MMT: Molecular Mechanisms of Aging Flashcards

1
Q

Define aging

A

Process of gradual and spontaneous change that leads to maturation through childhood and adolescence, and decline through middle and late age

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2
Q

Define senescence

A

Process by which the capacity for cell division, growth, and function is lost over time leading to incompatibility with life

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3
Q

Define longevity/life expectancy

A

Average time a person will live based on factors like gender and birth year

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4
Q

Define maximum lifespan

A

Maximum period organisms of a given species can live

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5
Q

Describe physiological changes associated with aging.

A

Our sensory declines, CNS declines, cardiovascular system declines, etc.

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6
Q

Describe age-related diseases.

A

Risk for diseases increase with age; age is the #1 risk factor for many diseases!

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7
Q

explain oxidative stress as a theory of aging

A

Oxidative stress: can impact almost all the organ systems in the body. Accelerated oxidative stress is linked to many diseases. It occurs when there is an imbalance between production and breakdown of ROS. This can damage mitochondria, DNA, protein processing, and metabolism. This results in a loss of cellular phenotype and cell death.

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8
Q

describe chronic inflammation as a theory of aging

A

Chronic inflammation: an imbalance between anti and proinflammatory molecules, with more proinflammatory molecules being present. This causes elevated cytokines that give rise to stress responses and causes the body to be less able to handle infection.

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9
Q

describe mitochondrial damage as a theory of aging

A

Mitochondrial damage: oxidative stress and inflammation can damage mitochondrial DNA. This leads to further production of ROS, damage of genetic material and other molecules, and decreased energy production. The decreased energy production leads to degeneration, cell swelling, and apoptosis. This leads to the aging process.

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10
Q

What can serve as natural defense against ROS and inflammation?

A

Glutathione, catalase, vitamin C and E, antioxidant enzymes, carotenoids, flavonoids

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11
Q

Explain the replicative senescence hypothesis of aging: Hayflick Limit.

A

This theory relies on the idea that as cells divide over time, the telomeres on chromosomes shorten. As they shorten, eventually they disappear. Without them, the ends of chromosomes would be vulnerable to “repair” processes, leading to chromosome fusion and abnormal functioning. In addition, once telomeres shorten enough the cell cannot divide which can also cause aging

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12
Q

Describe genes associated with aging.

A

Stress resistance genes, genes targeting inflammation, and genes that slow basic metabolism try to ease effects that lead to aging, however, quality control defects can lead to altered gene expression and errors to accumulate as cells divide, leading to diminished function of these genes.

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13
Q

describe progeria (Hutchinson-gilford)

A

juvenile onset accelerated aging caused by a point mutation in Lamin A gene, which is important in nuclear integrity and DNA repair. Aging occurs within months of birth. Shortened stature, thinned skin, large vesicles, heart conditions, etc. they tend to die in their teens or twenties from heart attack or stroke

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14
Q

Lamin A is associated with which premature aging condition?

A

progeria

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15
Q

describe werner syndrome

A

adult-onset premature aging. Mutations in the WRN gene, which is a DNA repair enzyme. Typically die in their 50’s from heart attack or stroke

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16
Q

WRN gene is associated with which premature aging condition?

A

werner syndrome

17
Q

Describe modifiable factors that can increase healthy aging

A

Diet, exercise, attitude, stress management, genetic engineering