Diseases of Aging - Induced by time

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It is not my intention to act as doctor, my knowledge is deep in very few areas of interest to me. However, certain broad area have to interned at very shallow level and these are likely to be of interest to some. Aging, understood as a universal chemical process and interventions to increase the health span, is one of the areas. Let us examine two very major diseases here - Parkinson and Alzheimer's. These are considered nonintervention, if you or loved have it then the best is to reduce the evil consequences as much possible.  But, TPE intervention makes sense in Alzheimer's. AMBAR is very cutting edge, and surprise is that the equipment is available in Delhi, due to unthinking but political move of AAP to battle Corona, made unused for NBE with cured patients, but the vaccines are unexpectedly here and usable. Means TPE is there, can be repurposed for fighting aging, a very useful disease with no recognition as one by FDA! I was amused to learn that Dr. DobriKirprov is the first doctor in the USA entitled to specialist status in TPE! The AMBAR project is old and in fact Drs. Conboy did the lessened recovery interpretation of their classic 2005 surgical hetero chronic blood exchange paper, in 1916 when funded by none other than Dr. de Grey. Naturally, Dr. Kirprov was coauthor in 1916 and also in 1920!

The blood-brain-barrier or BBB seems to defeat all improvements to brain, independent to blood. That (improvements) is a consequence of two new facts, even today not known to middle-aged Doctors in India who were taught by senior Doctors. First there is old age neurogenesis in hypothalamus, essential for short to medium term memory. Decline in neurogenesis is why all old people decline in fresh memories even though they can remember old things! The second fact is that the ratio of beta-amyloid in blood and brain is a constant. This is maintained by some beta-amyloid moving from the brain to diluted blood (where it unites with albumin). You see that aged brains show distinct beta-amyloid patches, essential to Alzheimer's! AMBAR shows that. Twin improvements in memory and reduced loss of sanity was objectively measured and showed 50-60% improvement! I attribute lack of world-wide processing as partly poor information spread and partly lack of TPE equipment.

Stupidity of doctors' about plasmapheresis, indicates a very wide open entrepreneur area with unused TPE equipment making TPE lot cheaper, hence applicable here - patient supply huge if improved self. Precisely sensible gamble, worst is no effect and minor pain! Low cost advertise-strategy will work here initially, with likely a huge wall of disincentives to overcome later. Self TPE is likely the smartest move in my life! Glutathione is a likely add to my NBE. If small lightened, will become walking ad proof! Since I intend life long NMN by IV, adding Glutathione will be trivial.

Parkinson is caused by loss of doipamine. It is fixed differently. Taget is mPTP described next which converts autphagy process to destructive. The activity of the mitochondrial permeability transition pore, mPTP, a highly regulated multi-component mega-channel, is enhanced in aging and in aging-driven degenerative diseases. mPTP activity accelerates aging by releasing large amounts of cell-damaging reactive oxygen species, Ca²⁺ and NAD⁺. The various pathways that control the channel activity, directly or indirectly, can therefore either inhibit or accelerate aging or retard or enhance the progression of aging-driven degenerative diseases and determine lifespan and healthspan. Autophagy, a catabolic process that removes and digests damaged proteins and organelles, protects the cell against aging and disease. However, the protective effect of autophagy depends on mTORC2/SKG1 inhibition of mPTP. Autophagy is inhibited in aging cells. Mitophagy, a specialized form of autophagy, which retards aging by removing mitochondrial fragments with activated mPTP, is also inhibited in aging cells, and this inhibition leads to increased mPTP activation, which is a major contributor to neurodegenerative diseases, such as Alzheimer's and Parkinson's diseases. The increased activity of mPTP in aging turns autophagy/mitophagy into a destructive process leading to cell aging and death. Several drugs and lifestyle modifications that enhance healthspan and lifespan enhance autophagy and inhibit the activation of mPTP. Therefore, elucidating the intricate connections between pathways that activate and inhibit mPTP, in the context of aging and degenerative diseases, could enhance the discovery of new drugs and lifestyle modifications that slow aging and degenerative disease.

Since CD38 is bad too, CD38-in-78C is a potent suppressor, in turn raising NAD+. No one seems to know why not used commonly. The Intertwined Nature of NAD+, CD38, and Senescence is missed.

If rapamycin strikes your fancy, please read this.