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health and the community > lectures 16-19 > Flashcards

lectures 16-19 Flashcards

1
Q

define what is meant by ageing

A

a set of gradual and spontaneous changes that occur in maturation from infant to adult

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2
Q

what are the main physical signs of ageing?

A
  • wrinkles on the face and body
  • sight, hearing, taste, and smell become less acute
  • hair begins to thin and turn grey
  • reduced bone density
  • slower reflexes and altered gait
  • less acute mental agility and declining memory
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3
Q

what % of the population is above 65 in the UK

A

18.5%

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4
Q

define what is meant by lifespan

A

the period of time in which the events of a species typically occur

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5
Q

what is meant by the maximum life span?

A
  • the maximum period of time members of any given species can live
    human’s is currently 122 years and 164 days
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6
Q

define what is meant by life expectancy

A

a measure of the average time we can expect to live based on the year of birth, current age, and sex

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7
Q

what causes a reduced life expectancy in Haiti?

A
  • it is the poorest population in the Western Hemisphere
  • few natural resources due to deforestation
  • corruption
  • low levels of education for much of the population
  • natural disasters cause mortality shocks but life expectancy often recovers quickley
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8
Q

does conflict cause mortality shock?

A

yes

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9
Q

do old or young people tend to be more affected by mortality shock?

A

young people

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10
Q

what 3 diseases show accelerated ageing?

A
  • Hutchinson-Gilford syndrome
  • Werner syndrome
  • Down’s syndrome
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11
Q

what is the incidence of Hutchinson Gilford progeria syndrome?

A

1 in 4 million to 1 in 8 million

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12
Q

what are the main features of HGP

A
  • slow growth + dwarfism
  • early loss of hair
  • disproportionately large head
  • stiff joints
  • coronary artery disease
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13
Q

what is the average life expectancy of those with HGP?

A

14 years

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14
Q

what is the genetic cause of HGP?

A
  • can be mapped to chromosome 1q
  • most cases are a single de novo base substitution resulting in a silent change in the LMNA gene
  • this mutation in exon II activates a cryptic splice resulting in production of a defective lamin A protein (progerin)
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15
Q

what does the LMNA gene code for?

A

the nuclear lamin A protein

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16
Q

what is the normal function of lamin A?

A
  • it forms intermediate filaments to be part of the cytoskeleton
  • forms a network with other lamins inside the nuclear envelope
  • in late passage, normal cells lamin A and lamin B mostly co-localise at the nuclear lamina
  • lamin A promotes genetic stability by maintaining levels of proteins that have key roles in repair of DNA double strand breaks
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17
Q

how does the production of progerin cause problems?

A
  • in HGPs there is an instability to rapidly repair DNA damages, causing aspects of premature ageing
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18
Q

why is HGPs not a perfect model for ageing?

A
  • males do not develop prostate issues
  • there is no increased risk of cancers
  • high blood pressure is rare
  • diabetes is rare
  • no Alzheimers
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19
Q

what are the physical characteristics and effects of Werner syndrome?

A
  • individuals typically grow and develop normally until they reach puberty
  • accelerated ageing in their 20s causes:
    greying and hair loss
    a hoarse voice
    thin skin
    abnormal fat deposition
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20
Q

what is the global incidence of Werner syndrome?

A

1 in 1 million

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21
Q

what pattern of inheritance does Werner syndrome follow?

A

autosomal recessive

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22
Q

what are the cellular features and causes of Werner syndrome?

A
  • there is limited cellular division capacity
  • caused by a mutation in the WRN gene (a DNA helicase)
  • mutations are typically loss of function
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23
Q

how does faulty telomere production cause Werner syndrome?

A
  • the telomeres that are normally replicated by lagging strand synthesis are not replicated efficiently
  • causes premature ageing of cells
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24
Q

overexpression of which enzyme in vitro counteracts WRN mutations?

A

telomerase

25
Q

why is it suggested that the nuclear lamina may also regulate DNA replication?

A

wild type WRn interacts with the nuclear lamin

26
Q

why is Werner syndrome not an effective model for ageing?

A
  • no prostate issues
  • generally no high blood pressure
  • no strokes
  • no Alzheimers
27
Q

what is the incidence of Down’s syndrome?

A

1 in 700 births

28
Q

what is the life expectancy of someone with Down’s?

A

60 years

29
Q

what suggests that Down’s is a good model for ageing?

A
  • premature greying/ hair loss
  • early vascular disease
  • early onset Alzheimers
30
Q

what suggests that Down’s is not a good model for ageing?

A
  • no prostate cancer
  • no cataracts
  • not associated with high blood pressure
31
Q

what are the genetic causes of Down’s syndrome?

A
  • trisomy 21 - 95% of cases
  • translocation Down’s - 4% cases
  • mosaic downs - 1% cases
32
Q

what is the Down’s critical region?

A
  • an area of about 30 genes in which Usp16 protein is over-expressed
33
Q

what is the Down’s critical region?

