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 2: A. APOE is transported across the blood brain barrier and accumulates in the amyloid-beta deposits and neurofibrillary tangles associated with AD because B. APOE is involved in the normal catabolism of triglyceride-rich lipoproteins. Question 3: A. Diets high in antioxidants that prevent oxidative injury by free radicals may lower the rate of AD development because B. Vitamin E supplementation has been shown to work similarly to the NMDA receptor antagonist, Memantine, but spares the patient the adverse effects including dizziness, headache, and lethargy. Question 4: A. All forms of AD share overproduction and/or decreased clearance of amyloid beta peptides because B. The main cause of sporadic AD is failure to clear amyloid beta peptide from brain tissue.
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 2:
A. APOE is transported across the blood brain barrier and accumulates in the amyloid-beta deposits and neurofibrillary tangles associated with AD because
B. APOE is involved in the normal catabolism of triglyceride-rich lipoproteins.
Question 3:
A. Diets high in antioxidants that prevent oxidative injury by free radicals may lower the rate of AD development because
B. Vitamin E supplementation has been shown to work similarly to the NMDA receptor antagonist, Memantine, but spares the patient the adverse effects including dizziness, headache, and lethargy.
Question 4:
A. All forms of AD share overproduction and/or decreased clearance of amyloid beta peptides because
B. The main cause of sporadic AD is failure to clear amyloid beta peptide from brain tissue.
Question 5:
A. Low levels of amyloid-beta-42 in the cerebral spinal fluid (CSF) is used as a biomarker for AD because
B. Post-mortem plaque count and amyloid-beta retention as seen in PET imaging correlate with CSF levels of amyloid-beta-42.
Question 6:
A. Some studies suggest a link between the risk of AD and elevated HDL cholesterol levels in midlife because
B. Cholesterol is carried in the brain primarily by high density lipoprotein complexes.
Question 7:
A. The APOE4 isoform is a relatively minor causative or contributing factor for AD because
B. There is no conclusive evidence for the involvement of APOE4 in tau phosphorylation or lipid
Question 8:
A. The most firmly established risk factor for dominantly inherited Alzheimer’s Disease is a homozygous APOE4 genotype because
B. Inherited allele 4 (e4) of APOE may enhance clearance of amyloid beta from the cerebrum.
Question 9:
A. Only 5-10% of AD cases can be correctly diagnosed based on CSF biomarkers because
B. The combination of low amyloid-beta-42 and high T-tau and P-tau in the CSF is not specific for AD.
Question 10:
A. Use of benzodiazepines, anticholinergics, or PPIs may enhance the penetrance of presymptomatic AD because
B. Some drugs increase vitamin B12 absorption, which increases amyloid-beta deposition.
Question 11:
A. Solanezumab may be useful during the prodromal phase of AD to delay onset and progression of clinically apparent disease because
B. Evidence suggests that accumulation of amyloid-beta is an early upstream initiator of the disease process.
Question 12:
A. Cerebral amyloid angiopathy is often found in cases of AD with parenchymal amyloid beta deposits because
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