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Physiology & Science: Ageing > Theories of ageing > Flashcards

Theories of ageing Flashcards

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1
Q

What are the 3 major views/groups of why we age?

A
  1. Wear and tear
  2. Adaptive evolutionary
  3. Non-adaptive evolutionary
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2
Q

What is the wear and tear theory and why can it not be the whole answer?

A
  • View organism as a machine that wears out
  • Some organisms wear out (eg. teeth), contributing to deleterious ageing
  • BUT some organisms can repair whole organs and not age
  • Therefore wear and tear cannot be the whole answer as if body has potential to repair itself, why don’t we?
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3
Q

Describe the adaptive evolutionary theory and its problems

A
  • Developed through process of evolution + natural selection
  • Conforms to popular Darwinian principles
  • Ageing selectively advantageous to species
  • Prevents old + worn out individuals competing
  • BUT.. advantage to population not individual
  • Ageing rarely seen in natural populations
  • Prevents old + worn out individuals competing
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4
Q

What are the 2 theories that underly non-adaptive evolutionary reasons for why we age?

A
  • Mutation Accumulation
  • Antagonistic pleiotropic genes
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5
Q

What is meant by the mutation accumulation theory?

A
  • Powers of natural selection decline w/ age
  • Early expressed genes affect most of population
  • Those expressed after reproduction are lost from evolutionary control
  • Ageing due to a miscallaneous collection of late acting deleterious genes
  • No experimental support for this theory
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6
Q

What is meant by the ‘antagonistic pleiotropic genes’ theory?

A
  • Genes have more than one effect
  • Early good effect therefore retained
  • Bad/deleterious late effect which contributes to ageing
  • Evidence in drosophila studies
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7
Q

Describe examples of evidence for the theory of antagonistic pleiotropic genes

A
  • Drosophila studies - 2 examples
  1. aa allele greatly increases early fecundity (fertility) and pleiotropically reduces longevity
  2. if breeding prevented until later in life over 15 generations lifespan extended by 1/3 but short-winged + flying ability reduced
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8
Q

What is the disposable soma theory?

A
  • development of non-adaptive evolutionary views
  • theory views organism as machine that transfers free energy -> progeny
  • success is to ensure survival of genes in most efficient way
  • disposable = prod with limited lifespan
  • soma = not of germ line
  • ‘your body is dispoable but you have to hand your germ line on’
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9
Q

Disposable Soma theory: Which process will any organism give most attention to and why?

A
  • The amount of energy expended on various possibilities will depend on the ecological niche occupied by that organism (eg. cat, mouse from lecture notes)
  • This will result in species specific longevity
  • For some fertility is priority
  • Others need to maintain soma for longer
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10
Q

What does the second law of thermodynamics suggest?

A
  • Entropy increases ie. we age + decay
  • We resist this with defensive + repair processes
  • Protective mechanisms eventually fail
  • Rate of ageing is determined by investment in self maintenance
  • We are programmed to survive not age
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11
Q

How do we age - what are the four groups of theories?

A
  • System level theories
  • Cellular/molecular level theories
  • Genetic theories
  • Genomic stability
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12
Q

A theory based on total body systems is the Neuroendocrine theory. What is it?

A
  • Suggests functional decrease in neurones + associated hormones is central to ageing process
  • HPA axis controls growth + dvpt so why not ageing?..
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13
Q

What is the evidence for the neuroendocrine theory?

A
  • Decreased pulsatile GH and GnRH release in ageing rats
  • Hypophysectomy + hormone replacement -> inc lifespan
  • DECO or death hormone proposed but never found
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14
Q

Cellular theories: Wear and tear + rate of living - what is it?

A
  • Some aspects of ageing look like wear + tear
  • Organisms w higher basal metabolic rate have shorter lifespan
  • Accumulation of damage may be important
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15
Q

Cellular theories: Cross link formation - what is it?

A
  • Many biological molecules develop cross linkage or bonds w passage or time, altering physical/chemical properties
  • Collage is able to cross link - leading to changes in skin, younger person has stretchier/resistant skin compared to old person.
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16
Q

Cellular theories: Heat shock proteins - what is it?

A
  • Heat shock proteins produced at time of cell stress
  • Disassemble damaged proteins + transport in new
  • Reduced production w/ age
  • Decreased ability to cope w stress leads to ageing
17
Q

Cellular theories: Hayflick phenomena - what is it?