A
  • an area of about 30 genes in which Usp16 protein is over-expressed
34
Q

what is Usp16?

A
  • ubiquitin specific protease
  • histones can be ubiquitylated by covalent attachment of ubiquitin
  • histones become ubiquitylated at DNA double strand breaks and acts as a focus for recruitment of DNA repair enzymes
35
Q

what mutation do nematodes possess to increase lifespan

A
  • age-1 gene mutation
36
Q

what is the dauer stage in nematodes?

A

feeding stops and movement is reduce in which no ageing occurs
- it reduces activity of the glucose pathway so no PI-3K is produced

37
Q

what is the general phenotype of centenarians

A
  • low bmi
  • low plasma triglycerides
  • low oxidative stress levels
  • high insulin sensitivity
  • higher plasma levels of active IGF-1
38
Q

what mutation is thought to increase risk of Alzheimer’s?

A
  • mutation of the APoE-4 gene
  • APoE regulates lipid homeostasis, so APoE-4 mutation can lead to plagues of amyloid beta in the brain
39
Q

what are proteasomes?

A
  • multi subunit particles with a barrel shaped catalytic core capped with regulatory particles
  • found in the cytosol and around nuclear pore complexes
  • proteins to be destructed are degraded there
  • the 20S core proteasome can degrade oxidised proteins (these damage regular proteins)
40
Q

what are the general roles of autophagy?

A
  • removal of aggregates, damaged organelles, and invading microbes
  • providing amino acids, nucleotides, lipids, and sugars under low nutrient conditions
41
Q

what is the mechanism of action of autophagy?

A

1 - an isolation membrane captures cytoplasmic contents
2 - an autophagosome is formed
3 - the auto-phagosome fuses with a lysosome
4 - this forms an autolysosome that digests the cytoplasmic cargo

42
Q

what is the main source of the isolation membrane?

A
  • primary source is the omegasome on the ER
  • multiple other sources are used
43
Q

how does an LC3-II protein capture cargo?

A

1 - LC3-II protein captures a cargo receptor that contains an LC3-interacting region motif that captures cargo
2 - autophagosome fuses with lysosome

44
Q

how is autophagy stimulated?

A
  • phosphorylated AKT activates FOXO-3a transcription factors whose targets stimulate autophagy
  • the mTOR complex 1 inhibits autophagy but AKT phosphorylation inhibits mTORC1
45
Q

what other molecule can inhibit mTORC1

A

Rapamycin

46
Q

how does caloric restriction upregulate autophagy?

A
  • it inhibits mTOR
  • it also upregulates FOXO-3a by producing SIRT-1
47
Q

list the primary hallmarks of ageing

A
  • genomic instability
  • loss of telomeres
  • epigenetic alterations
  • loss of proteostasis
48
Q

what is genomic instability caused by?

A
  • it is DNA damage caused by exogenous and endogenous threats
  • includes point mutations, translocations, chromosomes gains and loss, telomere shortening, and gene disruption caused by the integration of viruses or transposons
49
Q

how do telomeres show ageing?

A
  • telomeres regulate how many times a cell can divide - they shorten with each division
  • once telomeres shrink to a certain level, cells can no longer divide
50
Q

how are epigenetic alterations passed between generations?

A
  • the epigenetic marks of the female re passed to the ovum
  • protamines associated with sperm DNA are mostly replaced with acetylated histones from the ovum’s cytoplasm
51
Q

what are the antagonistic hallmarks of ageing?

A

(things that happen in response to ageing)
- deregulated nutrient sensing
- mitochondrial dysfunction

52
Q

what occurs in deregulated nutrient sensing?

A
  • the signalling pathway IGF-1 is the same as insulin, informing cells of glucose presence
  • its targets are FOXO and mTORC, so when IGF-1 levels decline with age, nutrient sensing decreases
53
Q

what occurs to induce mitochondrial dysfunction?

A
  • as ageing occurs, electron leakage increases, reducing ATP generation which should activate ROS and stimulate ageing
  • however ROS could trigger survival in stress conditions instead of ageing
54
Q

list the integrative hallmarks of ageing

A
  • cellular senescence
  • stem cell exhaustion
  • altered intracellular communication
55
Q

what is cellular senescence?

A

it is the processes by which the capacity for cell division, growth, and function is lost over time
accumulation of senescent cells increases inflammation and decreases tissue function

56
Q

what are the causes of stem cell exhaustion?

A
  • anaemia
  • osteoporosis
  • poor fracture repair
  • reduced intestinal function
  • poor muscle fibre repair
57
Q

how can stem cell exhaustion be prevented?

A

induced pluripotent stem cells can be artificially produced

58
Q

what are the effects of altered intracellular communication?

A
  • neuroendocrine dysfunction
  • inflammation
  • immunosenescnece
59
Q

how is obesity an ageing accelerator?

A
  • obesity causes SIRT1 inhibition and MTORC1 activation
  • high levels of white adipose tissues are associated with accelerated leucocyte telomere attrition

health and the community (6 decks)

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