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Biology Of Ageing Year2 > Age-related molecular disease > Flashcards

Age-related molecular disease Flashcards

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1
Q

What is incidence?

A

Number of new cases in a given time period.

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2
Q

What is the incidence rate?

A

Number of new cases/Number of persons at risk.

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3
Q

What is prevalence?

A

Total number of cases.

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4
Q

Prevalence rate?

A

Total number of cases/ Total population size.

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5
Q

What leads to a cancerous tumour?

A

An imbalance between apoptosis and and cell divsion.

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6
Q

How long does cancer take to develop?

A

Years to decades.

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7
Q

Where do cancers origanate from?

A

Single aberrant cell.

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8
Q

What is the affect of tumour supressing proteins on ageing?

A

Increases it.

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9
Q

What are 2 two types of cancer-critical genes?

A

Proto-oncogenes
Tumour suppressors

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10
Q

How do Proto-oncogenes cause cancer?

A

Mutated or overexpressed result in too much cell proliferation.

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11
Q

What was the first oncogene known?

A

Ras.

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12
Q

What are tumour suppressors?

A

Protects the cell from cancer.

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13
Q

What is gene X?

A

Tumour suppressor.

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14
Q

What happens when deletion or point mutation in coding sequences occurs?

A

Hyperactive protein is made in normal amounts.

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15
Q

What happens when a regulatory mutation?

A

Normal protein greatly overproduced.

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16
Q

What happens when gene amplification occurs?

A

Normal protein greatly overproduced.

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17
Q

What happens when chromosome rearrangement occurs?

A

Nearby regulatory DNA sequences cause normal proteins to be overproduced.
Fusion to actively transcribed genes produces hyperactive fusion protein.

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18
Q

How many mutations does it take for a somatic cell to become cancerous?

A

3.

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19
Q

What kinds of mutations lead to the overactivation of the cell cycle?

A

Ras or Myc.

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20
Q

What is the role of Rb?

A

Inhibits the cell cycle until cells are ready to divide.

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21
Q

How does the Rb control the cell cycle?

A

It is mutated which leads to the start of the cell cycle.

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22
Q

What happens when mitogenic signalling is excessive?

A

Inhibits the cell cycle.

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23
Q

Why is ageing a risk factor for cancer development?

A
  1. Time.
  2. Decline in quality control.
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24
Q

How can age-related decline in protein homeostasis contribute to cancer?

A

The gradual likelihood of mutations being accumulated as damaged protein isn’t being removed fast enough.

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25
Q

What is the function of p53?

A

Stops the cell cycle when cancer cells are formed.

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26
Q

What is diabetes?

A

A condition in which a person has high blood sugar.

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27
Q

What is type 1 diabetes?

A

The body does not produce enough insulin.

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28
Q

What is type 2 diabetes?

A

Cells do not respond to the insulin that is produced.

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29
Q

What are the risk factors for type 2 diabetes?

A

Genetic
Lifestyle
Age

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30
Q

What is insulin?

A

A hormone that is central to regulating energy and glucose metabolism in the body.

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31
Q

What is the function of insulin?

A

Causes cells in the liver, muscle, and fat tissue to take up glucose from the blood, storing it as glycogen in the liver and muscle.

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32
Q

What are the stages of insulin signalling pathways?

A
  1. Receptor binding
  2. Translocation of Glut-4 to the plasma membrane
  3. Glucose uptake
  4. Glycogen synthesis
  5. Glycolysis
  6. Fatty acid synthesis
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33
Q

What causes diabetes?

A

Mutations in genes.
Decrease in receptor concentration.
Excessive phosphorylation of IRS1.
Increase in oxidative stress.

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34
Q

What is IRS1?

A

Insulin receptor substrate proteins.

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35
Q

What are AGEs?

A

Advanced Glycation End-products.

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36
Q

What kind of reaction is AGEs?

A

Glycation reaction (addition of a carbohydrate to a protein).

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37
Q

What kinds of proteins does AGEs affect?

A

Proteins with long half-life.

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38
Q

What is the function of AGEs?

A

Makes proteins resistant to degradation.

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39
Q

What are the steps in the formation of AGE products?

A
  1. Formation of a Schiff base
  2. Formation of an Amadori product
  3. Amadori product is oxidised to produce AGE
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40
Q

What is the function of RAGE receptors?

