Replies to post #13512 on Tao Synergies Inc (TAOX)

[XenaLives]

Actually they are theorizing that aging itself has a specific cause.

Because Anavex 2-73 addresses mitochondrial dysfunction on a cellular level by encouraging autophagy and correcting miss folded proteins it may actually be a generalized treatment for aging.

The role of mitochondria in aging
Ana Bratic1,2 and Nils-Göran Larsson1,2


Over the last decade, accumulating evidence has suggested a causative link between mitochondrial dysfunction and major phenotypes associated with aging. Somatic mitochondrial DNA (mtDNA) mutations and respiratory chain dysfunction accompany normal aging, but the first direct experimental evidence that increased mtDNA mutation levels contribute to progeroid phenotypes came from the mtDNA mutator mouse. Recent evidence suggests that increases in aging-associated mtDNA mutations are not caused by damage accumulation, but rather are due to clonal expansion of mtDNA replication errors that occur during development. Here we discuss the caveats of the traditional mitochondrial free radical theory of aging and highlight other possible mechanisms, including insulin/IGF-1 signaling (IIS) and the target of rapamycin pathways, that underlie the central role of mitochondria in the aging process.

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Introduction
The exact reasons why we age are poorly understood. Aging is thought to be a degenerative process caused by accumulated damage that leads to cellular dysfunction, tissue failure, and death. A number of aging theories have been proposed (1–5), and the mitochondrial free radical theory of aging (MFRTA) has taken center stage for several decades (1). According to this theory, ROS are considered to be unwanted toxic byproducts of aerobic metabolism that induce oxidative damage to various cellular macromolecules due to their high chemical reactivity. The respiratory chain (RC), located in the inner mitochondrial membrane, is a main production site of superoxide, an abundant ROS in the cell formed at the level of complexes I and III during electron transport (Figure ?(Figure1).1). The superoxide anion is converted to hydrogen peroxide by SOD. Although hydrogen peroxide itself is not a free radical, it can be converted to the highly reactive hydroxyl radical in the presence of transition metals through the Fenton reaction (Figure ?(Figure1).1). The hydroxyl radical is considered to be the most damaging form of ROS, as it is highly reactive and causes oxidative damage to virtually every molecule type in the cell, including lipids, proteins, and nucleic acids.

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3582127/

[Cyosol]

There's this time lapse video of neurons interacting with each other:

If the onset of AD and the destruction of these connections are highly correlated, it would make sense that regrowing these connections would also reverse the damage caused by the disease.