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HAPIB > Module 6: Ageing > Flashcards

Module 6: Ageing Flashcards

1
Q

2 biological theories of ageing?

A
  1. Programmed Theory
  2. Error Theory
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2
Q

What is the programmed theory of ageing?

A

Considers ageing to have an internal clock

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3
Q

What is the error theory of ageing?

A

Considers ageing to be resultant of an accumulation of damage to essential macromolecules within cells, causing the demise of such cells and organs

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3
Q

What is senescence?

A

An irreversible block in cell proliferation; cells cease to divide

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3
Q

Maximum number of times somatic cells can divide?

A

Approximately 75-80

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4
Q

Three components of programmed theory of ageing?

A
  1. Programmed longevity theory
  2. Endocrine theory
  3. Immunological theory
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5
Q

What is programmed longevity theory?

A

Ageing is due to long-term genetic instability and changes in gene expression leading to senescence

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6
Q

What is endocrine theory?

A

Ageing is hormonally regulated

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7
Q

What is immunological theory?

A

Ageing is due to the immune system being programmed to decline over time thus becoming susceptible to infection and causing low-grade, chronic, persistent inflammation

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8
Q

Three components of error theory of ageing?

A
  1. Free radical theory
  2. DNA damage theory
  3. Wear and tear theory
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9
Q

What is free radical theory?

A

Ageing is the cumulative result of oxidative damage to cells/tissues, that arises primarily as a result of free radicals being a byproduct of aerobic metabolism

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10
Q

What is DNA damage theory?

A

DNA damage, via DNA mutations and breaks, overrides DNA repair occurring over time, thus contributing to genomic instability and the ageing process

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11
Q

What is wear and tear theory?

A

Ageing results from gradual deterioration of vital components of cells/tissues via ‘wear and tear’ over time

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12
Q

8 pillars of ageing?

A
  1. Cellular senescence
  2. Telomere shortening
  3. DNA damage/genomic instability
  4. Epigenetic drift
  5. Stem cell exhaustion
  6. Inflammaging
  7. Mitochondrial dysfunction
  8. Deregulated nutrient sensing
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13
Q

Why is senescence important?

A

Prevents propagation of mutated DNA to daughter cells, so acts as a natural barrier against cancer

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14
Q

Widely used markers of senscence?

A
  • Increased levels of senescence-associated β-galactosidase
  • Activation of genes: p16 and p14
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15
Q

Why does cancer still occur despite senescence?

A

Oncogenes override senescence programming and repress apoptosis, causing accumulation of mutated cells

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16
Q

Benefits of senescence? (5)

A
  • Embryonic development
  • Tissue regeneration
  • Immunity
  • Tumour suppression
  • Wound healing
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17
Q

Negative effects of senescence? (3)

A
  • Tissue regeneration
  • Chronic inflammation
  • Tumor promotion
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18
Q

How is ageing associated with senescence?

A

Ageing = senescent cells accumulate and build in number (so, if senescent cells eliminated, ageing may be reduced)

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19
Q

What are senolytics?

A

Small molecules, administered as drugs, that induce apoptosis of senescent cells by targeting their pro-survival pathways

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20
Q

What are telomeres?

A

Highly repetitive DNA sequences enclosing ends of chromosomes (shelterin complex)

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21
Q

Role of telomeres?

A

Highly protective against damage and fraying of DNA

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22
Q

What is telomerase?

A

Enzyme that maintains telomere length, which is generally not expressed in somatic cells

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23
Q

What impacts length of telomeres?

A

Length decreases with each cell division; thus, shortens over time

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24
Q

What is the main reason for ageing/cellular senescence?

A

DNA damage

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25
Q

3 main reasons for DNA damage?

A
  • External insults (e.g. UV, chemicals, pollutants, infections)
  • Internal insults (e.g. reactive oxygen species (ROS), which are metabolic by-products)
  • DNA replication/proliferation (i.e. rapid proliferation = increased DNA damage, whilst senescence/apoptosis decrease)
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26
Q

3 types of DNA damage?

A
  • DNA mutations
  • DNA breaks
  • Chromosome translocations
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27
Q

4 types of DNA mutations?

A
  • Silent mutation
  • Missense mutation
  • Nonsense mutation
  • Frameshift mutation
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28
Q

What is a silent mutation?

A

A change in DNA sequence, but no effect on protein sequence

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29
Q

What is a missense mutation?

A

A change in DNA sequence causing amino acid substitution

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30
Q

What is a nonsense mutation?

