Dementia by Alzheimers – possible solutions

Dementia by Alzheimers

Alzheimers may be preventable

or –

Hypothesis of the cause of Alzheimers and the origin of β-amyloid plaque.

Phillip D Wade, ND Adv. MPS, MATMS. B. Pharm, Dip Nutrition, Dip Botanical Med, 15/08/2010

                                                                                 Human brain
Update:

(i)            It has since been reported in the overview referenced herewith that ascorbic acid (AA) – also known as vitamin C – exists in brain neurones in concentrations that are vastly greater than in normal cells – even in much greater concentrations than in immune cells.

And that insufficient concentrations of AA can reduce significantly brain plaque formation.

And this would have great effect in reducing free radicles that are associated with contaminating lipid peroxides that can be shown to be a major cause of the destruction of brain cells that itself is the major cause of Alzheimer’s disease. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7285147/

(ii)           Given the above, maintaining adequate concentrations of AA in brain cell neurones may also minimise brain tumour development.

Introduction:

The following article, reproduced in plain language here, restates my hypothesis that was published in the Acnem journal of that year and accepted after some revisions by an academic committee of Peer Review.

Ethics prevent my including it here but please feel free to contact us for detailed information.

If you a reformed smoker or addicted to vapes, or wish to understand how to live with fats without slowly harming your brain or developing blood pressure from that issue, please contact me (Phil) and/or read on.

For those interested in knowing why the eating of contaminated and/or trans fats or cooking with vegetable oils may injure your brain and/or your retina with a slowly accumulating effect, please also read on.

Beta Amyloid Plaque and Neuro-fibrillary Tangles and actual cause of dementia by Alzheimer’s.- hypothesis

Low density lipoprotein (LDL) carrying potentially damaging peroxidated lipids can migrate into the brain by active absorption via foam cells and passive absorption via fatty layers in the brain and after disassembly into component parts destroy neuronal cell walls.

Some definitions:

LDL and HDL: these abbreviations stand for low density lipoproteins and high density lipoproteins – or “bad cholesterol” and “good cholesterol”. These “protein carriers” are needed to transport fats around the body because blood being a watery medium and fats will not mix unless the fats or oils are hidden within these protein balls.

Peroxidated fats or lipids are usually unsaturated oils that have been exposed to heat in air while cooking and have formed a chemical bond with oxygen. They are toxic to your cells. Also known as bad fats.

Contaminated fats are thoise fats that have been polluted by pesticides and that may have a toxic effect on your nerves – both in the brain and elsewhere. These too are bad fats.

Trans fats are also bad fats.

Cis fats are good fats – whether saturated or unsaturated.

Arterioles are small arteries that have branched off larger arteries.

Sub-hypothesis 1.

Fats in these lipoprotein “ferries” will normally adhere readily to arterial walls so that they may be transported into the arterial muscle layers by foam cells that provide energy for the normal, healthy, constant contraction that healthy arterial muscle must maintain every second of every day, asleep or awake.

This constant workload requires the continuous energy provided by “good” low-density lipids. Any surplus of good fats may migrate into brain fats and provide nourishment.

And that this form of energy is the major – if not only – source of energy for arterial cells. Not so as to be taken to excess of course.

Sub-hypothesis 2

When peroxidated or contaminated fats were attached to these then they are usually associated with arterial disease such as swollen arteries. This is because the foam cells will not allow the bad fats to be released into the arterial cells in case they kill the cell.

These bad fats are trapped in the muscle as the aqueous medium of watery lymph fluid that bathes the outside the artery walls in non-brain circulation will not allow fats into their patch as water and oil do not mix. So the bad fats build up in the artery wall. This condition is called athrosclerosis.

And so all fats in artery walls have developed a bad name as a result.

Sub-hypothesis 3

From brain arteries and arterioles, bad fats that have accumulated will migrate  into the brain’s fatty brain tissue.

Sub-hypothesis 4

Origin of the mysterious plaque formation.

