WBR0369
| Author | [[PageAuthor::Gonzalo A. Romero, M.D. [1]]] |
|---|---|
| Exam Type | ExamType::USMLE Step 1 |
| Main Category | MainCategory::Biochemistry, MainCategory::Pathology, MainCategory::Pathophysiology |
| Sub Category | SubCategory::Neurology |
| Prompt | [[Prompt::A research lab develops a new knock-in mouse model with a chimeric mouse/human exon containing 140 CAG repeats inserted in a gene located on the short arm of chromosome 4. These mice eventually develop increased locomotor activity and abnormal posturing at 1 month of age, followed by hypoactivity at 4 months and gait anomalies at 1 year. Behavioral symptoms preceded neuropathological anomalies.
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| Answer A | AnswerA::Decreased NE, 5-HT and DA |
| Answer A Explanation | [[AnswerAExp::Incorrect. These are the neurotransmitter changes associated in depression]] |
| Answer B | AnswerB::Increased DA |
| Answer B Explanation | [[AnswerBExp::Incorrect. This is seen in schizophrenia]] |
| Answer C | AnswerC::Decreased DA, increased 5-HT and increased Ach |
| Answer C Explanation | [[AnswerCExp::Incorrect. These changes are seen in parkinson’s disease]] |
| Answer D | AnswerD::Decreased GABA and Ach, increased DA |
| Answer D Explanation | [[AnswerDExp::Correct. These changes are associated with Huntington disease.]] |
| Answer E | AnswerE::Increased NE, decreased GABA and 5-HT |
| Answer E Explanation | [[AnswerEExp::Incorrect. These neurotransmitter changes are seen in anxiety]] |
| Right Answer | RightAnswer::D |
| Explanation | [[Explanation::This animal model is trying to develop Huntington disease in the monkeys, which is caused by a trinucleotide repeat (CAG), which caused damage to the caudate nucleus. Biochemically; human brains affected with this autosomal dominant disease have decreased GABA and Ach, increased DA.
References: First Aid 2013 page 461 |
| Approved | Approved::No |
| Keyword | |
| Linked Question | Linked:: |
| Order in Linked Questions | LinkedOrder:: |