A

Substitutes a stop codon for an amino acid, causing premature termination

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31
Q

What is a frameshift mutation?

A

Insertion/deletion of a nucleotide, changing all amino acids downstream from that sequence

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32
Q

6 types of DNA breaks?

A
  • Single-stranded break
  • Mis-match (wrong nucleotide, doesn’t connect)
  • Damaged base
  • Double-stranded break
  • Intra-strand crosslink (nucleotide connects twice to one strand; loop)
  • Inter-strand crosslink (one nucleotide connects to both strands)
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33
Q

What are chromosome translocations?

A

When regions of chromosomes break apart, then translocate and fuse with other chromosomes

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34
Q

How are chromosome translocations detected?

A

Karyotyping or FISH (fluorescence in situ hybridisation -> fluorescent DNA probes)

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35
Q

Impact of senolytic agents upon idiopathic pulmonary fibrosis?

A

Improved walking

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36
Q

Impact of senolytic agents upon osteoarthritis?

A

Reduced cartilage destruction inflammation

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37
Q

Impact of senolytic agents upon diabetes?

A

Reduced organ dysfunction

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38
Q

What does increased DNA repair cause?

A

Increased longevity

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39
Q

Characteristic of people who live >100 years?

A

Higher levels of DNA repair enzymes

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40
Q

What are reactive oxygen species (ROS)?

A

Chemical reactive species; molecules comprising an oxygen atom and an unpaired electron

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41
Q

How are ROS produced?

A

Natural by-product of aerobic metabolism and formation of ATP

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42
Q

What factors increase ROS production?

A

Ionising radiation, UV, heat, pollutants, smoke, diet (fatty foods)

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43
Q

What detrimental effects do ROS have?

A

Responsible for >100 human diseases; induce ageing

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44
Q

Roles of ROS? (2)

A

Cell signalling and immunity

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45
Q

How do ROS cause ageing?

A

Attack and oxidise DNA, lipids, carbohydrates, and proteins

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46
Q

What is oxidative stress?

A

Imbalance between ROS and body’s ability to detoxify/counteract their damaging effects via antioxidants (e.g. glutathione)

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47
Q

What are progeroid syndromes?

A

Group of rare monogenic disorders that mimic physiological ageing

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48
Q

What are monogenic diseases?

A

Arise from a single gene mutation that affects DNA repair/nuclear structure

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49
Q

Symptoms of Hutchinson Gilford Progeria Syndrome?

A
  • Rapid onset of ageing from childhood
  • Disproportionately large head, eyes, and ears, wrinkled skin
  • Growth retardation and sparse hair
  • increased incidence of cardiovascular pathology (e.g. heart attack/stroke)
50
Q

Cause of Hutchinson Gilford Progeria Syndrome?

A

Genetic mutation in LMNA gene causes abnormal variant of lamin A, instigating an unstable/damaged nuclear envelope and premature cell death

51
Q

What is epigenetics?

A

Change in gene expression; not dependent upon DNA sequence, but dependent on chemical modifications

52
Q

What is heterchromatin?

A

Highly compacted DNA, transcriptionally inactive (‘h’=on ‘h’old)

53
Q

What is euchromatin?

A

Loosely packed DNA, transcriptionally active (‘e’=’e’nergetic)

54
Q

What is epigenetic drift?

A

Divergence of epigenome due to age, which is influenced by environmental exposures

55
Q

What impacts epigenetics?

A

Environmental exposures: e.g. diet, chemical exposure, exercise, social activities, moods, mental states, ancestors, and parents

56
Q

2 main forms of epigenetic drift that instigate ageing?

A
  • Global DNA hypomethylation
  • Histone modifications
57
Q

Correlation between heterochromatin/euchromatin and ageing?

A

Decrease in heterochromatin and increase in euchromatin

58
Q

What is global DNA hypomethylation, and its correlation with ageing?

A
  • DNA methylation associated with gene silencing and heterochromatin
  • Low methylation (‘hypo’methylation) causes an open chromatin structure, increasing formation of euchromatin, leading to genetic instability via DNA damage
  • Aged cells lose cell type and gene expression due to hypomethylation
59
Q

What are histone modifications, and their correlation with ageing?

A
  • More than 30 types of histone modifications
  • As we age, incorporation of different histone variants into DNA leads to opening of chromatin structure (increased formation of euchromatin), meaning cells are exposed to DNA damage
60
Q

Role of stem cells?

A

Differentiate and produce specialised cells, thus generating new tissue by replacing often damaged cells

61
Q

Unique properties of stem cells? (4)

A

Uncommitted, immature, high degree of plasticity, and self-renew

62
Q

Single major driver of ageing?

