Scenario 3 Linda just turned 73 years old, and her doctor has diagnosed her with Alzheimer's disease. Although her family does not have a history of the disease, her children insisted that Linda get tested for genetic mutations related to Alzheimer's disease. The results showed that she does not have any mutations known to cause Alzheimer's disease. 1. How can you explain that Linda has Alzheimer's disease but she does not have any mutations linked to the disease nor a family history of it?

Scenario 3 Linda just turned 73 years old, and her doctor has diagnosed her with Alzheimer's disease. Although her family does not have a history of the disease, her children insisted that Linda get tested for genetic mutations related to Alzheimer's disease. The results showed that she does not have any mutations known to cause Alzheimer's disease. 1. How can you explain that Linda has Alzheimer's disease but she does not have any mutations linked to the disease nor a family history of it?

Human Anatomy & Physiology (11th Edition)

11th Edition

ISBN:9780134580999

Author:Elaine N. Marieb, Katja N. Hoehn

Publisher:Elaine N. Marieb, Katja N. Hoehn

Chapter1: The Human Body: An Orientation

Section: Chapter Questions

Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...

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Question 3 ) Listen Becker muscular dystrophy is due to a mutation in the same gene that causes the more severe Duchenne muscular dystrophy. This is an X linked recessive condition that causes muscular weakness that begins and a later age and progresses more slowly than Duchenne muscular dystrophy which is often lethal by age 20. One of my former students had a father who had this condition. She did not have the condition. If she has children with a male who does not have the condition, what is the chance that any daughters she would have would have the condition? 100 % 75% O 50% O 25% 0%
4). p53 (sometimes called TP53 for “tumor protein 53") is a human tumor suppressor gene that is mutated in the majority of human cancers (many tumor types). a. For each of the mutations described below (i-iv): is this a mutation you would expect to find when sequencing p53 alleles from tumor cells? Why or why not? i. A missense mutation encoding a hyperactive form of the protein. ii. A deletion of the gene. iii. An insertion in the promoter that increases transcription 10-fold. iv. A nonsense mutation. b. When sequencing the p53 gene in tumor cells, would you expect to find only mutant version(s) of the gene or a mix of mutant and wild type versions? c. For any of the mutations you said you would expect to find in tumor cells, would you expect tumor cells to be homozygous (same mutation on both chromosomes)? Why or why not? d. Individuals with Li-Fraumeni syndrome have a very high risk of tumors originating in various tissues due to inheritance of a loss-of-function mutant allele of…
Please answer all questions if possible. 1. Why are genetic screens useful? Why do biologists do screens? What are we trying to do? What is the Big Picture purpose? 2. Why would a researcher be interested in over- or mis- expression phenotypes?
Mutations can arise in the absence of a mutagen. please explain your answer true false
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