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DEV + ageing > ageing > Flashcards

ageing Flashcards

1
Q

what is longevity

A

the length of lifespan independent of ageing

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2
Q

explain how longevity and ageing are thought to have arised

A

longevity aligns with “reproductive fitness” evolutionarily, may have evolved to maximise opportunities to reproduce
vs
ageing might be a more random process arising form the impact of events over the life course.

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3
Q

what is ageing

A

poorly defined but represents a time dependent decline in physiological function

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4
Q

what and when was the first theory of ageing ( not thaaat important)

A

1890s, Weissman proposed that ageing happens because it benefits a species by removing the older members of the populations since it reduces the competition for resources between younger members thus improving reproductive fitness

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5
Q

what are the two major froups of ageing theories that have emerged since?

A

damage theories of ageing and program theories of ageing

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6
Q

what do damage theories generally support?

A

that the cumulative impact of environmental assaults throughout our lifespan causes ageing

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7
Q

give some examples of “envrionmental assaults” we experience in our lives

A

external impacts (eg UV exposure),

or from intrinsic physiological processes (eg Reactive Oxygen Species (ROS)

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8
Q

are damage or program theories more widely accepted?

A

damage, and better supported by evidence

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9
Q

despite what type of theory is accepted and supported by evidence, what is most likely closer to reality?

A

In reality, it is likely that there is no single thing which drives biological aging, but instead a combination of accumulating damage and (epi?)genetic dysregulation may underpin biological aging.

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10
Q

give 3 examples of program theories

A

Programmed longevity – this suggests that aging arises due to time-dependent changes in expression of key genes involved in growth or development.

Endocrine theory – this suggests that hormonal influences (eg GH-IGFI signalling) constitutes a biological clock that determines the rate of aging of an organism

Immunological theory– this suggests that progressive loss of immune system activity with increasing age leads to cellular stress and eventual death from impact of disease

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11
Q

give 5 examples of damage theories

A

Wear and tear theory – over time the components of cells and tissues eventually wear out, leading to the aging of the organism.

Rate of living theory – an organisms rate of basal metabolism determines its lifespan - the higher the basal metabolism, the shorter the lifespan (eg rodents vs humans)

Cross-linking theory – accumulation of cross-linked proteins over time impairs cellular function, slowing down bodily processes and leading to aging

Free-Radical Theory – reactive oxygen species (ROS) cause damage to cellular macromolecules, (DNA, proteins) and organelles, impairing function. Accumulation of this damage over time results in aging.

Somatic DNA damage theory – genetics mutations are acquired faster than they can be repaired. These accumulate over time leading to a breakdown of genetic integrity, resulting in aging.

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12
Q

what is the term “hallmarks of ageing” referring to?

A

In 2013 a group of biologists published an article with this title
which sought to identify common characteristics of ageing across multiple species
in an attempt to identify biological pathways that drive or contribute to ageing

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13
Q

criteria that had to be met by each hallmark of egeing

A

i) it should manifest during normal aging;
(ii) its experimental aggravation should accelerate aging; and
(iii) its experimental amelioration should retard the normal aging process and, hence, increase healthy lifespan

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14
Q

how many hallmarks were ther einitially and what functional domains can they be grouped in?

A

9:
3 Genomic hallmarks
3 cellular hallmarks and
3 biochemical hallmarks

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15
Q

what ageing processes fall under genomic instability

A

1) DNA damage is accumulated throughout life from exposure to external sources (eg UV radiation) or body processes (eg free radicals).

in nuclear DNA:
2) changes in copy number and chromosome stability during ageing
3) changes to nuclear architecture (how the DNA is arranged and packaged within the nucleus)
4)and to the mitochondrial DNA.

Failure to remedy these changes leads to cellular dysfunction, which accumulates, leading to aging.

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16
Q

what is some proof that aging and genetic integrity are linked?

A

Some premature aging syndromes (Werner, Blooms) arise from mutations in DNA repair enzymes

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17
Q

what are some epigenetic changes?

A

loss of DNA methylation, age-specific patterns of histone modification, and changes in the expression of enzymes that regulate DNA packaging and chromatin remodelling

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18
Q

how do epigenetic changes lead to ageing?

A

Together, these lead to
1) inappropriate expression of genes (transcriptional noise) and
2) changes in the packaging and accessibility of DNA to proteins,
which in turn can lead to impaired DNA repair and chromosome instability.

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19
Q

what are telomeres

A

ends of chromosomes that contain repeated DNA sequences

20
Q

why do telomeres shorten over our lifetime?

A

because DNA replication machinery can’t fully replicate them so they shorten with each round of cell division

21
Q

give the term for when a cell stops dividing because a telomere has reached critical shortness

A

senescence (Stop dividing)

22
Q

what do some cells contain that can maintain telomere length?

A

telomerase

23
Q

some proof that telomere lentgh is linked to ageing (its also one of the criteria for hallmarks)

A

experimental manipulation of telomere length or telomerase expression can modulate mammalian lifespan.

