biology of aging Flashcards

1
Q

what is aging

A

Longevity – length of lifespan independent of ageing.​

Ageing – more of a random process arising from the impact of events over the life course.

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2
Q

Name 2 physiological changes that occur when humans age

A

Reduction in brain volume or mass/

Decreased lung capacity/

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3
Q

Name 2 psychological changes that occur when humans age

A

Altered sleep patterns/ Cognitive decline/
increased depression risk

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4
Q

Compare program theories of ageing to damage theories of ageing

A

Program theories of ageing suggest that ageing follows a biological timetable. (1)

Damage theories suggest organisms experience environmental assaults (UV exposure, ROS) throughout their lifespan and that the cumulative impact of these assaults causes ageing (1)​

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5
Q

list 3 criteria for hallmarks of ageing- (an attempt to identify biological pathways that contribute to aging)

A

(i) it should manifest during normal ageing;

(ii) its experimental aggravation should accelerate ageing;

(iii) its experimental improvement should retard the normal ageing process and, hence, increase healthy lifespan

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6
Q

9 hallmarks of aging is split into what 3 functional domains

A

genomic hallmarks
cellular hallmarks
biochemical hallmarks

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7
Q

what is in genomic hallmarks

A
  1. genomic instability
  2. epigenetic changes
  3. telomere attrition
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8
Q

what is genomic instability and treatment

A

[DNA damage over time by environment ie (UV radiation/free radicles) is linked to aging.]

increasing age-> changes in chromosome stability, nuclear architecture, mitochondrial DNA. Failure to remedy these changes-> cellular dysfunction. Accumulation=aging.

treat: elimination of damaged cells

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9
Q

what is epigenetic changes and treatment

A

[Aging is associated with
distinct epigenetic changes,
loss of DNA methylation,]
age-specific patterns of histone modification,
changes in enzymes expression that regulate DNA packaging and chromatin remodelling

impaired DNA repair and chromosome instability

treat: epigenetic drugs

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10
Q

what is Telomere attrition and treatment

A

[Telomeres, repeated DNA sequences at chromosome ends, shorten with each cell division, leading to aging when critical shortness is reached.]

however, some cells, like stem cells, express telomerase, maintaining telomere length. Experimental modulation of telomeres or telomerase can affect lifespan, suggesting a role in aging.

treat- telomerase reactivation

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11
Q

what is covered in cellular hallmarks

A

1.stem cell exhaustion
2. changes in cell signalling
3. cellular senescence

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12
Q

what is stem cell exhaustion and treatment

A

reduced regenerative potential of tissues->hallmark of aging.

reduced cell cycle activity in aged stem cells->divide less frequently -> contribute less to repair + tissue maintenance, resulting in aging.
stem cells accumulate mutations = formation of neoplasias.

treat- stem cell based therapies

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13
Q

Stem cell exhaustion- what does changes in HSC/MSC/Satellite cell and IESCs with age lead to

A

Haematopoietic Stem Cells
-anaemia

Mesenchymal Stem Cells
-osteoporosis

Satellite Cells
-decreased repair of muscle fibres

Intestinal Epithelial Stem Cells
-decreased intestinal function

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14
Q

Changes in cell signalling and treatment

A

[changes in inflammation, hormonal changes, and reduced immune system activity- internal environment is responsible for aging]

Senescent cells can influence the cells around them to enter senescence too (bystander effect)
Prevention of chronic inflammation-> poss inhibiting aging.

treat- anti-inflammatory drugs

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15
Q

what is bystander effect

A

influencing cells around to enter senescence too through communication to neighbouring cells via gap junctions

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16
Q

what is cellular senescence and treatment

A

[suppression of cell cycle]
halts cell cycle in response to DNA damage, preventing proliferation of dysfunctional cells.
removal of senescent cells by the immune system reduces cancer and aging risks.

Aging reduces stem cell activity, impairing replacement of removed cells.
Senescent cells secrete pro-inflammatory cytokines, accelerating aging.

treat- clearance of senescent cells

17
Q

what are considered in the biochemical hallmarks

A
  1. Impaired mitochondrial function
  2. Impaired proteostasis
  3. Impaired nutrient sensing
18
Q

what is impaired mitochondrial function and treatment

A

[mother’s mitochondrial DNA damage cause aging]

dysfunction increases ROS damaging cellular macromolecules.

treat- mitophagy

19
Q

what is Impaired proteostasis and treaetment

A

Proteostasis maintains protein folding via chaperones and targets unfolded proteins for breakdown,

impaired prosteostasis-> their persistence can lead to aggregation, disrupting cell function and contributing to age-related disorders like Alzheimer’s and Parkinson’s.

treat- activation of chaperones and proteolytic systems

20
Q

Impaired nutrient sensing and treatment

A

Mutations reducing the activity of the GH- like (IGF-1) pathway prolong lifespan in animals, but extremely low levels are deadly. Dietary restriction extends lifespan in animals by activating the AMPK pathway.

treat- dietary restriction

21
Q

What term describes the hallmarks of ageing which are the causes of damage which underpin ageing?

A

Primary hallmarks
ie. genomic instability

22
Q

what are the 9 hallmarks of aging

A

1.genomic instability
2.epigenetic changes
3. telomere attrition
4. stem cell exhaustion
5. changes in cell signalling
6. cellular senescence
7. impaired mitochondrial function
8.impaired proteostasis
9. impaired nutrient sensing