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Originally posted by DaRAGE
Dementia will triple by 2050? WRONG!
Dementia will be cured by 2050! CORRECT!
Originally posted by Sinny
Thanks for posting OP, this is a serious cause and awareness needs to be raised.
I can honestly say Dementia is in my top 5 things I never want to have!
I've seen old people with it, and one of the most aweful things to witness, I'd rather die before the disease could touch me.
And spot on! The most important question here is, why??
Why the increase, I think it can be considered "pandemic".
Somethings not right here, and we need to figure out what.
Originally posted by drbatstein
This is by design, it is to drain old people of their life earnings before they die, to reduce the inheritance to the next generation. The system wants the next generation to have a need to submit to employment.
How do they do this? To you and me it's known as "The Old Persons Flu Jab", but to those in the know it's an injection which pushes you one step closer to Dementia/Alzheimer's. Once you've had a certain number of these injections you're almost certain to end up with Alzheimer's, then if you go to a care home your savings will start to quickly be drained back into the system
Alzheimer's and vaccination
www.whale.to...
"According to Hugh Fudenberg, MD, the world's leading immunogeneticist and 13th most quoted biologist of our times (nearly 850 papers in peer review journals), if an individual has had five consecutive flu shots between 1970 and 1980 (the years studied) his/her chances of getting Alzheimer's Disease is ten times higher than if they had one, two or no shots. I asked Dr. Fudenberg why this was so and he said it was due to the mercury and aluminum that is in every flu shot (and most childhood shots)."
Of course, after this he got smeared, as there are some things we're just not meant to knowedit on 6-8-2012 by drbatstein because: (no reason given)
Originally posted by zatara
Originally posted by DaRAGE
Dementia will triple by 2050? WRONG!
Dementia will be cured by 2050! CORRECT!
That is the best news I heared for a long time.
And you got this info from where...?
Some of the most common forms of dementia are: Alzheimer's disease, vascular dementia, frontotemporal dementia, semantic dementia and dementia with Lewy bodies. It is possible for a patient to exhibit two or more dementing processes at the same time, as none of the known types of dementia protects against the others. Indeed, about ten per cent of people with dementia have what is known as "mixed dementia", which may be a combination of Alzheimer's disease and multi-infarct dementia.[8][9]
Alzheimer's disease Enzymes act on the amyloid precursor protein and cut it into Aβ fragments, which then aggregate to form senile plaques characteristic of Alzheimer's patients. Alzheimer's disease is an incurable form of dementia which most often affects the elderly. Its cause remains largely unknown, but the disease is identified as a protein misfolding disease and is associated with toxic aggregations of the amyloid beta (Aβ) peptide, a fragment of the larger amyloid precursor protein.[42] High concentrations of misfolded Aβ cause protein oligomer growth that in turn contribute to Aβ misfolding. This cyclic process appears to be toxic and leads to neurodegeneration. The oligomer aggregates then collect into dense formations known as senile plaques, a pathological marker of Alzheimer's.[43][44] The severity of the disease depends not only on the amount of Aβ, but also on how it misfolds. However, due to the heterogeneous nature of these aggregates, experimental studies of the oligomer structure in atomic detail are difficult,[43][44] and simulations of oligomer aggregates are extremely computationally demanding due to their size and complexity.[45][46] In 2008 Folding@home simulated Aβ oligomerization in atomic detail over timescales of the order of tens of seconds. This was significant as previous simulations had been forced to use simplified models and been limited to several hundreds of microseconds: six orders of magnitude short of experimentally relevant timescales.[47] This study helped prepare the Pande lab for future aggregation studies and for further research to find a small peptide which may stabilize the aggregation process.[45] This is regarded as a promising approach to the development of therapeutic drugs for treating Alzheimer's patients.[48] The Pande lab is focusing their research on Alzheimer's with the goal of predicting the aggregate structure for drug design approaches as well as developing methods to stop the oligomerization process.[5] In 2008 Folding@home found several small drug candidates which appear to inhibit the toxicity of Aβ.[49] In 2010, these drug leads went from the test tube to testing on living tissue and, in close cooperation with the Nanomedicine Center for Protein Folding, continue to be refined.[5] In 2011, Folding@home completed simulations of several Aβ mutations that appear to stabilize the aggregate formation, which could aid in the development of therapeutic drug approaches to the disease as well as greatly assisting with experimental NMR spectroscopy studies of the oligomers.[46][50] In the same year, Folding@home began simulations of various Aβ fragments in order to determine how various natural enzymes affect the structure and folding of Aβ.[51][52]