Neurogenesis Unchanged by MTHFR Deficiency in Three-Week-Old Mice

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. 

Structural Dynamics of Amyloid-β Aggregation in Alzheimer’s Disease: Computational and Experimental Approaches

Authors:  Cecily Wing Hei Cheng, Matthew Wai Heng Chung, & Joseph Chi Fung Ng

The nucleation of amyloid-β (Aβ) oligomers, and the fibril formation that follows represents an important pathologic mechanism for Alzheimer's disease (AD). This has motivated the search for therapeutics that specifically target Aβ, which holds promise to be a cure for AD. However, conventional biophysical approaches like X-ray crystallography and nuclear magnetic resonance (NMR) spectroscopy fall short of capturing this highly dynamic process. The aggregation of amyloid fibrils has been unravelled by a mix of novel approaches.