A

AGE binding to RAGE receptors leads to increased oxidative stress and inflammation.

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41
Q

What is the molecular pathway activated by AGE at its normal levels?

A

Binds to AGER1 and then is degraded.

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42
Q

What is the molecular pathway activated by AGE at its increased levels?

A

Binds to RAGE receptors.
Upregulates pro-inflammatory signalling.
Increase in RAGE receptors.
Increase in inflammation and oxidative stress.

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43
Q

What are cardiovascular diseases?

A

Involving the heart or blood vessels.

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44
Q

What is Atherosclerosis?

A

The artery wall thickens due to the build-up of fatty materials such as cholesterol.

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45
Q

What is ischemia?

A

Insufficient blood supply to the heart due to blocked arteries.

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46
Q

What occurs in the body due to ischemia?

A

Cellular ATP decrease.
ROS production increase.
Mitochondrial dysfunction.
Activation of autophagy.

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47
Q

What is reperfusion?

A

Blood supply returns after ischemia.

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48
Q

What occurs in the body during reperfusion?

A

Oxidative damage
Inflammation
Cell death

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49
Q

What causes cardiovascular diseases?

A

Multiple mutations usually.
Oxidative stress.
Formation of cross-linked proteins (AGEs).

50
Q

What happens when the formation of cross-linked proteins occurs in arteries?

A

Stiffens the arteries which leads to higher pressure and results in the heart overcompensating.

51
Q

What are cataracts?

A

Clouding of the lens leading to loss of vision.

52
Q

Why do cataracts occur?

A

Lens proteins denature and degrade over time.

53
Q

What molecular mechanism result in cataracts?

A

Oxidative stress.
Protein aggregation.

54
Q

What is AMD?

A

Age-related macular degeneration.

55
Q

What is AMD?

A

Gradual loss of central vision.

56
Q

What are the types of AMD?

A

Dry and wet

57
Q

What is dry AMD due to?

A

Build up of waste products called drusen.

58
Q

What is wet AMD?

A

Abnormal blood vessels form under the macula and cause cellular damage.

59
Q

What are the causes of AMD?

A

Oxidative damage
Advanced glycation end products.
Loss of proteins homeostasis.

60
Q

What are Neurodegenerative diseases (proteinopathies)?

A

Range of diseases which mainly affect neurons in the human brain.

61
Q

What are the clinical features of Neurodegenerative diseases?

A

Movement disorder.
Dementia.

62
Q

What are the main pathological features of neurodegenerative diseases?

A

Loss of brain cells (neurons)
Protein aggregation

63
Q

What are the clinical features of Alzheimer’s?

A

Progressive dementia

64
Q

What are the clinical features of Parkinson’s?

A

Movement disorder

65
Q

What are the clinical features of Huntington’s disease?

A

Dementia
Motor and psychiatric problems.

66
Q

What are the affected regions of the brain during Alzheimer’s?

A

Hippocampus and Cerebral cortex

67
Q

What are the affected regions of the brain during Parkinson’s disease?

A

Substania nigra
Hypothalamus

68
Q

What are the affected regions of the brain during Huntington’s disease?

A

Striatum
Cerebral cortex

69
Q

What are the proteins involved in Alzheimer’s?

A

Amyloid-Beta
Tau

70
Q

What are the proteins involved in Parkinson’s?

A

Alpha-synuclein
Parkin
UCH-L1

71
Q

What are the proteins involved in Huntington’s disease?

A

Huntingtin

72
Q

What happens to the brain in dementia?

A

Loss of neurons and tissue from the brain in dementia.

73
Q

What happens to the brain during ageing?

A

It decreases in size.

74
Q

What happens when there is too much apoptosis in the body?

A

Oxidative stress
Excessive calcium influx
Mitochondrial dysfunction
Toxic proteins
P53 upregulated.

75
Q

What are the genetic factors that cause Alzheimer’s?

A

Small amounts due to inherited mutations most are sporadic.

76
Q

What are the genetic factors which cause Parkinson’s?

A

Some forms due to mutations in family.

77
Q

What are the genetic factors which cause Huntington’s disease?

A

An inherited mutation in Huntington’s disease.

78
Q

What kind of structures appear in Alzieher’s disease?

