The pathology of ageing Flashcards
How does a cell’s division capability change over time
Progressively undergoes fewer divisions
What is a hay flick limit
This is the maximum number of cell divisions in a species
What type of mammals tend to have high hay flick limits
Those with a larger lifespan
What metric does the hay flick limit define
The shortening of the telomeres with each successive division
Why are short-lived cells less effected by debris than longer-lived cells
They divide cytoplasmic debris with each of their daughter cells. This does not happen with long-lived cells
Where does accumulated cytoplasmic debris originate from
- Peroxidation of lipids forms indigestible lipofuscin
- Intracellular aggregates of defective proteins
- Defective mitochondria
What is the inbuilt genetic mechanism of aging theory (clonal senescence)
- Genetically we have an allowed lifespan that is finite
Why do no wild animals live to the allowed lifespan of the genetic raging theory
Due to predation, infections and accidents
Describe the replication senescence
- Some cells stay with us from birth to death and we lose these cells during our daily life
- Accumulation of lethal damage causes whole organism to succumb (e.g. CNS and cardiac)
What is an accumulation of ‘lethal damage’
Cross-linking between proteins and DNA
Damage to mitochondria
Where do free radicals form
- Macrophages
2. Neutrophils
How does defective repair result in raging
- Hayflick phenomenon states cells can only divide a limited number of times under genetic control
- If i damage the gastric mucosa, there may come a time where the cells can no longer replicate to heal the ulceration
How does telomeric shortening cause ageing
- Become too short that DNA polymerase in unable to find the start position for transcription
- Associated with hay flick limit of cells
What is sarcopenia
Part of the frailty syndrome
- Reduced metabolic rate
- Chronic poor nutrition
- loss of muscle
How does skin age
- Loss of elastic recoil due to less collagen and elastin