Biology of Ageing 1 Flashcards
specific types of intracellular degradation
aggrephagy
lysophagy
ribophagy
mitophagy
ferritinophagy
reticulophagy, nucleophagy
xenophagy
proteophagy
lipophagy
pexophagy
types of DNA repair that occurs in response to:
- base mismatch
- ss break/damage
- bulky lesion/crosslinks
- ds breaks
- base mismatch - mismatch repair
- ss break/damage - base excision repair
- bulky lesion/crosslinks - nucleotide excision repair
- ds breaks - homologous recombination/non-homologous end joining
what are the two main theories of ageing and what they mean
examples of each
program theories of ageing: fundamental limitation (telomere attrition, stem cell exhaustion)
damage theories of ageing: deterioration accumulation (mitochondrial dysfunction, chronic inflammation)
program theories of ageing
irreversible process controlled by internal factors that we can only slow down
damage theories of ageing
reversible process affected by external factors that can be rejuvenated when we remove the risk factors
how does deterioration accumulation lead to fundamental limitation
mitochondrial dysfunction leads to chronic inflammation
increased immune cell activation leads to proliferation and differentiation
leads to telomere attrition with every division
leads to stem cell exhaustion
primary hallmarks of ageing
genomic instability
telomere attrition
epigenetic alterations
loss of proteostasis
disabled macroautophagy
antagonistic hallmarks of ageing
cellular senescence
mitochondrial dysfunction
dysregulated nutrient sensing
integrative hallmarks of ageing
stem cell exhaustion
altered intracellular communication
chronic inflammation
dysbiosis
why do humans have longer spans than mice despite having shorter telomeres
shortening rate predicts species life span not starting length
methods of telomere length measurement
southern blotting gel
Q-PCR (due to repetitive DNA seq)
genome wide sequence
fluorescence in situ hybridisation
what happens when p53 is stabilised by mutation
what statement does this prove
remain cancer free for longer but die sooner due to senescence
tumour suppressors drive cellular senescence
early ageing-related phenotype mouse
reduced body size and kyphosis present (excessive rounding of upper back)
reduction in cortical bone thickness and absence of trabecular bone
osteoporosis and muscle atrophy so shape cannot be held well
beneficial consequences of cell senescence
embryonic development
wound healing and regeneration
tumour suppression
ambiguous consequences of cell senescence
reprogramming
deleterious consequences of cell senescence
tumour development
stem cell exhaustion