Glial cells in the brain already possess their own apolipoprotein – Apo E. Thats because glial cells and astrocytes produce their own lipids to provide nourishment and myelin to brain cells. So any surplus lipoprotein wil be broken down for re-use by their own enzyme that is specific to Apo E. But it will not be capable of completely “digesting” Apo B.

So what remains is the 42-unit peptides – the mysterious plaque.

Sub-hypothesis 5

Origin of neurofibrillary tangles found in affected brains.

The apolipoprotein B will be itself contaminated with the free radicle content of the lipids that it transported.

This hydrophilic protein will be attracted to the like protein material of the neuronal wall structures such as trabeculae etc, damaging them, causing cell death and creating tangled neurones.

So neurofibrillary tangles are simply dead brain cells.

Conclusion:

LDL-cholesterol containing free radicles and trans-structures, will readily concentrate into fatty brain tissue and once a critical concentration is reached, will almost certainly lead to cell death of neurones.

The proof that these peroxidated and contaminated LDLs are surrounded by the particular protein called Apolipoprotein B lies in the work done by Poirer (1), who identified that the apo-l receptors occur in the brain and appear to be involved in neurogenesis.

Apolipoprotein E is the protein fraction of  glial LDL.

Finally, Alexander Johs et al (2006) showed, via a small angle, neutron scattering technique, that the structure of Apolipoprotein B was composed of 4,536 amino acid units.

I have found that when you divide 42 into this (the number of amino acid units in one of the 2 types of β-amyloid plaque, it divides  by 108 exactly.

Therefore Apo B carries contaminated fats into the brain, releases them, becomes incompletely digested by the Apo E enzymes leaving the 42-unit “plaque”, and this leads ultimately to the death of the brain cells.

And this is a major cause of dementia by Alzheimer’s.

QED.
Progression over time and brain protection from free radicles

This process will obviously take years and its progression will depend on

•  1)   Passive absorption from the arterial wall

•  2) The quantity and regularity of exposure to lipid free radicles and nerve-paralysing nicotinoid pesticides

•  3)  the brain’s ability to neutralise these free radicles with superoxide dismutase and other endogenous cellular antioxidant strategies.

•  4)  Dietary input of antioxidants supporting these systems, such as ascorbic acid (Vit C), Vitamin E, selenium, ascorbic acid, carotenoids, Coenzyme Q10, α-lipoic acid, bioflavonoids and other natural dietary antioxidants such as polyphenols and proanthocyanadins as well as material needed to repair and regenerate neuronal cell walls such as omega-3 fatty acids, enzymes and their vitamin and mineral co-factors such as zinc, magnesium B6 et al.

•  5) Rate of production of endogenous Myelin and therefore corresponding satisfactory dietary input of choline and inositol

•  6) Health of glial cells in producing the myelin and their enzyme co-factor availability

•  7) Dietary input of substrate for (4) and (5) and efficiency of gall bladder in processing fats to effectively emulsify dietary fats for transport to the liver for due metabolism.

•  8) Rate of breakdown of myelin from ingested or inhaled exogenous solvents such as as organic alcohols, aldehydes, acetones and non-polar solvents such as chloroform, turpentine, kerosene, diesoline and petroleum, to name a few.

  • 9) The rate of neuroplasticity versus the rate of cell death
Normal protein absorption hypothesis

Neuronal cells are like any other cells and require protein to be made available to them for normal metabolic requirements but by a different route, given that they have no direct blood supply. Healthy lipoprotein would provide one such source. So, an intracellular enzyme system would be employed to effect the breakdown of this to component amino acids as in any other type of cell.

Therefore, normal lipoprotein will be able to break down into amino acids by existing healthy cellular enzymatic production. These healthy proteins may also be available to be absorbed through specific neuronal cell wall receptors in the normal way and be able to be utilised more directly in building more healthy neuronal structure in the normal course of brain neuronal events involving neuro-plasticity in the normal memory-generation process.

 

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