A

Loss of stem cell number and function

63
Q

3 main possible changes to stem cells due to ageing?

A
  • Reduced potential to differentiate -> less specialised cells
  • Reduced potential to proliferated -> less stem cells -> less specialised cells
  • Enhanced potential to differentiate -> less stem cells
64
Q

Causes of changes to stem cells due to ageing?

A

DNA damage, telomere shortening, senescence, abnormal cellular signalling/metabolism, epigenetic changes

65
Q

Where do neural stem cells generally reside?

A

Subventricular zone and hippocampus

66
Q

What neural cells can stem cells differentiate into?

A

Neurons, astrocytes, oligodendrocytes

67
Q

What blood cells can haematopoietic stem cells differentiate into?

A

Platelets, erythrocytes, myeloid cells, lymphoid cells

68
Q

Where do haematopoietic stem cells generally reside?

A

Red bone marrow

69
Q

What occurs to haematopoietic stem cells with age, and what effects does this have?

A
  • Increased haematopoietic stem cells and myeloid cells
  • Decreased lymphoid cells
70
Q

Where do mesenchymal stem cells generally reside?

A

Bone/bone marrow

71
Q

What bone cells can mesenchymal stem cells differentiate into?

A

Adipocytes, osteoblasts, chondrocytes

72
Q

What occurs to mesenchymal stem cells with age, and what effects does this have?

A
  • Increased adipocytes = more bone marrow fat accumulates
  • Decreased osteoblasts = less trabecular/spongy bone
73
Q

Where do muscle stem cells generally reside?

A

Skeletal muscle; surrounding muscle fibres

74
Q

What occurs to muscle stem cells with age, and what effects does this have?

A

Decreased differentiation = reduction in muscle repair/mass

75
Q

What is the somatotropic axis?

A
  • One of the main hormone pathways
  • Involves growth hormone (GH) and IGF-1; mutations in these genes expand lifespan
  • Minimal activation of pathway promotes lifespan, maximum activation of pathway decreases lifespan
76
Q

What stimulates growth hormone secretion?

A

When food is ingested and broken down, dietary factors stimulate release of GH into anterior pituitary

77
Q

Role of growth hormone?

A

Stimulates production of IGF-1

78
Q

Role of IGF-1 (insulin-like growth factor 1)?

A

Informs cells glucose is present, causing them to take up said glucose = growth

79
Q

What occurs with excessive IGF-1 stimulation?

A

Causes more metabolism and proliferation, promoting DNA damage and hence ageing

80
Q

Impact of cutting calories (diets) upon ageing?

A

Increase longevity

81
Q

Why do diets slow ageing?

A
  • Reduce GH/IGF-1 pathway, reducing metabolism/cell growth and hence DNA damage
  • Sirtuins activated due to nutrient scarcity, increasing metabolic efficiency and thus genomic stability
  • Activates autophagy
82
Q

What are sirtuins?

A

Enzymes that repair/modify DNA and proteins, causing genetic stability and increasing metabolic efficiency

83
Q

What is autophagy?

A
  • ‘Self-eating’
  • Homeostatic pathway in which cellular components that have worn out are degraded and recycled, stimulating development of new organelles
84
Q

Impact of ageing upon autophagy?

A

Autophagy declines with age, causing accumulation of dysfunctional organelles and macromolecules

85
Q

What is inflammaging?

A

Chronic, sterile, low-grade inflammation that develops with age, leading to cell and tissue destruction

86
Q

3 layers of skin?

A
  1. Epidermis (avascular; epithelial cells)
  2. Dermis (CT; collagen/elastin fibres)
  3. Hypodermis (fat cells)
87
Q

What occurs to skin layers with age?

A
  • Lose layer of fat cells in hypodermis
  • Lose collagen and elastin fibres in dermis
  • Decrease in vascularity
88
Q

What does age-related degrade in epidermis/dermis/hypodermis cause?

A

Loss of skin elasticity (sagging and wrinkling)

89
Q

What does age-related lack of vascularity in skin cause?

A
  • Accumulation of waste products
  • Less nutrients/O2 going to skin cells
  • Less effective thermoregulation
90
Q

What does age cause to hair?

A

Melanocytes lost in hair follicles due to undergoing cell cycle arrest, thus leading to grey, dry, thinning hair

91
Q

What is photoageing?

A

Degeneration of skin in proportion to UV exposure (skin spots, skin cancer, wrinkling)

92
Q

What body system degenerates the least with age?