A
  • Fibroblasts grown in culture undergo a set number of divisions then stop
  • More divisions if from younger source
  • Repeated in other cell types
  • Biological clock
  • HeLa cell line from Ca breast unlimited divison
18
Q

The genetic theory can explain for how ageing occurs. What observations/experiments suggest genes are important in this?

A
  • Twin studies
  • Long lived families
  • Species specific longevity
19
Q

In which 3 organisms were genes identified that shorten and lengthen life?

A

Drosophila, yeast, nematodes

In nematodes, there’s a mutation that doubles 3/52 lifespan by increasing superoxide dismutase

20
Q

What are telomeres and what is their purpose?

A
  • Chromosome tail, repeated short DNA base sequence
  • Stabilise chromosome during cell division
  • Shorten with each division
21
Q

How are telomeres relevant to explaining ageing?

A
  • Telomeres reach a critical length at which no further divisions can occur -> shorter -> ageing
  • Explain Hayflick phenomena (cellular theory) but more importantly telomere length regulates gene (ISG15) expression in human cells
  • In germ cells + tumour cells, telomerase is made, which re-expands the telomere and allows for continued cell divison
22
Q

Genomic stability can account for how ageing occurs. What is error catastrophe?

A
  • Errors occur at transcription and translation that result in abnormal protein production, it’s usually corrected when protein is replaced
  • If the abnormal protein is important in DNA repair/protein synthesis -> may lead to a cascade + cell death
  • Accumulation of such errors may result in ageing
23
Q

Genomic stability: What is meant by somatic mutation and DNA repair?

A
  • Based on irradiation shortening the life span of mice so perhaps ageing due to background radiation causing damage to DNA?
24
Q

Why is somatic mutation now considered unimportant in relation to ageing?

A
  • Occurence rate is too low
  • DNA repair sufficient enough
25
Q

Despite the unimportance of somatic mutation, repair may fail in combination with toxic agents eg. UV light or O2 radicals. What evidence is there for this?

A
  • DNA repair more efficient in man than in mouse
  • Also more efficient in germ cells
  • Ability to repair declines w/ ageing (more cancer cells seen)
26
Q

Genomic stability: What is the free radical theory?

A
  • Highly reactive chemical compounds arise from enzymatic and non-enzymatic reactions
  • These damage cellular DNA
  • Several enzymes (superoxide dismutase, catalase, glutathione peroxidase) & vit E, C, carotene protect cells/prevent damage
  • Protection reduces with age
27
Q

Genomic stability: What is the mitochondrial theory?

A
  • Ageing due to mitochondrial DNA damage
  • High exposure to O2 radicals
  • No protein coat to mitochondrial DNA (less protected than nuclear DNA)
  • Damage and mutation increase with age
  • Genetic mitochondrial dysfunction syndromes mimic ageing
28
Q

What is cell senescence?

A

Cellular senescence is the phenomenon by which normal diploid cells cease to divide. In culture, fibroblasts can reach a maximum of 50 cell divisions before becoming senescent. This phenomenon is known as “replicative senescence”, or the Hayflick limit. It’s basically ageing.

29
Q

What factors can act on a pre-senescent cell to make it enter into its senescent phase?

A
  • Dysfunctional telomeres
  • DNA damage
  • Oxidative stress
  • Strong mitogenic signals
  • Chromatin perturbations
30
Q

What 3 main things occur within the senescent phenotypic cell?

A
  • Growth arrest
  • Altered gene expression
  • Apoptosis resistance
31
Q

Senescent cell numbers inc with age + are at the site of age related pathologies. In which organ dysfunctions is senescence prominent in?

A
  • Osteoarthritis
  • Pancreatic*
  • Neurogenesis*
  • Haemopoiesis*

*function decreases associated with P16 dependent senescence

32
Q

What impacts does cellular senescence have?

A
  • Altered gene expression
  • Up-regulation of genes controlling extracellular matrix degrading enzymes, inflammatory cytokines + growth factor
  • Disrupt normal tissue structure + function
  • Stimulate growth of pre-malignant cells
33
Q

The observed changes of ageing are the result of many separate processes, such as?

A
34
Q

Describe the method of calorie restriction in aim to increase lifespan. What are its problems?

A
  • Calorie restriction in rats increases lifespan
  • But results in delayed puberty + increased infection and death in pre-puberty, but if rats make it beyond puberty, then they live longer
  • Some evidence in humans eg. Okinawa diet
35
Q

What other lifestyle/everyday factors have impact on the ageing process?

A
  • Exercise decreases ageing
  • Sexual activity decreases ageing
  • Overcrowding increases ageing

Physiology & Science: Ageing (13 decks)

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