24
Q

what do cellular hallmarks generally refer to

A

changes in cell behavior or function over the lifecourse,
that might contribute to aging through failure to maintain or repair tissues or organs.

25
Q

how does stem cell exhaustion lead to ageing

A

1) Cell cycle activity in aged stem cells is reduced, leading to less division, and thus less contribution to repair and maintnance of tissues, resulting in aging.

2) stem cells may also accumulate mutations leading to the formation of neoplasias

26
Q

what are some results of changes in HSCs

A

anemia, myelodysplasia

27
Q

what are some results of changes in MSCs ( Mesenchymal stem cells)

A

osteoporosis, decr fracture repair

28
Q

what are some results of changes in satelite cells

A

decr repair of muscle fibres

29
Q

what are some results of changes in IESCs

A

decr intestinal function

30
Q

what does the “changes in cell signalling” hallmark of ageing refer to?

A

1) ageing is associated with age- related changes in inflammation, hormonal changes and reduced immune system activity
2) senescent cells can influence the cells around them to enter senescence too - bystander effect- through communication of neighbouring cells via gap junctions.

31
Q

what age potential is seen in relation to changes in cell signaling hallmark?

A

Manipulation of signalling pathways, or prevention of chronic inflammation, may present attractive strategies for inhibiting aging.

32
Q

how does cellular senescence happen in non- aged cells

A

Senescence is the stable arrest of the cell cycle, and occurs in response to DNA damage, and prevents the ongoing proliferation of these dysfunctional cells.

These cells are efficiently removed by the immune system, preventing progression to cancer or aging, with removed cells are replaced by stem cell activity.

33
Q

what is the difference with senescense in aged cells?

A

In aged cells, senescence still occurs, but stem cell activity is less efficient, so removed cells do not get replaced as effectively, thus the demand for replacement cells may increase, thus exhausting the capacity of the stem cells. Senescent cells also secrete pro-inflammatory cytokines, which may contribute to aging.

34
Q

what have been some focuses in anti ageing research?

A

“cell signalling” hallmark : Manipulation of signalling pathways, or prevention of chronic inflammation, may present attractive strategies for inhibiting aging.

“cellular senescence”: Improving the mechanisms by which the body can clear senescent cells has been a focus of anti-aging research, as summarised in the short video below.

35
Q

what do biochemical hallmarks relate to

A

Biochemical hallmarks relate to cellular changes in metabolism or biochemistry, which over time may contribute to cell damage and dysfunction, leading to aging.

36
Q

mechanisms of imparied mitochondrial function leading to ageing

A

1) loss of efficacy of respiratory train which results in less energy availability for cellular processes.
2) age-related mitochondrial dysfunction leads to increased reactive oxygen species (ROS) which can damage cellular macromolecules
3) Accumulation of mtDNA mutations may lead to reduced bioenergetics, contributing to a decrease in cellular processes and aging.
4)Mitochondria may also become permeabilized (‘leaky’) with age, triggering apoptosis and inflammation.

37
Q

is the normal state of proteins folded or unfolded

A

folded

38
Q

what are some factors that can elad to the unfolding of proteins

A

ER stress, heat shock, oxidative stress

39
Q

what is proteostasis

A

Proteostasis controls the normal folding and maintenance of proteins in their folded state through chaperone (heat shock protein) activity).

40
Q

what normally happens to unfolded proteins and what is an abnormal process?

A

Normally, unfolded proteins are targeted for autophagy, or breakdown by the proteosome.

However, persistence of unfolded proteins leads to their aggregation, disrupting normal cell function,
(associated with numerous age-related disorders (eg Alzheimers, Parkinsons).

41
Q

what does impaired nutrient sensing refer to

A

Mutations that impair the function of the activity of the Growth Hormone (GH) – Insulin-Like Growth Factor I (IGFI pathway

42
Q

what does impaired nutrient sensing lead to in terms of ageing

A

these mutations are associated with increased lifespan and healthy aging in model organisms,
although very low levels of GH-IGFI signalling are incompatible with life.

43
Q

what else in terms of impaire dnutrient sensing has been shown to expand lifespan in model organisms?

A

In parallel, dietary restriction has been shown to extend lifespan in model organisms, through the AMPK pathway.

44
Q

what is th enewest theory of ageing

A

the information theory of ageing

45
Q

what does the information theory of ageing suggest?

A

suggests that acquisition of epimutations (harmful epigenetic changes) over the lifecourse leads to aging through loss of ‘youthful epigenetic information’.

46
Q

how is the new “ information theory” of ageing being tested?

A

a team at Harvard have been working to use the Yamanaka factors (a collection of 4 transcription factors (OCT4, SOX2, KLF4 and MYC)
that when artificially-expressed together in mature cells can reprogram them to an embryonic, pluripotent state)
to ‘reset’ the epigenome of cells in aging tissues and animals.

47
Q

suggest (with a few words for each) an anti ageing strategy to adress each of the hallmarks of egeing

A

DEV + ageing (4 decks)

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