A

Endocrine system

93
Q

Effects of ageing upon endocrine system?

A
  • Reproductive/growth/thyroid hormones decline; release and secretion rates slow
  • Target cell sensitivity decline
94
Q

Why is Type II diabetes more common with age?

A

Decreased insulin sensitivity = accumulation of glucose in blood

95
Q

Difference in brain mass with age?

A

Brain weighs 50% less by age 75

96
Q

Effects of ageing upon nervous system? (4)

A
  • Cerebral and neural atrophy (loss of brain matter)
  • Neurons accumulate waste product (lipofuscin)
  • Degeneration of myelin, as it becomes patchy, thus slowing signals
  • Reduced neurotransmitter production
97
Q

What aspect of intellectual function suffers the most with age?

A

Short-term memory

98
Q

Effect of ageing upon bones?

A

Decrease in bone mass/bone mineral density (osteopenia)

99
Q

Effect of ageing upon bone cells?

A

Osteoblasts less active than osteoclasts

100
Q

Why is there less bone growth/formation with age?

A
  • OBs < OCs
  • Sex hormones (estrogen (F) and testosterone (M)) trigger less bone growth
101
Q

Why are joint diseases more commonplace with age?

A

Less abundant synovial fluid, thin/absent articular cartilage, narrowed joint space, formation of bone spurs

102
Q

What is muscle atrophy?

A

Replacement of muscle with adipose tissue (fat)

103
Q

Impact of ageing upon composition of muscle cells?

A

Have fewer myofibrils and mitrochondria

104
Q

Impact of ageing upon production of blood cells?

A

Dramatic reduction in erythropoiesis and leukopoiesis

105
Q

What is anaemia?

A

Lack of or dysfunctional RBCs, leading to less O2 to tissues

106
Q

What is coronary atherosclerosis?

A

Plaque build-up in heart blood vessels, potentially leading to angina, infarction, heart block

107
Q

What are varicose veins?

A

Bulging, enlarged veins, that occur due to vessels stiffening and not expanding effectively, because of weaker valves; can increase BP

108
Q

Impact of ageing on heart structure, SV, CO?

A
  • Thinner heart walls
  • Decreased SV and CO
109
Q

Main effect of ageing upon respiratory system? Why?

A

Declining pulmonary ventilation, because costal cartilage is less flexible and there is reduced capacity for expansion

110
Q

Effect of ageing upon mucociliary escalator?

A

Mucociliary clearance compromised, so less able to clear lungs of irritants/pathogens, rendering more susceptible to respiratory infection

111
Q

Why does ageing cause reduced gas exchange?

A

Lungs have less elastic tissue and fewer alveoli, so less surface area

112
Q

Extent of renal atrophy that occurs with age?

A

Kidneys 40% smaller by age 90 due to a loss of nephrons; impaired filtration rate

113
Q

Effect of ageing upon fluid balance?

A

Less effective fluid balance -> less responsive to ADH -> sense of thirst reduced, dehydration commonplace

114
Q

Effect of ageing upon urinary systems of elderly males?

A

80% of aged men have benign prostate enlargement, making it harder to control bladder and void urine, causing urine retention

115
Q

Effect of ageing upon females systems of elderly women?

A

Sphincters weakened, causing incontinence; nervous system can impact micturition reflex

116
Q

Effect of ageing upon saliva?

A

Saliva reduced, so dental health negatively affected because saliva contains enzymes that kill pathogens in the oral cavity

117
Q

Effects of ageing upon nose and mouth?

A

Reduced sense of smell/taste, gum recession

118
Q

Effects of ageing upon esophagus?

A

Decrease in peristalsis and sphincters lose tension, causing acid reflux

119
Q

Effects of ageing upon liver?

A

Shrinkage of liver -> less hepatocytes -> less able to detoxify substances

120
Q

Effect of ageing upon stomach?

A

Stomach wall’s elasticity reduced -> decreased bicarbonate and gastromucosal production, as well as delayed gastric emptying of chyme; also gastric mucosa atrophies -> less HCl and intrinsic factor

121
Q

Effect of ageing upon pancreas?

A

Decreased secretion of pancreatic protease and lipase, meaning less nutrients

122
Q

Effect of ageing upon small intestine?

A

Gut-associated lymphoid tissue capacity compromised, decreasing peristalsis

123
Q

Effect of ageing upon large intestine?

A

Slowed peristalsis, causing constipation

124
Q

What is lifespan?

A

Maximum attainable age

125
Q

What is life expectancy?

A

Average length of life in a given population

HAPIB (8 decks)

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