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Human Development > The cellular aspects of ageing > Flashcards

The cellular aspects of ageing Flashcards

1
Q

what is ageing

A
  • Gradual and spontaneous changes occur in maturation from infant to adulthood, these changes underpin a normal physiological decline seen in middle and late adulthood
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2
Q

ageing is a

A
  • Ageing is a biological process not a disease
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3
Q

what are the consequences of ageing

A
  • Reduce tissue and physiological function
  • Decreased resistance to stress – physical and psychological
  • Increased susceptibility to disease
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4
Q

what are the two broad categories of ageing

A

cancer and degenerative disease

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5
Q

what are the degenerative diseases of ageing

A

Alzheimer’s, kidneys disease, heart disease, autoimmune disease, cogntivie decline

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6
Q

what levels does ageing occur at

A
  • Molecules
  • Cell
  • Tissues
  • Organs
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7
Q

how do cells respond to damage or stress

A

Cells respond to damage or stress via cell death (apoptosis) and arrested cell growth (cell senescence)

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8
Q

what are factors that influence life expectancy

A
  • Disease Processes
  • Medical Treatment
  • Lifestyle Choices
  • Nutrition
  • Heredity
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9
Q

what is tumour suppression genes

A
  • these are genes that have evolved to protect from cancer, they can cause the damage cells to die or arrest growth
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10
Q

How do you use genes to study ageing

A
  • Classic genetic approach

- Isolate and study mutants with altered ageing

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11
Q

what are the hallmarks of ageing

A
  • Telomere attrition
  • Cellular senescene
  • Mitochondrial dysfunction
  • Deregulated nutrient sensing
  • Loss of proteostatsis
  • Epigenic alterations
  • Genomic instability
  • Stem cell exhaustion
  • Altered intracellular communication
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12
Q

what does ageing result from

A
  • Cell intrinsic factors

- Cell extrinsic factors

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13
Q

what does the hay flick limit prove

A

cell senscene theory

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14
Q

describe how the hay flick limit works

A
  • They isolated fibroblasts from human tissue and put it in a cultred nutrient media
  • Cells divide and form a confluent layer
  • Discard half of cells and allow the rest to grow confluency
  • Fibroblast replication slows and stops at 50 passages
  • Cell have reached the hayflick limit and undergo replicative senescene
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15
Q

describe the action of telomerase in normal DNA replication

A
  • End of the chromosome is not cpopeid exactly which leaves an unreplicated gap
  • The enzyme telomerase filsl the gap by attaching bases to the end of the chromosome to exnted it and make it longer again
  • Telomerase keeps the telmoers longer to prevent information from being lost
  • Over time tleomerase levels decrease and the telmoers become hsorter and shorter
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16
Q

describe the telomeric theory of senescene

A
  • This is an extension of the hayflick limit
  • Telomeres are specialised DNA sequences at the end of the chromosomes
  • Non coding repeat of sequences TTA GGG
  • Telomeres shorten with each cell division
  • When the telomeres become too short the cells enters senescence
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17
Q

where are shortened telomeres found

A

– Atherosclerosis
– Heart disease
– Hepatitis
– Cirrhosis

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18
Q

describe how telomeric theory link to cancer

A

• 90% of cancer cells have been found to possess telomerase.
– Telomerase prevents the telomere from shortening.
– This allows the cancer cells to reproduce, resulting in tumor growth.
– Balancing act between cellular ageing and cancer

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19
Q

how does alternated intracellular communication lead to ageing

A
  • Signals between cells change over ageing
  • Biological clocks act through hormones to control the pace of ageing
  • The hormones affect growth, methabolism, temperature, inflammation and stress
  • For example menopause
20
Q

How does the immune system decline lead to ageing

A
  • A programmed decline in the immune system leads to an increased vulnerability to disease, ageing and death
  • Decrease in thymus dependent immunity and the hormones that are secreted by the thymus
21
Q

what is a free radical

A

• A free radical is a molecule with an unpaired, highly reactive electron

22
Q

what does a free radical do to cells and organs

A

• During aging, damage produced by free radicals causes cells and organs to stop functioning.

23
Q

name a type of free radical

A

• One type of very reactive free radical is the oxygen free radical, which may be produced during metabolism or as a result of environmental pollution.

