Saturday, August 31, 2013

Senile Memory Loss

Senile Memory Loss

Andre Willers
31 Aug 2013
Synopsis :
A pill to remember things . Will an overdose remember fantasies ?
Discussion :
1.Such a pill will be on the market soon . This research is about 3 days old (as at 31 Aug 2013)
Protein RbAp48 is a protein that can be used as an nutritive supplement , bypassing any pesky legal requirements .
2.Since some analogue of it seems to be in cocoa , it is even natural .
3. How it works .
The gene RBBP4 encodes for the protein RbAp48 . This protein then causes a cascade of reactions by loosening the histone windings of the chromosomes , in controlled order . See Appendix C .
But things get screwed up if not enough RbAp48 is produced .
The cascade does not start .
Memory fades as the necessary fetch-and-carry molecules are not being produced .
Like a company where the file clerks are on strike .
Appendix 0 gives some background .
Appendix A a popscience account of the research .
Appendix B is something that can done immediately .
Drink cocao or eat chocolate .
Appendix C is a fairly general view of genetics .
If you are unclear about histones , see
5.What can be expected .
This report See Appendix A) is about 3 days old . Expect a massive , quick response from the nutraceutical establishment .
I myself is going to see the effect of drinking 2 cups of cocao per day .
PTSD therapy . Antibodies to RbAp48 precisely delivered should excise any bad memory .
People in PTSD stress should steer away from cocao .
Know yourself !
Appendix 0
Chromatin remodeling is the dynamic modification of chromatin architecture to allow access of condensed genomic DNA to the regulatory transcription machinery proteins, and thereby control gene expression. Such remodeling is principally carried out by 1) covalent histone modifications by specific enzymes, i.e., histone acetyltransferases (HATs), deacetylases, methyltransferases, and kinases, and 2) ATP-dependent chromatin remodeling complexes which either move, eject or restructure nucleosomes.
Function[edit source | editbeta]
This gene encodes a ubiquitously expressed nuclear protein that belongs to a highly conserved subfamily of WD-repeat proteins. It is present in protein complexes involved in histone acetylation and chromatin assembly. It is part of the Mi-2/NuRD complex complex that has been implicated in chromatin remodeling and transcriptional repression associated with histone deacetylation. This encoded protein is also part ofcorepressor complexes, which is an integral component of transcriptional silencing. It is found among several cellular proteins that bind directly to retinoblastoma protein to regulate cell proliferation. This protein also seems to be involved in transcriptional repression of E2F-responsive genes.[3]
Clinical significance[edit source | editbeta]
A decrease of this protein in the dentate gyrus part of the hippocampus in the brain is suspected to be a main cause of memory loss in normal aging.[4]

Appendix A
Protein clue to old-age memory loss
By James GallagherHealth and science reporter, BBC News
Why does memory decline in old age?
A clue to why memory deteriorates with age has been found by US researchers.
Experiments on mice suggested low levels of a protein in the brain may be responsible for memory loss.
It is hoped the discovery could lead to treatments to reverse forgetfulness, but it is a big leap from the mouse to a human brain.
The study, published in the journal Science Translational Medicine, said age-related memory loss was a separate condition to Alzheimer's disease.
The team at Columbia University Medical Centre started by analysing the brains of eight dead people, aged between 22 and 88, who had donated their organ for medical research.
They found 17 genes whose activity level differed with age. One contained instructions for making a protein called RbAp48, which became less active with time.
Memory boost
Young mice genetically engineered to have low RbAp48 levels performed as poorly as much older mice in memory tests.
Using a virus to boost RbAp48 in older mice appeared to reverse the decline and boosted their memory.
One of the researchers, Prof Eric Kandel, said: "The fact that we were able to reverse age-related memory loss in mice is very encouraging.
"At the very least, it shows that this protein is a major factor, and it speaks to the fact that age-related memory loss is due to a functional change in neurons of some sort. Unlike with Alzheimer's, there is no significant loss of neurons."
It is still not known what impact adjusting levels of RbAp48 in the far more complex human brain will have or even if it is possible to manipulate levels safely.
Dr Simon Ridley, from Alzheimer's Research UK, said: "While the findings may seem clear cut from these studies, in reality people reaching older age may well have a combination of changes happening in the brain - both age-related and those involved in the early stages of Alzheimer's.
"Separating early changes in Alzheimer's from age-related memory decline in the clinic still presents a challenge, but understanding more about the mechanisms of each process will drive progress in this area."

Appendix B

Cocoa 'might prevent memory decline'

