EXAM 4

This exam has a total of 16 points. Each point corresponds to a numbered question. The numbered question is to be answered. The correct answer to a numbered question will give you one point. If the answer is partially correct, partial credit will be given as a decimal value. If the answer is incorrect, no credit will be given. If the question is unanswered, no credit will be given so it is better to guess than to leave a question blank. The number of points earned will be divided by the total number of points on the exam and multiplied by 100 to get your grade. Good luck!

In the background section the authors wrote “The major pathological hallmarks of AD include widespread neuronal and synaptic loss, excessive presence of astrocytes, and aggregation of multiple proteinaceous deposits for instance β-amyloid plaques and neurofibrillary tangles.” Why would neuronal and synaptic loss be a problem? (1 point)

In the background section the authors wrote “The number of hypotheses are proposed along the years to describe the root cause of AD such as the production of β-amyloid, cholinergic hypothesis, excitotoxicity and oxidative stress hypothesis as summarized in Fig. 1.” Are these null hypotheses, alternate/alternative hypotheses, or both? (1 point)

How do you know that your answer to question 2 correct? (1 point)

Why does Acetycholine (Ach) inhibitor activation lead to a ACH deficit? (1 point)

Where in the neuron would an ACH deficit occur? (1 point)

How do you know that your answer to question 5 is correct? (1 point)

In the background section the authors wrote “AD is also characterized by the cholinergic deficit in the affected brain. The acetylcholine-releasing neurons especially their cell bodies which lied in basal forebrain degrades selectively in AD affecting cognitive functions and memory as these neurons are vital in the normal functioning of cerebral cortex and related structures.” Are these cell bodies pre or post synaptic? (1 point)

How do you know that your answer to question 7 is correct? (1 point)

Why would AChE-1 inhibitors be therapy for AD? (1 point)

In the background section the authors wrote “Thus, NMDA receptor antagonists could be advantageous therapeutically in the management of AD.” Why would NMDA receptor antagonists be therapeutic in the management of AD? (1 point)

In the methods section the authors wrote “The target proteins i.e. AChE (4EY7), BACE-1 (2HM1), MAO-A (2Z5X) and NMDA (1PBQ) were selected.” Why is AChE a target protein? (1 point)

In the methods section the authors wrote “The target proteins i.e. AChE (4EY7), BACE-1 (2HM1), MAO-A (2Z5X) and NMDA (1PBQ) were selected.” Why is NMDA a target protein? (1 point)

In the discussion section the authors wrote “The active site comprises of catalytic site of AChE (Glu334,Ser 203 and His447), acyl-binding pocket (Phe297and Phe295), oxyanion hole (Ala204, Gly120 and Gly121), quaternary ammonium binding locus (Trp86) and finally, PAS (Trp341, Trp286, Tyr124, Tyr72 and Asp74), which groups at the active site gorge’s entry [35].” What naturally binds in AChE’s active site? (1 point)

In the discussion section the authors wrote “Similarly, monoamine oxidase (MAO) an enzyme majority involves in the oxidation of numerous vital monoamine hormones and neurotransmitters such as adrenaline, noradrenaline, dopamine, and serotonin [36}.” What is MAO doing? Be more specific than answering “oxidation”. (1 point)

What kind of an agent does your answer to question 14 make MAO to be? (1 point)

How do you know that your answer to question 15 is correct? (1 point)

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