Growing old {aging, development} changes DNA, protein, hormones, cells, tissues, and organs.
causes
Autoimmunity or immune-system breakdown can cause aging. Pituitary hormone and/or thymosin decrease can cause aging. Thymus thymosin keeps immune system active. Structural-molecule changes, as collagen has more cross-links and stiffens, can cause aging.
effects
Aging impairments typically result from disease, trauma, or disuse, not age itself.
effects: biology
Brain deterioration causes most aging effects. Random brain activity increases. Serum globulin becomes higher. Fracture-healing rate decreases.
effects: behavior
Performance ability peaks at 26 and then slowly declines. Slower decision making, especially for tasks in which responses cause signals for next response, slows activities slightly. Older people pay attention to responses more, rather than to next task.
Older people learn facts and skills more slowly but do not forget more rapidly. Verbal ability peaks at 50 and sharply declines after 70.
effects: senses
Signals from sense organs to brain and among brain parts become weaker. Ability to understand speech does not decrease with age, unless people cannot hear frequencies below 1800 Hz, three octaves above middle C. Trauma causes most hearing loss. Aging causes reduced sensitivity to vibration and pain. Smell loses sensitivity.
Aging causes reduced fine-joint-movement sensitivity, reduced clear-focus distance, reduced resting pupil size, increased yellow eye pigment, reduced overall acuity, slight visual-field narrowing, color-discrimination loss, and increased glare susceptibility.
effects: personality
Personality has few trends with age. Adjusting to aging does not relate to health or wealth.
individual differences
Aging rate and effects differ among individuals, and differences become greater with age.
defenses
Aging defenses are apoptosis, suppressor genes, gene redundancy, DNA editing, RNA editing, DNA repair, anti-oxidant free-radical scavenging, defective-protein removal, and damaged-cell removal by immune system.
long life
Physical fitness, genetic factors, low mental pressure, low-fat diet, low-calorie diet, psychological well-being, and living in highlands can contribute to long life. Lowering body temperature and food-intake rate slows aging in animals.
theories
Mammals, even wild animals in zoos, age after adulthood. Perhaps, genetics determines aging, and childhood, sexual maturity, adulthood, and senescence involve separate genetic programs. Perhaps, aging results from diminished energy, slower repair, and increased damage. Perhaps, aging results from free-radical oxidation.
Species have age limits {age limit}. Age limits and population structure can maximize reproductive fitness. People can live to 130 years.
Oxygen-containing molecules can gain electrons, make free radicals, and react with cell molecules {anti-oxidant theory of aging}. Superoxide dismutase (SOD) returns oxygen-containing molecules to normal. Antioxidant vitamins can scavenge free radicals.
Lifetimes {lifespan} can increase by delaying reproduction.
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