Enhanced version of my Alzheimers/dementia theory

I'm not sure how much more I will get done. Surely not ever get round to publishing my theories of schizophrenia, "psychoticism", psychosis (which Eysenck's 'psychoticism' is not the essence of!), extraversion, neuroticism, neuroses, IQ, genius, dream sleep, etc.

The last thing I was working on was in 2003 an enhancement of my paper "Does longer-term memory never become overloaded, and would such overload manifest as Alzheimer's and other dementia?" (published in 2000, see PubMed).

I will try to put here a link to a "reprint/preprint" of my unfinished draft update, which is basically a revision of my 2000 paper which I was working on revising to incorporate the enhanced ideas, and left off in 2003 when I got too tired to continue. I think the later pages remained un-updated. But first I'll just add some separate explanation about the enhancement.

Basically, the enhancement is an additional level (or process) of overload, arguably the most important. It is overload in intra-cellular information. It explains why tau becomes hyperphosphorylated and tangled.

It has been noted that this tau AD pathology starts many years earlier with the most complex neurons, namely the pyramidals in the hippocampus called the CA1 or dentate granules or something I forget which.

Neurons have a very complex shape, loads of branches of axons and dendrites and thousands of synapses connecting them to other neurons. These shapes are not just random, rather they are the very embodiment of our ideas, memories and such like information. There has to be some means within each cell of organising and remembering that correct, and changing, shape. This is all the more so given that any two neurons never form more than one synapse together.

There must therefore be some rigorous mechanism for storing the "design" of the cell, storing it in the nuclear RNA and transporting design messages outwards along the cell's axons and dendrites.

So we are looking for some molecule that travels out from the nucleus and has means of carrying information in a code. Like the molecular code in DNA and RNA.

The tau molecule has about 34 (if I recall correctly) sites of adjustable phosphorylation. So the phosphorylation of tau could have the capacity to encode about 17 billion different messages. That's a lot! It does indeed travel out from the nucleus to the synapses etc.

Bear in mind that the design information of the cell has to be recorded as a sequence of changes rather than just the first or the latest design. And some of these cells experience a seriously large amount of changes as learning progresses.

And natural selection is less than perfect. That's especially the case in respect of extreme circumstances, extreme age and extreme data input. So those most complex neurons, located in the hippocampus, eventually find their tau molecules trying to register more data than natural selection has prepared them for. So their tau phosphorylation becomes "hyperphosphorylation" as is well-known. And that affects the shape of the molecule, causes the tau molecule to become curled and tangled. And thus the degeneration into AD begins. I thought of all this before 2003 but so what, no-one gives a damn ... [update, shock horror three papers in 2013/4 have cited my 2000 published dementia theory even though there's this great update I haven't published yet].... Cheers anyway!