The Molecular Basis of Aging & Disease Flashcards

1
Q

Define longevity

A

How long an organism lives

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2
Q

Define senescence

A

Time related deterioration

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3
Q

Define mortality rate

A

The probability of death in a given period of time

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4
Q

What is semelparity?

A

Genetically programmed senility and death after reproduction

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5
Q

Name a species which undergoes semelparity

A

Pacific salmon

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6
Q

What are the four distinct mortality phases in humans?

A

1) Raised mortality in infancy
2) low mortality until midlife (~60 years)
3) high mortality from midlife to old age
4) Reduced mortality in extreme old age

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7
Q

Name two ways to find out which genes protect/ promote aging, death and damage in life?

A

Genetic linkage studies and genome wide association studies

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8
Q

What kind of diseases of premature aging can be found using genetic linkage studies?

A

Monogenic, causal

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9
Q

What kind of diseases can be found using GWAS?

A

Complex with many SNPs and low effect size

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10
Q

What are progeroid syndromes?

A

A group of genetic disorders characterised by clinical features mimicking physiological ageing at an early age

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11
Q

True or false: Progeroid syndromes are monogenetic?

A

True

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12
Q

What is segmental progeria?

A

A progeroid disease affecting multiple tissues. It is autosomal recessive.
An example is Werner Syndrome (gene: WRN)

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13
Q

What is unimodal progeria?

A

A progeroid disease which affects one main tissue. It is autosomal dominant. An example is familial Alzheimer’s disease (gene: APP)

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14
Q

What is the most common feature of accelerated aging in progeroid syndromes?

A

A loss of genome integrity

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15
Q

What do progeroid syndromes tell us?

A

There are similarities between the molecular hallmarks of aging and human progeroid symptoms. There is a powerful argument that molecular defects which cause these syndromes are the major causative agents of agent.

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16
Q

What are the primary hallmarks of aging (causes of damage)?

A

Genomic instability, telomere attrition, epigenetic alterations and loss of proteostasis

17
Q

What are the antagonistic hallmarks of aging (responses to damage)?

A

Deregulated nutrient sensing, mitochondrial dysfunction and cellular senescence

18
Q

What are the integrative hallmarks of aging (culprits of the phenotype)?

A

Stem cell exhaustion and altered intercellular communication