Answered: Answer the following “cause-effect”…

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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Answer the following “cause-effect” true/false questions using the answer key: A: Only statement A is true. B: Only statement B is true. C: Both statements A and B are true, but B is not the exclusive cause of A.. D: Both statements A and B are true, and B is the exclusive cause of A. E: Neither statement A nor B is true. Question 12: A. Cerebral amyloid angiopathy is often found in cases of AD with parenchymal amyloid beta deposits because B. Lewy bodies are common in the setting of low AD neuropathologic changes causing significant vascular brain injury. Question 13: A. Diabetes, mid-life hypertension, mid-life obesity, and physical inactivity are risk factors for AD because B. The clinical and behavioral symptoms of cerebrovascular disease can be similar to that of AD.  Question 14: A. Reduced metabolism of amyloid-beta-42 is a current hypothesis of disease progression in older adults because B. Inhibition or dysfunction of clearance mechanisms for amyloid-beta-42 from the extracellular space promotes accumulation of neuritic plaques and neurofibrillary tangles in neurons. Question 15: A. Amyloid-beta-42 is thought to be a pathogenic peptide involved in AD in part because B. Most mutations in APP, PSEN1 and PSEN2 are associated with an overproduction of amyloid-beta-42. Question 16: A. Destabilization of cytoskeletal elements by hyperphosphorylation can contribute to the pathogenesis of AD because B. The microtubule-associated protein Tau aids in microtubule assembly and stabilization. Question 17: A. Amyloid-beta that is released from neurons into the extracellular space is non-toxic because B. Diffusible amyloid-beta cannot aggregate to form plaques that damage adjacent synapses. Question 18: A. Tau levels are measurable in the CSF of all individuals, including healthy individuals and those with AD because B. The AD CSF profile refers to the combination of low CSF amyloid beta-42 and high T-tau and P-tau levels, and is used as a diagnostic measure due to its high sensitivity. Question 19: A. The definitive diagnosis of AD is made based on changes in memory, cognition, and function because B. In the pre-symptomatic period of dominantly inherited AD, there is a decline in CSF levels of amyloid-beta 42. Question 20: A. Donepezil is a cognition-enhancing drug approved for use in AD because B. Donepezil reduces the effect of acetylcholine on postsynaptic nicotinic receptors. Question 21: A. Cerebrovascular disease has been associated with worse cognitive performance in patients with AD because B. Decreased blood flow before beta amyloid deposition contributes directly to amyloid accumulation due to the reduced clearance of amyloid. Question 22: A. Amyloid-beta deposits occur in the walls of blood vessels in the brain of AD patients because B. Diffusible amyloid-beta oligomers are taken up by astrocytes and endothelial cells via low-density lipoprotein receptor-related protein 1. Question 23: A. Pathological forms of tau may account for the spread of AD in the brain because B. Hyperphosphorylation of tau protein leads to transmission of pathologic forms of tau between neurons.

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The questions inquired are related to the cause-effect relationship between two statements, each relating to a particular viewpoint of Alzheimer’s Disease (AD). They investigate different aspects of AD. These questions require an understanding of both explanations and their interrelation to decide whether one is the select cause of the other, both are independently true, or neither is true.

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