Unit 2 Biological systems Flashcards

How do our Biological systems change as we age?

1
Q

What are some examples of age-related changes in the cardiovascular system?

A

Thickening of the left ventricle wall, reduced/irregular heartbeats, and reduced elasticity of arteries.

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2
Q

How does aging affect the digestive system?

A

Weakened esophageal contractions, reduced elasticity of the stomach, and increased vulnerability to lactose intolerance.

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3
Q

Name some age-related changes in the endocrine system.

A

Reduced reproductive hormones, thyroid hormone, and increased insulin resistance.

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4
Q

How is the immune system affected by aging?

A

Increased vulnerability to infection, increased autoimmune responses, and reduced responsiveness to vaccinations.

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5
Q

What changes occur in the integumentary system with age?

A

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

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6
Q

List some age-related changes in the musculoskeletal system.

A

Reduced bone density, reduced muscle mass, increased rigidity of ligaments and tendons, and thinning of cartilage.

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7
Q

How does aging affect the reproductive system?

A

Menopause, “andropause,” and changes in sexual functioning.

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8
Q

What are some respiratory system changes due to aging?

A

Reduced peak airflow, reduced gas exchange, and increased breathlessness.

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9
Q

How does aging impact the urinary system?

A

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

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10
Q

What changes occur in the nervous system with aging?

A
  • Reduced visual/auditory/tactile acuity (our lenses become more yellow, hair cell sin ear lessen so can’t hear high frequency, lower balance,
  • decline in ability to taste sweet and salty) - decreased olfactory and gustatory sensitivity,
  • STRUCTURAL AND FUNCTIONAL CHANGES TO THE BRAIN
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11
Q

What is dopamine associated with?

Where is dopamine produced in the brain?

How does dopamine functionality change with age?

A

Dopamine is associated with attention, memory, movement, and reward/reinforcement.

Dopamine is produced in the substantia nigra and ventral tegmental area (VTA) in the midbrain.

Dopamine functionality decreases with age, with reductions in receptors, synthesis capacity, and transporters (are on the presynaptic and reuptakes dopamine) ranging from 3.7–14% per decade from young adulthood to older adulthood.

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12
Q

What is serotonin associated with?
Where is serotonin produced in the brain?
How does serotonin functionality change with age?

A

Serotonin is associated with mood, feeding, sleep, and sexual behavior.

Serotonin is produced in the raphe nuclei of the brainstem.

Serotonin functionality decreases with age, with reductions in receptors, synthesis capacity, and transporters ranging from 1.5–7% per decade from young adulthood to older adulthood.

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13
Q

What is neuroplasticity?

A

Neuroplasticity, or brain plasticity, refers to the brain’s ability to change its structure and function in response to learning and experience, such as the development of new neurons and neuronal connections.

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14
Q

What are some environmental interventions that support neuroplasticity in the aging brain?

A

Environmental interventions that support neuroplasticity include diet, enriched environments, exercise, and training programs.

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15
Q

Structual changes of the brain due to age related changes to the Nervous system

A

Brain Atrophy: Decrease in brain volume by 0.2% per year after age 35, and by 0.5% per year after age 60.

Shrinkage of Specific Regions:
Prefrontal Cortex: Executive functions (attention, decision-making, problem-solving).
Hippocampus: Memory.
Cerebellum: Balance, motor coordination, and control.
Gyri: Outward folds of the brain shrink.
Sulci: Inward folds of the brain widen.

Grey Matter Deterioration: Loss of neurons, decrease in dendrite size and number, and fewer synapses among neurons.

White Matter Deterioration: Loss of neuronal axons, reduction of myelin (the sheath that insulates axons).

Enlargement of Cerebral Ventricles: Cavities that contain cerebrospinal fluid (CSF) enlarge.

Changes in Cerebral Vasculature: Decreases in blood flow in specific brain regions.

Loss of Microglial Cells: These cells are responsible for triggering inflammation and removing dead or injured neurons.

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16
Q

Functional changes (nervous system)

A
  1. Dopamine
  2. Serotonin
17
Q

What theories have been proposed to explain biological aging?

A

Genetic theories of aging, telomere theory of aging, free radical theory of aging, and biologically-based interventions for age-related diseases

18
Q

Gene Theory of Aging

A

The Gene Theory of Aging suggests that aging is controlled by genes that influence longevity and disease. Key points include:

  • Certain species don’t age (e.g., some worms), but most species do, and their lifespan varies (e.g., tortoise lives up to 177 years, mouse lives only 3 years).
  • In humans, maximum lifespan is around 122 years, with genes playing a role in how long we live.
19
Q

Examples of genes associated with DISEASE

A
  • Kidney and Brain Expressed Protein KIBRA gene (Chromosome 5): Linked to memory impairment and late-onset Alzheimer’s disease.
  • Lipoprotein A (LPA gene) (Chromosome 6): Associated with atherosclerosis, coronary artery disease, and stroke.
  • SH2B3 gene (Chromosome 12): Related to cancer, coronary artery disease, diabetes, and rheumatoid arthritis.

