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biological system Flashcards

1
Q

aging is accompanied by a number of universal and anticipated changes to biological systems

A

cardiovascular, digestive, endocrine, immune, nervous, integumentary, musculo-skeletal, reproductive, respiratory, urinary

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2
Q

Cardiovascular

A

Thickening left ventricle wall resulting in larger, less efficient heart; reduced and irregular heartbeat; reduced elasticity of arteries

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3
Q

digestive

A

Weakened esophageal contractions;esophageal sphincter; reduced elasticity of stomach; increased vulnerability to lactose intolerance

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4
Q

endocrine

A

Reduced reproductive hormones, reduced thyroid hormone; insulin resistance

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5
Q

immune

A

Increased vulnerability to infection (produces less proteins); increased autoimmune responses (body attacks itself; ie arthritis); reduced responsiveness to vaccinations

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6
Q

Nervous

A

Reduced visual(eyes become more yellow)/auditory(loss of hearing)/tactile acuity; decreased olfactory and gustatory sensitivity; structural and functional changes to brain;

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7
Q

integumentary

A

Thinning of epidermis, dermis, subcutis, reduced elasticity of skin, reduced ability to filter UV radiation

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8
Q

musculo-skeletal

A

Reduced bone density, muscle mass, increased rigidity of ligaments, tendones; thinning of cartilage

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9
Q

reproductive

A

Menopause (decreased estrogen production); “andropause”; changes in sexual functioning

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10
Q

respiratory

A

Reduced peak air flow; reduced gas exchanges; increased breathlessness

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11
Q

urinary

A

Reduced kidney size, increased rigidity and decreased capacity of the bladder; urinary incontinence

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12
Q

With respect to structural changes to brain; research has demonstrated brain atrophy with age:

A

Decreases in volume of 0.2% per year after age 35 and 0.5% per year after age 60
Shrinkage of gryi and widening of sulci
Shrinkage of specific regions (vulnerable regions include: prefrontal cortex, hippocampus, cerebellum)

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13
Q

Age related structural changes to brain

A

Shrinkage of gyri (outward folds)
Widening of sulci (inward folds)
Shrinkage of prefrontal cortex
Shrinkage of hippocampus (memory)
Shrinkage of cerebellum

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14
Q

1)Dopamine

A

Associated with attention, memory, movement, reward/reinforcement

produced in substantia nigra and ventral tegmental area (VTA) in midbrain

Evidence suggests dopamine functionality decreases with age

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15
Q

Decreases across the dopamine system (ie:receptors, synthesis capacity, transporters) range from —-per decade between young adulthood and older adulthood

A

3.7-14%

Transporter on presynaptic cell takes back some dopamine that is not reuptaken

Synthesis of dopamine decreases the lease/remains stable

Largest decline in Transporters (reduction of 14%)

Reuptake of dopamine decreases

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16
Q

2)Serotonin

A

Associated with mood, feeding, sleep, sexual behavior

Produced in the raphe nuclei of brainstem

2 billion neurons in our brain associated with the use of serotonin

Evidence suggest serotonin functionality decreases with age

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17
Q

Decreases across the serotonin system range from —- per decade between young adulthood and older adulthood

A

1.5-7%

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18
Q

Despite structural and functional changes noted above, research has demonstrated ongoing —–of the brain in older adulthood

A

neuroplasticity

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19
Q

Neuroplasticity(brain plasticity);

A

examples include development of new neurons (in hippocampus,olfactory bulb) and neuronal connections/synapses

As we get older we are still able to create new synapses

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20
Q

theories proposed to explain biological aging

A

1)genetic theories of aging
2)telomere theory of aging
3)free radical theory of aging

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21
Q

genetic theory of aging

A

aging is determined by genes that influence longevity and disease

aging is observed by majority of species

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22
Q

Maximum life span for various species:

A

correlation between brain size and lifespan( bigger brain=higher life span)

Small correlation between body size and lifespan (bigger bodies have shorter life span)

High Metabolic rate tend to have shorter life spans (loose negative correlation)

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23
Q

Gompertz law:

A

human mortality rate doubles every 8 years

Suggesting genes play a role in our life span

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24
Q

Maximum life span for humans is 122 years, where max life span of chimpanzees is 37 years.

