Cellular Ageing Flashcards
what are the characteristics of ageing and senescence
slow occrung process
compromises entire musculature leadings to frailty
unavoidable.
changes to HAIR
– Gradual thinning & graying of the hair results from a cessation of pigment production of both men & women
– Hair loss is cause by destruction of the germ centers that produce hair follicles
– Men usually do not lose facial hair as they age
– Women develop patches of hair on their face especially on their chin
changes to physical appearance
- In women, especially near menopause age as the ovary functions slow down then there can be more DHEA or androgens produced thus causing an increase in facial hair or hirsutism. As the woman begins to produce more androgens rather than estrogens she may begin to experience an increase in facial hair.
changes to skin
4 steps to make a wrinkle
• the outer layer of skin becomes thinner through cell loss
• the collagen fibers that make up the connective tissue lose much of their flexibility, making the skin less able to regain its shape after a pinch
• elastin fibers in the middle layer of skin lose their ability to keep the skin stretched out
• the underlying layer of fat, which helps provide padding to smooth out the contours, diminishes.
changes to body build
- A decrease in height
- Fluctuations in weight and shifts in body composition
- Muscle atrophy
- Compression of spinal vertebrae / can spinal deform and osteopeorosis of the spine
changes in the skeletal system
– The loss of bone
– Osteoporosis –defined as a decrease in bone mass & strength
– Osteoarthritis – a degenerative joint disease
• Osteoperosis is particular bad in women because of e2 where as men are protected to a degree from testosterone.
changes in the cardiovascular system
– The main function of heart is pumping blood
– Age-related structural changes in the heart
• the accumulation of fat deposits
• the stiffening of the heart muscle due to tissue changes
• Typically the left ventricle is less effective at pumping and accumulation of fat within the cardiomyoctyes – contributing to impaired ability to act As a pump
examples of cardiovascular disease
- Ischemic heart disease
- Cardiac Arrhythmias
- Angina -narorowing of vessles pain in heart and dwon the arms
- Myocardial infarction
- Atherosclerosis -plaque deposits impair blood flow and create further hypertension particually in arterioles
- Cerebrovascular Disease
- Hypertension
changes in the respiratory system
– Age-related to structural and functional
– With increasing age, the rib cage and the air passageways become stiffer
– Changes in the maximum amount of air we can take into the lungs in a single breath
– Respiratory disease
• Emphysema
changes In the reproductive system
– Women
• The major reproductive change in women during adulthood is the loss of the ability to bear children
• Begins in the 40s, as menstrual cycles become irregular and by the age of 50 to 55 it is usually complete - menopause
• A variety of physical and psychological symptoms
– Men
• Men do not have a physiological & cultural event to mark reproductive changes
• Do experience a normative decline in the quantity of sperm
changes in vision
• The major changes in visual functioning can be group into 2 classes :
I. changes in the structures of the eye
» disease: cataracts & glaucoma
II. changes in the retina
» usually begin 50s
» disease: macular degeneration & diabetic retinopathy (glucose impairs the small vessels behind the eye)
- Age related decrease in the ability to focus on nearby objects -presbyopia
- Age related decrease the ability to see detail and to discriminate different visual patterns -acuity
changes in hearing
greatest loss with high pitched tones / presbycusis
tinnitus can occur
inability to hear over background sound which is always present in the outside world
changes in taste
taste changes lead to a natural decline in appetite and therefore calorie intake
changes in smell
ability to detect doors remains in 60’s, until it then rapidly declines.
changes in the digestive system
eg intestine / gallbladder / liver
overall affecting macro intake for MPS and metabolic functioning leading to lack of substrates for new tissues (eg leaking protein into fences from inadequate absorption
how does telomere shortening cause cell senescence
somatic cells usually lack telomerase activity, meaning there telomeres shorten with each cell division
cells may go into crisis after reaching zero telomere length
reactivation of telomerase however ables cells to survive crisis and to become immortal
explain oxidative damage theory
95% off cells energy is produced in the mitochondria and therefore most oxygen is utilised there. however oxygen is damaging in high concentrations - being toxic to most animals and plants.
protein turnover requires ATP to bond AA covalently and therefore oxidative damage is hungering muscle mass down the line by interfering with MPS and MPB
What is the evidence for oxidative damage theory
house fly experiment example
or
correlations between species-specific levels of antioxidant defences and lifetime energy expenditure.
how would you test oxidative damage theory
- Construct long-lived and short-lived animals and then assay their antioxidant defense levels.
- Construct animals with genetically altered levels of antioxidant defense enzymes and then test for lifespan.
what is mitochondrial free radical theory
damage to mitochondrial genome, impairing mitochondria gene expression.
leading to inability of mitochondria to replicate and divide further leading to a reduction in energy production
with damaged mitochondria replicating taste retain than intact mitochondria.
- good to look at as, DNA is well preserved in mitochondria - genes are so few and and so not subject to great variation.
what Is altered protein theory.
changes to protein impairing cellular process in a progressive manner until submittal levels reached.
what can reduce protein function
post translational changes such as
- covalent modifications
- protein carbonyl levels raising
- protein modifications such as glycation
what is HAYFLICKS LIMIT
cells are only capable of a limited number of population doublings in culture
when is cellular senescence triggered
when cells acquire one or a few critically short telomeres
how does telomerase work
addition of TTAGGG repeats (hexameric) onto the telomeric ends of chromosomes, thus compensating for the erosion of telomeres that occurs in its absence
can telomerase give rise to more cancers
some cells are immortal because there telomerase is switched on eg blood cells and cancer cells.
evidence as to why telomeres can’t be the only reasoning behind cellular senescence
labs have mice with long telomeres such as 30-40kb but live much shorter than humans of 5-15kb telomeres
