aging and disease Flashcards
how senescence and apoptosis causes aging?
senecence= cells age and stop diving but do not die. the process of growing old
apoptosis = the death of cells
why do different species have a different lifespan and use example of naked mole.
due to different genomes
naked mole- survive 20 mins without oxygen.
they don’t age
rarely gets cancer due to high levels of DNA repair to maintain correct protein folding.
3 examples of age specific mortality in pacific salmon, drosophila fruit flies and humans?
salmon- semel parity= genetically programmed senility (physical and mental decline in old age) and death after reproduction
fruit flies- none live beyond 75 days
low mortality straight to high mortality.
humans- reduced mortality in extreme old age. due to genetics.
explain the relationship between aging and cancer, CHD, dementia and epilepsy.
cancer- biapahsic. declines at extreme old age
CHD- sex specific. not constantly increasing with age. declines at 95> extreme ages
dementia- not more common in female. just less males in population die to them dying from CHD
epilepsy-
not all diseases are age related
what is progeriod syndromes?
a group of genetic disorders that mimic physiological aging at an early age.
genome integrity is lost.
the definition of monogenic and complex trait
monogenic= genetic trait caused by one gene that causes age related traits e.g alzeihmers gene(APP)
autosomal recessive
complex trait- many SNP of trait with a mix of different alleles
e.g. Werners syndrome
autosomal dominant
what is the most common features of progeriod syndromes?
disruption in metabolism and genome integrity.
what mutated gene promotes the worm C.elegans longevity.
Age-1 doubles adult life expectancy by insulin signalling
explain how the worm c. elegans lives longer using
-alleles
-dauer Larvae
- age 1 and daf. 23 gene. (same gene just different alleles)
starved worm (Dauer Larvae live longer)
wild type allele= promotes death
recessive mutant allele= partial loss of function- doubles life expectancy
daf-23= makes Dauer larvae even with plenty food = lives longer
age 1= mutant doesn’t make dater larvae but does live twice as long.
how the dauer formation is regulated by the insulin signalling pathway by calorie restriction.
- insulin regulating receptor
-transcription gene
-AKT
receptor- DAF 2
transcription gene - DAF - 16
activated AKT due to calorie restriction - no insulin = DAF 16 tuned on
leads to PARTIAL LOSS OF FUNCTION mutation = dauer development
(if DAF-16 is on a bit = normal development = long lived)
(if DAF-16 is off = normal development = short life)
understand how telomeres are shortened by cell cycles and how they are grown?
-p53 gene
-telomerase
telomere dysfunction = senescent cells. old people have more senescent cells.
p53 gene= senescent cells through telomere shortening
once all repeats are gone this shortening continues and deletes genes. called senescent state.
due to p53 they have become senescent
how do we survive when telomeres are removed after every cell replication?
telomerase is an enzyme that grow new telomeres.
somatic cells don’t have temperas which protects them from cancer as cancer cells have telomerase.
what is the hay flick limit?
the limit on cell replication of somatic cells imposed by the shortening of telomeres with each division. This end stage is known as cellular senescence.
how is loss of protein homeostasis a key hallmark of aging
as protein aggregation causes misfolded proteins
how is alzeihmers and Parkinson’s disease characterised by neuropathological lesions?
alzheimers=
1) amyloid plaques
2) tau fibrils
3) mutations in tau gene are linked to other dementia
parkinsons=
1) Lewy bodies
