B io Factsheet
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Number 147
Ageing
•
An adult organism is not a static being but continues to change and develop,
until the developmental processes are brought to an end by death. The
word ‘ageing’ describes the developmental changes that lead, over time,
to the deterioration of the mature organism and finally to the organism’s
death. Ageing is a complex process which involves interactions between a
number of biochemical mechanisms. The effects of these act at the molecular,
cell, tissue and whole organism levels.
The complex of interacting ageing processes that lead to death is called
senescence. Ageing:
• is species specific – it seems to be an inborn property which results in
particular species having particular life spans; For example, at 5 years
old a human baby’s tissues will still be growing and differentiating,
whereas 5 year old mouse tissues will be fully mature and showing
signs of ageing/deterioration;
• correlates with the organism’s investment in repair, particularly in
DNA repair.
• is affected by diet and by exercise. The ageing processes appear to be
slowed by having a good diet and by regular exercising.
DNA damage may occur due to somatic-cell mutations which occur
during the normal cell divisions which enable growth, repair or
replacement of tissues. These somatic-cell mutations may be triggered
by exposure to radiation, particularly the background cosmic and Xradiation.
Long-lived species counteract this by having high levels of DNA repair
enzymes and they invest much energy in maintaining the stability of
their DNA.
Short-lived species, which have early ageing, have low levels of DNA
repair enzymes and invest little energy in maintaining the stability of
their DNA.
•
•
Fig. 2. Activity of DNA repair systems in different mammals
Mean lifespan /years (log scale)
100
Exam Hint: If you are asked to write an essay on ageing, it is important
to distinguish the normal process of ageing, which occurs in healthy
organisms, from premature ageing caused by disease and
associated pathological changes. Normal ageing processes can be
modified and accelerated by pathological processes. Do not be drawn
into writing an essay about disease and death.
The fact that ageing and longevity (length of life) is characteristic to particular
species suggests that ageing and longevity are determined by genes:-
Human
Elephant
Horse
Longer-lived mammals
invest more energy and
materials in repair enzymes
and processes
Dog
10
Hamster
Rat
Mouse
Shrew
Thus, there is a general trend – larger animals tend to have longer lifespans
than smaller animals. There is thought to be a genetic trait, related to the
ability of the organism to repair DNA damage which occurs throughout life.
0
Relative DNA repair activity
0
Primates
Carnivores
Galapagos tortoise
Ungulates Rodents
Animals
1
Nile crocodile
Birds
Frog
10
Sparrow
Horse
20
Domestic cat
30
Domestic dog
40
Brown bear
50
Gorilla
60
Herring Gull
70
Mouse
80
Brown rat
90
Elephant (Indian)
100
Modern human
Fig 1. Mean normal lifespan of some animal species
Reptiles
Amphibians
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147 Ageing
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Examples of genetically coded detoxification enzymes produced by
mammals (and by many other groups of organisms) include peroxidases,
alcohol and lactic dehydrogenases and transdeaminases.
A similar pattern exists for the genetic coding and production of antioxidant
molecules in different species.
• Antioxidants detoxify dangerous chemicals (free radicals) that are byproducts of certain metabolic processes. They can cause molecular/
DNA/RNA damage resulting in deterioration of cells, tissues or whole
organisms. The damage caused may contribute to the ageing process.
during cell
metabolismmitochodria
convert glucose
into energy
Glucose
Remember - some dietary constituents also have excellent antioxidant
properties. For example, vitamins A, C and E. As well as their probable
action in slowing the ageing process, there is considerable statistical
evidence to show that a normal intake of these vitamins gives some
protection against developing certain cancers (bowel and bladder) and
cardiovascular disease.
Oxygen
The fact that offspring of long-lived parents tend to have long lives supports
the idea that ageing has a strong genetic component, simply because offspring
inherit their genes from their parents.
Mitochondria
Further evidence for a genetic component in ageing comes from the study
of identical twins. Identical twins (with identical genomes) tend to age in a
similar fashion and at a similar rate. For example, they tend to develop
similar skin lines and creases at similar ages, and their eyesight and hearing
ability becomes similarly impaired at similar ages.
Cell
membrane
Chromosome
Nucleus
Oxygen
radical
cell membrane
damage
energy released
energy and oxygen
radicals formed
So to summarise the evidence that ageing has a genetic component (Fig 3).
Fig 4. Evidence that ageing has a genetic component
Offspring live long if parents do
DNA damage in
mitochondria
Oxygen radical damages
cell membrane, DNA in
mitochondria and DNA
damage in nucleus
DNA damage in
nucleus
•
Species have
characteristic
longevity
For example, highly reactive products like hydrogen peroxide, if not
destroyed quickly, will cause cell damage and deterioration. Hydrogen
peroxide is detoxified by peroxidase enzymes.
