PT147.S1.Q21 > Question

SECTION 1 · lr

Question 1 Question 2 Question 3 Question 4 Question 5 Question 6 Question 7 Question 8 Question 9 Question 10 Question 11 Question 12 Question 13 Question 14 Question 15 Question 16 Question 17 Question 18 Question 19 Question 20 Question 21 Question 22 Question 23 Question 24 Question 25 Question 26

SECTION 2 · rc

PASSAGE 1

Question 1 Question 2 Question 3 Question 4 Question 5 Question 6 Question 7

PASSAGE 2

Question 8 Question 9 Question 10 Question 11 Question 12 Question 13 Question 14

PASSAGE 3

Question 15 Question 16 Question 17 Question 18 Question 19 Question 20 Question 21 Question 22

PASSAGE 4

Question 23 Question 24 Question 25 Question 26 Question 27

SECTION 3 · rc

PASSAGE 1

Question 1 Question 2 Question 3 Question 4 Question 5 Question 6

PASSAGE 2

Question 7 Question 8 Question 9 Question 10 Question 11 Question 12 Question 13

PASSAGE 3

Question 14 Question 15 Question 16 Question 17 Question 18 Question 19 Question 20 Question 21

PASSAGE 4

Question 22 Question 23 Question 24 Question 25 Question 26 Question 27

SECTION 4 · lr

The author concludes that Alzheimer’s risk can be reduced by converting homocysteine into other substances. This is based on the fact that people with above-average levels of homocysteine have higher risk of being diagnosed with Alzheimer’s.

The author assumes that there’s no other explanation for the correlation between above-average homocysteine levels and increased risk of Alzheimer’s.

A correlation between above-average homocysteine and Alzheimer’s allows for outliers. There can be Alzheimer’s patients with normal or even below-average homocysteine levels.

If the effects are unrelated to Alzheimer’s, then they have no impact on the conclusion, which is focused only on whether Alzheimer’s can be reduced by converting homocysteine to those substances.

This just suggests B vitamins and folic acid should be taken in other forms besides vitamin-mineral supplements. The author never suggested any specific form in which we take B vitamins and folic acid.

This suggests that there’s also a genetic component to Alzheimer’s. But there could be a genetic component to having higher homocysteine levels. In addition, it’s possible for there to be multiple, independent causes of Alzheimer’s.

This provides an alternate explanation for the correlation observed. If Alzheimer’s increases homocysteine, we’d expect people with Alzheimer’s to have higher levels of homocysteine, even if homocysteine doesn’t cause Alzheimer’s.

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