Human cells can divide up to 50 times {aging, cell} {cell, aging}. All cells, except cancer cells, have programmed lifespans. Gene redundancies can affect cell lifespans.
diseases
Genes or accumulated defects can cause old-age diseases. Defects include frame-shift mutations and nucleic-acid-coding, transcription, translation, microsatellite, gene-expression, and post-translational-modification errors.
cell changes
In aging, neurons have more Nissl bodies, are larger, have more axons, have more synaptic bulbs, have more dendrites, and have more myelination. Nerve-fiber length, size, and compactness increase.
cell death
Cells first deteriorate, then become senescent, then stop dividing, and then die.
telomeres
Telomeres decrease in length with each replication. After telomeres reach threshold length, cells can have senescence.
chemicals
In aging, nucleic-acid-to-protein ratio changes. Somatic-cell DNA mutates. DNA-repair-mechanism efficiency decreases. Oxygen uptake decreases. Anti-oxidants have less effect. Lysosomes increase. Intestine calcium-ion transport decreases. Cholesterol excretion decreases.
chemicals: free radicals
DNA damage affects biological aging and Alzheimer's disease. Free radicals from mitochondria and other chemical reactions can damage DNA, but vitamin E binds free radicals.
chemicals: protein
In aging, enzymes can change. Cell amyloid deposits can increase. In amyloidosis, frame-shift mutations cause protein-folding errors.
chemicals: proteins and slower aging
Sirtuins can slow aging.
Mouse, worm, and fruitfly Daf protein is similar to human insulin. Mouse, worm, and fruitfly TOR gene repression slows aging by decreasing cell growth and regulating glucose metabolism.
Mouse, worm, and fruitfly Fox0 is similar to human IGF-1. Yeast, worm, and fruitfly TOR gene repression slows aging by decreasing cell growth and regulating glucose metabolism.
Fruitfly Methuselah protein is similar to human CD97 protein. Decreased fruitfly Methuselah protein slows aging by resisting stress and increasing neuron signaling.
Worm Clock (clk-1) protein is similar to human CoQ protein. Worm Clock gene repression slows aging by regulating CoenzymeQ synthesis.
Worm Amp-1 protein is similar to human AMPK protein. Increased Amp-1 protein slows aging by regulating stress responses and metabolism.
Decreased mouse and rat growth hormone slows aging by decreasing body size.
Decreased mouse P66Shc protein slows aging by decreasing free-radical creation.
Mouse catalase is similar to human CAT protein. Increased mouse catalase slows aging by changing hydrogen peroxide.
Mouse Prop1 or pit1 protein is similar to human Pou1F1 protein. Decreased mouse Prop1 or pit1 protein slows aging by regulating pituitary gland.
Increased mouse Klotho protein slows aging by regulating insulin, IGF-1, and vitamin D.
Yeast, worm, and fruitfly SIR2 gene makes sir2 protein. Humans SIRT1 gene makes sirt1 protein. Sirtuins {silent information regulators} {sirtuin} slow aging, by mediating stress responses and deacetylating histones to make DNA coil tighter and prevent extra DNA production. Low calorie intake, high salt, high heat, and low nitrogen intake can increase PNC1-gene production, remove nicotinamide, and increase sirtuins. Low calorie intake causes mitochondria to respire instead of ferment, making low NADH and high NAD and increasing sirtuins. Red-wine and knotweed have resveratrol, which increases sirtuins.
Glycosylation make products {advanced glycosylation endproducts} (AGE) that damage DNA, lipids, and proteins.
Small deposits {drusen} can be outside cells.
Species-specific germline genes {gerontogene} can affect aging rates or maximum lifespans.
Fatty proteins {lipofuscin} can be in cells.
Human fibroblasts in culture can only divide 50 times {replicative senescence} {replication limit}. For species, allowed-doubling number is proportional to lifespan.
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Date Modified: 2022.0225