2H2O2
2H2O +
High levels of anti-oxidant =
long life (production of antioxidants is genetically
controlled)
O2
peroxidase (catalase)
•
Evidence that ageing is
partly controlled by genes
Long-lived organisms maintain high concentrations of antioxidant
molecules and expend much energy in cellular detoxification whereas
short-lived species do not. Fruit flies bred with a gene that produced
higher levels of an antioxidant (superoxide dismutase or SOD) lived
longer than those without the antioxidant (Fig 3).
Identical
twins age
similarly
High levels of DNA/RNA
repair enzyme = long life
(production of antioxidants is genetically
controlled)
The effects of ageing: senescence
As animals age, they tend to become physically weaker and various
physiological processes decline. Senescence effects all parts of the body,
including the brain. Some of the changes are listed in the table below:
Fig 3. SOD1 flies
Table 1. Average decline in a human male from ages 25 to 75 years
100
Characteristic
90
Survivorship (percent)
80
Peak bone density
Percentage
decline
30
70
Weight of brain
44
60
Number of neurones in spinal cord
37
Velocity of nerve impulses in myelinated neurones
10
Blood supply to cerebral hemispheres
20
SOD1 flies
Normal files
50
40
30
Number of taste buds
64
Power of accommodation (focussing)
45
Cardiac output at rest
30
20
Vital capacity of lungs
44
10
Number of nephrons in kidneys
44
Maximum glomerular filtration rate
30
Maximum O2 uptake during exercise
60
0
0
10
20
30
40
50
60
Life Span (days)
70
80
90
2
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147 Ageing
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As a human grows older:•
•
•
• The immune system becomes less efficient so the likelihood of
suffering disease and disability increases. Ultimately the person
is confronted with a situation to which there is no effective
response and death occurs.
Cataracts develop - lens becomes more opaque, scattering
light, and eventually leading to blindness causing visual
impairment
Glaucoma - involves structural changes of the optic
nerve as a result of increasing pressure in the eye.
This happens when the aqueous humor is prevented
from draining from the eye properly
Muscle mass decreases, the speed and strength of
muscles decreases and the number of muscle fibres
decreases. Bones become more brittle and break
more easily.
•
Falls in the level of sex hormones may have side
effects which can cause ageing effects. In women
particularly, after the menopause, the fall in
oestrogen levels may result in loss of calcium from
bones. This can cause development of brittle bones
and osteoporosis. Women may be given hormone
replacement therapy (HRT) to counteract this.
•
Physiological processes that maintain our organs and
systems become less sensitive, less accurate and slower.
•
Nervous reaction times become slower.
•
Maximum heart rate is lowered by about one beat for each
year a person ages, and the resting heart rate also declines.
•
Basal metabolic rate (BMR) declines - after the age of 60,
BMR slows down at a rate of about 3% each year.
• As cells age they tend to accumulate more metabolic
wastes, for example, highly reactive peroxides which may
cause cell deterioration. Ageing cells tend to synthesise
less antioxidant molecules, which destroy the damaging
wastes, than younger cells and so cell damage is more
likely in ageing tissues.
•
The number of nerve cells in the brain declines
with age and so the brain becomes smaller. Nerve cells in
the brain either cannot regenerate or do so very slowly.
Thus dead or damaged brain cells are not replaced as
quickly as they are lost. The brain of a 90-year-old
probably has about 10 per cent fewer nerve cells than the
brain of a 30-year-old.
Because of the loss of brain cells, one might think that brain
function would also decline with ageing, but this is not
necessarily so. Providing certain pathological conditions,
for example, senile dementia, are absent, although a small
degree of memory loss often occurs, some intellectual skills
can actually increase with age and gaining experience. Many
biologists believe that a decrease in brain function is not an
inevitable result of ageing. It is probable that memory loss,
personality changes, and other malfunctions are due to disease
processes which might be treated or even prevented.
Senile dementia and Alzheimer’s disease
Senile dementia is a progressive loss of intellectual abilities which usually
starts after the age of 65. It is characterised by:
•
•
a gradual decline in reasoning powers,
•
•
memory loss, which eventually may become severe,
•
a tendency to be easily confused,
•
personality changes.
Alzheimer’s disease is now thought to be caused by a variety of factors,
both genetic and environmental. There is often a family history of the
disease suggesting a strong genetic component. It is now known that
exposure to aluminium is not a causative factor.
Alzheimer’s disease is the fourth biggest killer in economically developed
countries after heart disease, cancer, and stroke.
Further Reading
Scientific American Vol 14 No. 3. 2004 - The Science of Staying Young
Senile dementia is a symptom of a variety of diseases of which Alzheimer’s
disease is the commonest.
