ReviewTrimethyltin-induced hippocampal neurodegeneration: A mechanism-based review

- TMT induces neurodegeneration selectively involving the limbic system (particularly, hippocampus).
- Behavioral abnormalities (i.e., memory deficit and epilepsy) are shown in rodents exposed to TMT.
- This article reviews in vivo and in vitro underlying mechanisms for TMT-induced hippocampal neurodegeneration.
- This review provides effective strategies for potential therapeutic approaches for neurodegenerative diseases.

Trimethyltin (TMT), a toxic organotin compound, induces neurodegeneration selectively involving the limbic system and especially prominent in the hippocampus. Neurodegeneration-associated behavioral abnormalities, such as hyperactivity, aggression, cognitive deficits, and epileptic seizures, occur in both exposed humans and experimental animal models. Previously, TMT had been used generally in industry and agriculture, but the use of TMT has been limited because of its dangers to people. TMT has also been used to make a promising in vivo rodent model of neurodegeneration because of its region-specific characteristics. Several studies have demonstrated that TMT-treated animal models of epileptic seizures can be used as tools for researching hippocampus-specific neurotoxicity as well as the molecular mechanisms leading to hippocampal neurodegeneration. This review summarizes the in vivo and in vitro underlying mechanisms of TMT-induced hippocampal neurodegeneration (oxidative stress, inflammatory responses, and neuronal death/survival). Thus, the present review may be helpful to provide general insights into TMT-induced neurodegeneration and approaches to therapeutic interventions for neurodegenerative diseases, including temporal lobe epilepsy.