown that families taught how to handle common dementia problems, and given support, are able to keep their loved ones at home for longer. Hoffman said such training programs are far cheaper than nursing homes.

Alzheimer's sufferers gradually lose the ability to do the simplest activities of daily life and can survive that way for a decade or more. A recent study suggests memory loss from aging could start as early as 45, HealthPop reported.

In meetings around the country last summer and fall, families urged federal health officials to make sure the national plan addresses how to help patients live their last years at home without ruining their caregivers' own health and finances.

According to a study in the Lancet Neurology, simple lifestyle changes may go a long way in staving off Alzheimer's disease. The study found that by reducing risk factors - such as obesity and blood pressure - by 25 percent, it could mean 3 million fewer cases of Alzheimer's worldwide, HealthPop reported.

Here are 7 ways to reduce your risk for Alzheimer's disease:

Government seeking $1T campaign against Alzheimer's

I was so saddened by this video, and then I became angry as hell. our family has been hit with not only Alzheimer’s, but also the Heidenhain Variant Creutzfeldt Jakob disease. These Transmissible Spongiform Encephalopathies have been spreading for decades, and thanks to Corporate interest, they were all simply lied about and or just swept under the rug. now look where we are, and yes, I believe that science has shown that Alzheimer’s disease is transmissible. NOW, think why the explosion of Alzheimer’s disease victims?

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.
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.
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

Tuesday, October 4, 2011

De novo induction of amyloid-β deposition in vivo
Molecular Psychiatry advance online publication 4 October 2011; doi: 10.1038/mp.2011.120

Wednesday, September 21, 2011
PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)

Researchers’ Discovery May Revolutionize Treatment of ALS

Friday, August 13, 2010
Creutzfeldt-Jakob disease (CJD) biannual update 13 August 2010 UK Iatrogenic CJD Incidents Report
Tuesday, March 29, 2011



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