It is not the first time cocoa has been linked with health benefits
Drinking cocoa every day may help older people keep their brains healthy, research suggests.
A study of 60 elderly people with no dementia found two cups of cocoa a day improved blood flow to the brain in those who had problems to start with.
Those participants whose blood flow improved also did better on memory tests at the end of the study, the journal Neurology reported.
Experts said more research was needed before conclusions could be drawn.
It is not the first time cocoa has been linked with vascular health and researchers believe that this is in part due to it being rich in flavanols, which are thought to have an important role.
In the latest study, researchers asked 60 people with an average age of 73 to drink two cups of cocoa a day - one group given high-flavanol cocoa and another a low-flavanol cocoa - and consume no other chocolate.
Blood flow
Ultrasound tests at the start of the study showed 17 of them had impaired blood flow to the brain.
There was no difference between those who drank flavanol-rich cocoa and those who had flavanol-poor cocoa.
But whichever drink they were given, 88% of those with impaired blood flow at the start of the study saw improvements in blood flow and some cognitive tests, compared with 37% of people whose blood flow was normal at the beginning of the study.
 “Start Quote
A cocoa-based treatment would likely be very popular, but it's too soon to draw any conclusions about its effects”
Dr Simon RidleyAlzheimer's Research UK
MRI scans in 24 participants found that people with impaired blood flow were also more likely to have tiny areas of brain damage.
"We're learning more about blood flow in the brain and its effect on thinking skills," said study author Dr Farzaneh Sorond a neurologist at Harvard Medical School.
"As different areas of the brain need more energy to complete their tasks, they also need greater blood flow. This relationship, called neurovascular coupling, may play an important role in diseases such as Alzheimer's."
The researchers said the lack of difference between the flavanol-rich and flavanol-poor cocoa could be because another component of the drink was having an effect or because only small amounts were needed.
Dr Simon Ridley, head of research at Alzheimer's Research UK, said this was a small study but that it added to a wealth of evidence.
"A cocoa-based treatment would likely be very popular, but it's too soon to draw any conclusions about its effects.
"One drawback of this study is the lack of a control group for comparison, and we can't tell whether the results would have been different if the participants drank no cocoa at all."
But he added: "Poor vascular health is a known risk factor for dementia, and understanding more about the links between vascular problems and declining brain health could help the search for new treatments and preventions."
Appendix C

Monday, February 22, 2010
The Beauty of the Genetic Code .
The Beauty of the Genetic Code .
Andre Willers
22 Feb 2010

The present TerraIII genetic code is elegantly optimized to give the most robustness possible per unit of information .

Discussion :
You have to be familiar with the concepts in:
1. "NewTools:Reserves" and Beth(n) orders of Randomness .
2.NewScientist of 23 Jan 2010 p34 "Another kind of evolution"

Brief recap of Reserves argument :
We take any identifiable entity , slice and dice it with an order of randomness like that of a coin (ie Beth(0) ) . We then calculate a minimum reserve (which is equivalent to the least errors of all possible Beth(0) paths per benefit . )
This works out at 1/3 on the average over Aleph(0) infinities .

The Beauty of the Genetic Code :
Four Base pairs (A,U,C,G) in triplet codons give a possible 4*4*4 = 64 codons .
But together , they code only for 20 amino acids , plus a Stop and a Semi-Start .

This gives
20/64 = 31.22% for 20 amino acids
21/64 = 32.81% for 20 amino acids + Stop
21.3333…/64 = 33.3333… for 20 amino acids + Stop + Semi-Start
22/64 = 34.375 %

Stop = (UGG) , (UGA) , (UAG) ,
Start = (AUG) , but this also codes for methionine . Hence the decimal notation . The system cannot come closer to 1/3 because of quantal considerations . Try it and see .
This also is the portal for the Epigenetic System ( note use of methiolization) .

Beautiful !!

Consider the ways of Gaia .

Linear and Sideways evolution .
Linear :
The standard , gene and chromosome based inheritance
Equivalent to Beth(1+x) in our notation .
1>= x >=0

Sideways :
Genetic material exchanged without going through all that genotype-phenotype procedures .
Equivalent to Beth(1-x) in our notation .
1>= x >=0

Note that the system could not possibly get as close to the optimum reserve without this stage .

The Breeder , genetic engineer .
Equivalent to Beth(2+x) in our notation . Humans or proto-humans .
Infinity>= x >=0

This gives a full spectrum of Beth capabilities .
(Negative Beth is outside the scope of this discussion)

You will notice that the system becomes chaotically unstable as x->0 from any direction . At that point , the system will exhibit symptoms of great stress and bifurcation . Once over the hump , it steadies either in an evolutionary manner (in
Probability = 1 - ( Beth(n+1)/Beth(n) ) ^0.5 . Admittedly a rough estimate .)

Or in a devolutionary manner , evolutionary manner here described as degrees of complexity .

Stable Gene Engineering :
1.Keep the same Triple-Base Codon Cell-Machinery .
The easiest . Existing cells can be used . Increase the number of bases to 5 .
Then we can optimally reliable make 1/3*5^3 = 40 amino acids + stop + semistart .
Different kinds of Stop and Start would be advisable .
So , maybe 18 new amino acids + 2 different types of Stop + SemiStarts

This would not even be hard .
Well within present technological capability .
(Wanna make an animal with a Kevlar skin ? Well , you can using this method .)

The system would even be self-assembling under the right condition . The main thing is the optimal stability .

This is already evolving as we speak . There a fifth base occasionally involved . So there is a fruitful interaction point .

2.Make 4-Base Codon Cell-Machinery .
A real remake . Not within human capability at the moment .

3.General :
nAminoAcids + nStops + nStarts = 1/3 * ( (nDNA-bases) ^ (nBasesPerCodon) )
where the prefix n denotes "number of"

A further stability would be introduced if nStarts ~ 1/3 * nStops in a fractal fashion .
This because life-forms evolve in a pedal-to-the-metal fashion . The problems are the brakes .

There is a relationship between the Beth level and the nBasesPerCodon . The minimum number sufficient for Beth(2+) is nBasesPerCodon=3 .
Else there is insufficient complexity .

Now go out there and evolve !

Andre .
Posted by Andre at 10:15 AM

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