Authors: Greg D. Owens, Patrice D. Smith, Nafisa M. Jadavji
The primary pathway for removing homocysteine, a potentially neurotoxic molecule, from circulation is via 5-methyltetrahydrofolate. This molecule is converted from folate via an enzyme known as methylenetetrahydrofolate reductase (MTHFR). Polymorphisms in the MTHFR gene have been linked to various pathologies (e.g. neurological disease) and animal models have been developed to study the in vivo effects of the deficiency. These models have revealed increased levels of apoptosis in the cerebellum and hippocampus and potential modulation of neurogenesis, which may contribute to the pathologies viewed.