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Pages:
1 page/≈275 words
Sources:
1 Source
Style:
APA
Subject:
Life Sciences
Type:
Essay
Language:
English (U.S.)
Document:
MS Word
Date:
Total cost:
$ 3.96
Topic:

Mammalian Aging: Can Human Longevity be Increased?

Essay Instructions:

Keep the following guiding questions in mind as you complete this activity taking care to ensure your response address them:
•Can human longevity be increased? 
Complete the assigned readings (Activity One). 
Prepare an essay of about 200 words addressing the following: Define mammalian senescence and discuss two specific animals and what we know about how they age, including aging on a molecular level. Discuss the experimental evidence and one proposed genetic cause for each animal. What are some likely causes of the differences in aging? What is especially interesting or significant about your animal case study? 
You should not need or use any references other than the class materials. 
Make sure to write in your own words as much as possible, using quotation marks and internal citations if you must cite the text directly. Always include page numbers if you cite the text.

Essay Sample Content Preview:

Mammalian Aging
Student’s Name
University Affiliation
Mammalian Aging
Aging is an organic process that makes all animals to grow old. Hypotheses have it that mutations in the mitochondrial DNA, mtDNA accumulate in the body tissues and initiate the aging process. Mutations cause mitochondrial dysfunction that results in aging. Scientists have knowledge of the aging of two specific mammals that are mice and humans. Aging humans have the characteristics of high levels of somatic mtDNA. On the other hand, experimental evidence from mice proves that a mouse that experiences a deficiency of mitochondrial DNA polymerase accumulates mtDNA and show characteristics of accelerated aging. The causes of difference in aging of animals relate to their ancestors but differ with their close kingdom associates such as reptiles and amphibians. The phenotype of aging in animals is similar in most if not all animals (Finch & Austad, 2012).
Research does not associate mtDNA with elevated defects in the proliferation of cells or levels of oxidative stress, but they induce apoptotic markers in the body tissues that cause a rapid turnover in cells. The experiment with mice found that levels of apoptotic markers increase with aging in mice. Therefore, the accumulation of mtDNA that initiate apoptosis is the central mechanism causing mammalian aging. The proposed genetic model for aging in mice and humans is that accumulation of somatic mtDNA and other cell types respiratory dysfunction of the chains initiates a variety of phenotypes that cause...
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