In Alzheimer’s disease there is a gradual build-up of:
•
an insoluble, abnormal protein, called beta-amyloid, which forms
deposits called plaques outside neurones,
•
a protein, called tau, which becomes abnormally, highly phosphated
and forms tangles within the nerve cells. The tangles interfere with the
functioning of the normal microtubules of the nerve cells.
•
The neurons most affected are in the cerebral cortex (memory) and in
the hippocampus (memory and personality)
Acknowledgements:
This Factsheet was researched and written by Martin Griffin.
Curriculum Press, Bank House, 105 King Street, Wellington, Shropshire, TF1 1NU.
Bio Factsheets may be copied free of charge by teaching staff or students, provided that their
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permission of the publisher. ISSN 1351-5136
3
Bio Factsheet
147 Ageing
www.curriculum-press.co.uk
Specimen questions
1. (a) Define the terms ‘ageing’ and ‘senescence’.
Answers
2
1. (a) ageing describes the developmental changes that lead, over time, to
the deterioration of the mature organism and finally to the organism’s
death;
senescence is the complex of interacting ageing processes which
eventually lead to death;
2
(b) Suggest four reasons for thinking that ageing processes are partly
genetically controlled.
4
(c) A suitable dietary intake of vitamins A, C and E are thought to
slow the ageing process. Suggest why.
4
Total 10 marks
(b) identical twins age at similar rates and in similar ways;
long-lived families tend to have long-lived offspring but shortlived families tend to have short-lived offspring;
ageing is species specific and species are characterised by their
genes/DNA;
organisms which activate their genes which synthesise DNA repair
enzymes tend to live longer than organisms which do not invest in
DNA repair;
organisms which activate their genes to synthesise antioxidant
molecules tend to live longer than organisms which do not;
max 4
2. Suggest explanations for each of the following:
(a) The average length of life of human red blood cells is 120 days but
humans live for many years.
2
(b) A person who is alcoholic may suffer liver damage leading to
replacement of normal liver cells with fibrous tissue. The remaining
undamaged liver cells age more rapidly than liver cells in a person
of similar age who is not alcoholic.
2
(c) The percentage of women in the 30 to 39 age group who break a
femur is only 0.01%.
The percentage of women in the 60 to 69 age group who break a
femur is 2.7%
2
(c) vitamins A, C and E have strong antioxidant properties;
metabolism produces free radicals/oxidising agents;
these can damage cells/cause deterioration of tissues and so speed
up ageing;
antioxidants destroy the free radicals before they can cause serious
harm;
4
Total 10 marks
(d) The brain becomes smaller during ageing yet intellectual ability
may not decline.
2
Total 8 marks
3. The graph below shows the expected life spans of modern humans and
stone-age humans.
2. (a) individual cells and tissues in the body do not live as long as the
organism;
regeneration/replacement occurs/most body cells are regularly
replaced by mitosis and differentiation;
2
Proportion of population surviving of birth population /%
100
(b) the number of healthy liver cells in the alcoholic person is greatly
reduced;
but they still have to cope with the workload of a normal liver and
so become ‘worn out’ more quickly;
2
75
50
(c) in post-menopausal women the levels of female sex hormones
decrease;
a side-effect of this is that calcium leaches out of the bones which
thus weaken/ref brittle bone disease/osteoporosis;
2
25
(d) the number of neurones in the brain decreases during ageing and
thus the brain becomes smaller;
but experience and accumulated knowledge may enable the remaining
neuronal circuits to work more efficiently;
2
Total 8 marks
3. (a) few, if any, Stone-age humans lived beyond the age of 40 but over
85% of modern humans live beyond the age of 40;
the greatest death rate in Stone-age humans occurred over the first
10 years of life, when 50% of the population died;
the greatest death rate in modern humans occurs between the ages
of 60 and 80, when about 60% of the population die;
3
0
0
20
40
Age/years
60
80
(b) because ageing processes are partly controlled genetically they are
probably similar in Stone-age humans and modern humans;
thus other factors are probably causing early death in Stone-age
humans/longer life in modern humans;
reference to Stone-age humans having a poor diet compared with
highly refined, varied,
nutritious modern diets/ Stone-age humans were hunter-gatherers
and so expended a lot of energy and time to obtain enough food;
reference to disease –Stone-age humans had few cures and no access
to the drugs and medical care available to modern humans;
Stone-age humans were more at risk of injury/death due to accidents
(when hunting) and due to attack by predators than modern humans;
5
Total 8 marks
(a) Describe the differences between the two sets of graphical data.
3
(b) Suggest reasons for the differences between the two sets of data.
5
Total 8 marks
4