Flow Chart of Biochemical Interactions Causing Human Aging





J.D. Furber

Legendary Pharmaceuticals, PO Box 14200, Gainesville FL 32604-2200



The many observable signs and symptoms of human senescence have been hypothesized by various researchers to result from several primary causes. Close inspection of the biochemical pathways associated with each of the hypothesized causes reveals several parallel cascades of events with multiple interactions and feedback loops among them.

As an aid to keeping track of the many processes and interactions, a flow chart is presented. Promising intervention points for the development of new therapeutics are also highlighted on the flow chart.

The mechanisms which are incorporated into the flow chart include:
-- Nonenzymatic glycation of long-lived proteins and nuclear DNA.
-- Mutations accumulate in the mitochondrial genomes of postmitotic cells.
-- Increasing acetylation of histones opens heterochromatin, permitting inappropriate expression of nuclear genes.
-- Lipofuscin accumulates in lysosomes of postmitotic cells.
-- Increased redox poise alters signaling and enzyme activities.
-- Redox damage and crosslinking of long-lived macromolecules in postmitotic cells and extracellular matrix.
-- Stiffer blood vessels promote stroke and heart disease.
-- Telomere shortening induces altered phenotype and halts cell division in some cells.
-- Apoptosis, necrosis, and cell loss lead to tissue wasting,
neurodegeneration, and organ malfunction.
-- Alterations in neuroendocrine and immune systems.
-- Rate of repair & turnover of macromolecules & organelles slows.
-- Senescent cells export toxic reactive species and inflammatory cytokines.
-- Abnormal aggregations of proteins damage brain cells.
-- Induction of cancer.

Theoretically powerful points for the development of new interventions would include:
-- Slowing or reversing the accumulation of lipofuscin in lysosomes of postmitotic cells.
-- Slowing or reversing the accumulation of AGE crosslinks in extracellular collagen, elastin, and blood proteins.
-- Preventing homoplasmic takeover of postmitotic cells by mutant mitochondrial DNA.
-- Enhancing proteasome turnover of damaged macromolecules.

This flow chart will be maintained on the Web as a reference to researchers, and will be updated as new information comes to light.

[ www.LegendaryPharma.com/senescence.html#Mechanisms ]




Key words: senescence, aging, biochemistry, interactions, causes







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