Neurodegen 01

Topic: Anatomy

Created on Sunday, February 8 2009 by gliageek

Last modified on Sunday, February 8 2009.

 
        A) LRRK2
 
        B) Superoxide dismutase 1
 
        C) Presenilin 1
 
        D) Prion P102L
 
        E) Beta-amyloid precursor protein
 

 

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This question was created on February 08, 2009 by gliageek.
This question was last modified on February 08, 2009.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

ANSWERS AND EXPLANATIONS

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A) LRRK2

This answer is incorrect.

LRRK2 mutations are the most common cause familial late onset Parkinson disease  (See References)

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B) superoxide dismutase 1

This answer is incorrect.

SOD1 mutations underlie a small proportion of familial ALS  (See References)

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C) Presenilin 1

This answer is correct.

Cotton-wool plaques are typically seen in early-onset familial AD secondary to mutations in presenilin-1  (See References)

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D) Prion P102L

This answer is incorrect.

This is the most common mutation in patients with Gerstmann-Straussler-Scheinker disease. GSS shows abundant multicentric amyloid plaques in the cerebral and cerebellar cortices.  (See References)

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E) beta-amyloid precursor protein

This answer is incorrect.

Mutations in the B-APP gene result in Lewy body variant of AD  (See References)

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References:

1. Graham, D.I., and Lantos, P.L. (2002). Greenfield's Neuropathology, 7th ed. Arnold Press, New York. (ISBN:0340742313)

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anatomy
Neurodegen 01
Question ID: 020809087
Question written by gliageek. (C) FrontalCortex.com 2006-2009, all rights reserved. Created: 02/08/2009
Modified: 02/08/2009
Estimated Permutations: 120