A
  • Extracellular amyloid plaques
  • Intracellular tau tangles
  • Neuritic plaques
79
Q

What are neuritic plaques?

A

Aggregation of altered glial cells and swollen dendrites containing abnormal tau protein.

80
Q

What is the effect of tau modification on aggregation?

A

Can now hyperphosphorylate and also be cleaved by caspases.

81
Q

What is the amyloid hypothesis?

A

The initial event which triggers neuronal degradation in Alzheimer’s disease is enhanced amyloid-β generation and aggregation.

82
Q

What are the aggregates in Parkinson’s disease called?

A

Lewy bodies

83
Q

What are Lewy bodies made up of?

A

α-synuclein
Ubiquitin
UCH-L1
Parkin (an E3 ligase)
Synphilin-
Tau

84
Q

What is α-synuclein encoded by?

A

SNCA gene

85
Q

How big is α-synuclein?

A

Small (14KDa) soluble protein

86
Q

What is α-synuclein?

A

Natively unfolded structure

87
Q

What is the function of α-synuclein?

A

Binds to membranes in a α-helical structure.
Regulate dopamine release.

88
Q

Where are α-synuclein?

A

Abundant in the brain – found at presynaptic terminals.

89
Q

What is α-synuclein degraded by?

A

Degraded by CMA and ubiquitin - proteasome pathway.

90
Q

What are the 2 types of arthritis?

A

Rheumatoid arthritis (RA)
Osteoarthritis (OA)

91
Q

What is RA caused by?

A

Inflammation

92
Q

When does RA occur?

A

Can occur at any age.

93
Q

What is OA?

A

A degenerative disease

94
Q

When does OA occur?

A

Incidence increases with age.

95
Q

What occurs at joints during OA?

A

Cartilage thins and bone ends rub together.

96
Q

What is the articular cartilage?

A

Mostly extracellular matrix.

97
Q

What does the extracellular matrix within the articular cartilage contain?

A

Aggrecan (proteoglycan) and collagen.

98
Q

What is cartilage homeostasis maintained by?

A

Growth factors and Cytokines

99
Q

What kinds of growth factor are used in cartilage homeostasis?

A

TGF-Beta and BMPs

100
Q

What kinds of cytokines are used in cartilage homeostasis?

A

IL-1, IL-6 and TNF-Alpha

101
Q

What is MMP?

A

Matrix metalloproteinase

102
Q

What is ADAMTS?

A

A disintegrin and metalloproteinase with thrombospondin motifs.

103
Q

What are the main molecular mechanisms of OA?

A
  1. Overproduction of cytokines
  2. Lower growth factor activity
104
Q

What is osteoporosis?

A

Normal gradual bone loss occurs at a faster pace.

105
Q

When does gradual bone loss begin?

A

From the age of 35.

106
Q

How much bone is replaced each year?

A

10% in adults.

107
Q

How is bone removed?

A

By resorption by osteoclasts

108
Q

What produces new bone?

A

Osteoblasts

109
Q

What kinds of signalling pathways allow maintenance of bone density?

A

Parathyroid hormone (PTH)
Wnt signalling
Growth hormones
Cytokines

110
Q

What is the function of PTH in bone remodelling?

A

Increases number and activity of osteoclasts.

111
Q

What is the function of Wnt signalling in bone remodelling?

A

Stimulates osteoblast activity.

112
Q

What is the function of bone hormones in bone remodelling?

A

Stimulates activity of osteoblasts and osteoclasts

113
Q

What is the function of cytokines withing bine remodelling?

A

Regulate different stages

114
Q

What is the function of cytokines withing bine remodelling?

A

regulate different stages

115
Q

What genetic factors lead to osteoporosis?

A

Mutations in LRP5
Polymorphisms in genes in Wnt pathway

116
Q

What is sarcopenia?

A

Sarcopenia results when there is an excessive loss of muscle mass.

117
Q

When does muscle mass begin to decline?

A

From the age of 25.

118
Q

At what rate does muscle mass decrease?

A

0.5-1% per year.

119
Q

What are the causes of sarcopenia?

A

Genetics
Reduced physical activity
Lack of repose to nutrients
Dysfunctional autophagy

120
Q

Can you think of the reasons for any of there co-morbidities?

A

Biology Of Ageing Year2 (23 decks)

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