Interventions (like gene therapy) to combat genes that contribute to age-related diseases and reduced life span.
Virus introduces the good alleles into the cells, and provide them with healthier versions of their genes

20
Q

Telomere theory of Aging

A
  • Telomeres are protective caps at the ends of chromosomes that prevent DNA damage during cell division.
  • With each cell division, telomeres shorten, eventually reaching a critical length where cells can no longer divide, leading to cellular senescence (cells stop dividing).
  • Cellular senescence contributes to aging as these non-dividing cells can secrete harmful substances, increasing inflammation and damaging nearby cells.
  • Telomere shortening is associated with aging-related diseases, and maintaining telomere length may help delay aging.

Aging is determined by telomeres and their impact of cellular division

Hayflick limit: Cells undergo a finite number of divisions, and the number of divisions possible declines with ago
Ex. Human fetal tissue -50, but lung tissue in adults -20 (check slides)

Telomeres = non coding portion at end of chromosome. Repeats of 6 base pair sequences: TTAGGG

(As a fetus you have 16,000 repeats of TTAGGG)
Telomeres decrease in length as we grow older

With each cell division, telomeres shorten (30-120 base pair sequences lost); when telomeres shorten to a “critical length”, cells are no longer able to divide, and then they turn into SASPs

Currently, Telomerase Gene Transfer is being investigated, using virus introducing altered DNA into cells, a gene that produces the code sequences and add them to the chromosomes and the telomerase increased the number of divisions
Implication of too much telomerase is Cancer. If we continue to add to the length and keep dividing, you get have malignancy, and uncontrollable division of cells.

21
Q

Free radical theory of Aging

A
  • Aging is caused by damage from free radicals (reactive oxygen species - ROS).
  • Free radicals are highly reactive molecules with unpaired electrons.
  • ROS are generated during normal metabolic processes, like energy production in the mitochondria.
  • These free radicals damage cells by attacking macromolecules such as proteins, lipids, and DNA.
  • Over time, the accumulation of this damage contributes to aging and age-related diseases.
  • Antioxidants (like vitamins C and E) can neutralize free radicals, potentially reducing damage.
  • Or Caloric Restriction
22
Q

What is the Hayflick limit?

A

The finite number of times a normal cell population will divide before it stops, typically around 50 divisions for fetal cells and 20 for adult cells.

23
Q

What is cellular senescence?

A

A state where cells stop dividing and adopt a form called senescence-associated secretory phenotype (SASP), which promotes inflammation and can lead to age-related diseases.

24
Q

What is senescence-associated secretory phenotype (SASP)?

A

SASP refers to the form that senescent cells adopt. These cells secrete inflammatory molecules that can damage surrounding tissues, promote the growth of malignant cells, and contribute to age-related diseases.

25
Q

What are telomeres?

A

Telomeres are protective caps located at the ends of chromosomes that protect them from degradation and fusion with other chromosomes. They shorten with each cell division (30-120 base pair sequences lost) , eventually leading to cellular senescence when they reach a critical length.

26
Q

What are reactive oxygen species (ROS)?

A

ROS are highly reactive molecules containing oxygen, such as free radicals. These molecules cause damage to cellular structures like DNA, proteins, and lipids, contributing to aging and age-related diseases.

27
Q

What is adenosine triphosphate (ATP)?

A

ATP is the primary energy carrier in cells, produced in the mitochondria during cellular respiration. It powers most of the cell’s activities by releasing energy when one of its phosphate bonds is broken.

28
Q

What are macromolecules?

A

Macromolecules are large biological molecules necessary for life, including proteins, lipids, nucleic acids, and carbohydrates. They are often damaged by ROS, which contributes to cellular aging.

29
Q

What is gene therapy and how is it used in aging research?

A

Gene therapy involves introducing corrected or protective genes into cells to combat genetic factors that contribute to age-related diseases. Researchers are investigating its potential to treat diseases linked to aging by targeting specific age-related genes.

30
Q

What is telomerase gene transfer and how does it relate to aging?

A

Telomerase gene transfer is a method being researched to combat telomere shortening. Telomerase is an enzyme that extends telomeres, potentially allowing cells to divide beyond their normal limit and delaying the onset of age-related decline.

  • Both genetic mutations (due to protective caps are now lost) and SASP play significant roles in the aging process and the development of age-related diseases like cancer. So telomerase gene transfer will delay the onset of both.
  • Implication of too much telomerase is Cancer. If we continue to add to the length and keep dividing, you might get malignancy, an uncontrollable division of cells.
31
Q

What are antioxidants and how do they relate to aging?

A

Antioxidants, such as vitamins C and E, neutralize reactive oxygen species (ROS), reducing oxidative damage to macromolecules like DNA and proteins. They are being studied as a possible intervention to slow the aging process and prevent age-related diseases.

32
Q

How does caloric restriction affect aging?

A

Caloric restriction, a 20-40% reduction in caloric intake, has been shown to reduce the onset of age-related diseases and increase life span in various species by slowing metabolism and reducing the production of ROS.

  • can extend 30 years
  • remains controversial.
33
Q

Genes associated with AGING

A
  • Genes like APOE on Chromosome 19 (lipid transport, influences brain injury repair)
  • FoxO on Chromosome 6 (controls cell death and cancer prevention) are examples of longevity-related genes.

BUT these also overlap with association to gene-related DISEASES.

  • Aging genes affect processes like cell death and repair, leading to differences in how long and how well we age.