A

Given that these two species share 98% of their DNA, scientists have suggested that relatively small number of genes influence aging

25
Q

Examples of genes that are associated with longevity:

A

1)apoliproprotein E (APOE) gene
2)Forkhead BOX O (FoxO) gene

26
Q

Apolipoprotein E (APOE) gene:

A

located on chromosome 19; associated with lipid transport and repair of brain injury

27
Q

Forkhead Box O (FoxO) gene:

A

located on chromosome 6; associated with apoptosis, autophagy, and tumor suppression

28
Q

FoxO 3

A

Allele 3 (FoxO 3)appears to be associated with longer life span (more likely to be found in centenarians and supercentenarians)

29
Q

Apoptosis (FoxO)

A

organized (systematic) cell damage (cells commit suicide)

30
Q

Autophagy

A

utilizes intracellular materials, brakes them down, and recycle for use WITHIN the cell

31
Q

Tumor suppression:

A

cancer (uncontrolled division of cells)

32
Q

Examples of genes associated with disease

A

1)kidney and brain expressed protein (KIBRA) gene
2)Lipoprotein A (LPA) gene
3)SH2B adapter protein 3 (SH2B3)

33
Q

——– of variance of longevity in humans is due to genes; as we get older, genes play more important role of influencing aging

A

25-30%

34
Q

Gene wide association study (GWAS)

A

looks at whole genome and looks for variance of genes between people

35
Q

Candidate genes study

A

looks at how a candidate genes functions in individuals in relation to aging

36
Q

interventions to combat age-related diseases and reduced life span

A

1)gene therapy

37
Q

gene therapy

A

replace bad DNA with good DNA through genetic engineering

We create DNA that has good allele and then transfer DNA to host

38
Q

1st way of gene therapy

A

injecting DNA in bloodstream and absorbed by cells

39
Q

2nd way

A

inject DNA in tissue and hope it replicates the good DNA

40
Q

3rd way (most popular):

A

create good DNA and attach it to a virus, virus create beneficial DNA and enters cells of host (virus introduces good DNA into the host)

41
Q

Telomere theory of aging:

A

aging is determined by telomeres and their impact on cellular division

42
Q

Hayflick limit (telomere theory)

A

cells undergo a finite number of divisions; the number of possible divisions declines with age

Lung tissue of older adults could only divide 20 times

43
Q

cellular senescence

A

Cells that no longer divide are in a state of arrest and adopt a new form called senescence-associated secretory phenotype (SASP)

44
Q

The stopping of cellular division is associated with—–

A

telomeres

45
Q

SASPS

A

remain active and secrete molecules that promote inflammation, alter structure of surrounding tissues, and stimulate growth of malignant cells

SASPs diffuse bad molecules into our tissues/cells

46
Q

SASPS —– as we age

A

accumulate

Moreover, SASP- like cells are found in affected tissues of patients with age-related diseases (ie osteoarthritis, atherosclerosis, alzheimer’s)

47
Q

where are telomeres located

A

non coding portion at the end of chromosomes; they protect the ends of chromosomes from DNA degradation and fusion with other chromosomal ends

48
Q

telomeres are —— as we get older

A

decreasing in length

49
Q

what can telomeres do?

A

Telomeres give us the opportunity to extend life span potentially

researchers are investigating interventions (telomere gene transfer) to combat telomere shortening

50
Q

Free Radical theory of aging

A

aging is determined by reactive oxygen species which cause cumulative damage to cells

51
Q

Reactive oxygen species (ROS)

A

chemically reactive oxygen-containing molecules (ie oxygen radicals)

52
Q

where is ROS generated?

A

The majority of ROS are generated by mitochondria as byproducts of adenosine triphosphate (ATP) production: ATP is the main energy source of ells

53
Q

what do ROS do?

A

ROS attack and damage cellular macromolecules including proteins (protein fragmentation)

lipids (“leaky” cellular membrane:transport across our membranes are affected and resulting in loss of beneficial molecules)

and DNA

54
Q

With age, damaged cellular macromolecules accumulate due to

A

increased production of ROS, decreased efficiency of repair systems, or both

Accumulation of damaged cellular macromolecules by ROS ultimately leads to cell death

55
Q

Interventions for ROS

A

With respect to caloric restriction as an intervention, research in varied species (ie fish, hamsters, rats, dogs) has demonstrated than a 20-40% decrease in caloric intake reduce the onset of age-related diseases (cancer, cardiovascular disease) and increase life span by 20-50%

56
Q

Caloric restriction

A

When we reduce calories, metabolism slows down, we reduce the accumulation ROS, leads to less macromolecule damage (controversial method)

57
Q

With respect to functional changes to the brain, research has demonstrated changes in neurotransmitter with age

A

Neurotransmitter: chemical that enables the transmission of nerve
impulses between neurons

receptor(binding site for neurotransmitters on receiving cell)

58
Q

studies that have excluded participants with cardiovascular risk factors or Covert brain disease have failed to reproduce some of these findings

A

covert brain disease: disease that has not yet become apparent

studies have excluded participants with these conditions have shown little or no deterioration of gray matter

59
Q
A

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