**Core Concept**
Familial amyloidotic polyneuropathy (FAP) is a rare genetic disorder characterized by the deposition of insoluble amyloid fibrils in peripheral nerves, leading to progressive neuropathy. This condition is primarily caused by mutations in the transthyretin (TTR) gene, which encodes a transport protein responsible for carrying thyroxine and retinol in the blood.

**Why the Correct Answer is Right**
Mutant transthyretin (TTR) is the primary cause of FAP. The mutations lead to the misfolding of the TTR protein, resulting in the formation of amyloid fibrils that deposit in peripheral nerves. This deposition causes nerve damage, leading to symptoms such as numbness, tingling, and weakness in the hands and feet. The pathogenesis of FAP involves the accumulation of mutant TTR protein in the endoneurium, leading to the disruption of nerve function.

**Why Each Wrong Option is Incorrect**
**Option A:** Amyloid associated protein (AA protein) is a type of amyloid protein associated with secondary amyloidosis, which is not related to FAP. AA protein is produced in response to chronic inflammation and is not caused by a genetic mutation.
**Option B:** Mutant calcitonin is associated with medullary thyroid carcinoma and multiple endocrine neoplasia type 2 (MEN 2), but it is not related to FAP.
**Option D:** Normal transthyretin is a transport protein that is not associated with FAP. While normal TTR can form amyloid fibrils under certain conditions, it is not the primary cause of FAP.

**Clinical Pearl / High-Yield Fact**
It's essential to remember that FAP is a genetic disorder caused by mutations in the TTR gene, and it can be inherited in an autosomal dominant pattern. The diagnosis of FAP is often made based on clinical presentation, family history, and genetic testing.

**✓ Correct Answer: C. Mutant transthyretin**