Abstract
Transthyretin (TTR) is the protein transporter of thyroxine and retinol. Several TTR mutations are associated with familial amyloid polyneuropathy, a neurodegenerative disorder characterized by extracellular deposition of TTR aggregates and fibrils in the peripheral nervous system. Several reports suggest new TTR functions in the nervous system particularly in nerve regeneration and in neuroprotection in Alzheimer’s disease. The fact that TTR increases axonal growth during peripheral nervous system, regeneration and allows an appropriate retrograde transport may represent the missing link explaining the preferential deposition of mutated TTR in the peripheral nervous system of familial amyloid polyneuropathy patients. This paper discusses the details explaining the role of TTR during nerve regeneration.
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