24
Q

how do mitochondria cause free radical damage

A

Mitochondria – get electron leaks, these generate free radicals, they cause damage and it carry’s on and on
Reactive oxygen species (ROS) are produced predominantly as a result of electron ‘leak’ during mitochondrial oxidative phosphorylation.
Mitochondrial dysfunction that occurs with ageing results in increased production of ROS

25
Q

what are the bodys defence system to free radicals

A

– Natural antioxidants in the body, such as bilirubin.
– Enzymes such as superoxide dismutase (SOD), catalase, & glutathione peroxidase.
– Dietary antioxidants such as beta carotene, and the vitamins C and E.

26
Q

How do the antioxidant works

A

they have a large number of electron in the shell, they donate an electron to the oxygen free radical and stablise the free radical

27
Q

what do we use free radical for

A

immunological response system.

28
Q

how are free radicals used in the immunological response system

A
  • Macrophages engulf bacteria

- Free radical reactions produced inside the macrophage oxidize and kill bacteria

29
Q

what is autophagy

A

– this is a intraceullar degradation system that delivers cytoplasmic constituents to the lysosome

30
Q

what is used to degrade and get rid of the unfolded protein

A
  • Autophagy and proteasomal degradation get rid of the unfolded protein
31
Q

how can an unfolded protein get refolded

A

chaperones

32
Q

what does aggregation lead to

A

leads to ageing

proteins

33
Q

what does cross linked proteins result in

A
  • The accumulation of cross-linked proteins damage cells and tissue slowing down bodily processes
34
Q

give an example of a disease that can be caused by cross linking proteins

A

Alzheimers disease

  • Aggregation and cross linking of the beta amyloid protein
  • Also get crossing linking which makes it harder to get rid of

Another example
- Non-enzymatic glycosylation reactions occur when glucose molecules attach to proteins causing a chain of chemical reactions resulting in a structural change to the proteins.

35
Q

what are the consequences of cross linking proteins

A
  • Loss of flexibility of connective tissue

- Microvascular changes in arteries

36
Q

what is genomic instability

A
  • Refers to a high frequency of mutations within the genome
37
Q

when does a somatic mutation result from

A
  • Ageing results from an imbalance between the rate of DNA repair and accumulation of DNA damage.
  • When the damage exceeds repair, the cell malfunctions
38
Q

what are the factors of ageing

A
  • Mulfacturial
  • Progressive
  • Deleterious
39
Q

what is nutrient sensing

A
  • Nutrient sensing is a cell’s ability to recognize and respond to fuel substrates such as glucose.
  • Homeostatic mechanisms respond to different hormones (e.g. insulin; IGF-1) to maintain blood glucose at physiological levels
40
Q

what happens to nutrient sensing during ageing

A
  • In old age, these mechanisms become disrupted and result in consequences which underpin disease including:
  • Reduced insulin sensitivity resulting in glucose intolerance
  • Increase in visceral fat mass
41
Q

what postpones senescene

A

Caloric restriction postpones senescence
- Food restricted rats show less evidence of cancer, atherosclerosis,
and autoimmune disease.

42
Q

name some process fo epigenetic alternations

A 
DNA methylation 
Chromatin structure 
Histone modification 
Regulatory RNA 
Spatial organisation of chromosomes
43
Q

what does stem cell exhaustion of … lead to

  • HSCs
  • MSCs
  • satellite cells
  • IESCs
A
  • anaemia and myelodysplasia
  • oeteoporosis and decreased fracture repair
  • decreased repair of muscle fibres
  • decreased intestinal function
44
Q

what are the ways that we can reverse ageing

A

– loose stem cells, eliminate damaged cells, epigenetic drugs – can reverse some of the changes, activate chaperones to reactivate the proteins, telomerase reactivation, elimination of damaged cells

45
Q

what happens to hearts as we age

A
  • The valves of the heart thicken and become stiffer.
  • The number of pacemaker cells decrease. Fatty & fibrous tissues increase about the sinoatrial (SA) node. Slightly slower heart rate.
  • The heart wall thickens, so the amount of blood that the chamber can hold may actually decrease.
  • The heart may fill more slowly.

Human Development (28 decks)

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