Vitamin B12 offers neuronal cell protection by inhibiting Aβ-42 amyloid fibrillation

Protein misfolding and aggregation has been implicated as the cause of more than 20 diseases in humans such as Alzheimer's and Parkinson's and systemic amyloidosis. Retardation of A beta-42 aggregation is considered as a promising and challenging strategy for developing effective therapeutics against Alzheimer's disease. Herein, we demonstrated the effect of vitamin B12 (VB) on inhibiting amyloid formation by employing ThT fluorescence assay, circular dichroism, ANS fluorescence assay, dynamic light scattering measurements and transmission electron microscopy and cell viability assay. Our results demonstrate that vitamin B12 (VB), inhibits A beta-42 aggregation in a concentration dependent manner. Further VB also provide protection against amyloid induced cytotoxicity in human neuronal cell line. This study points towards a promising strategy to combat A beta-42 aggregation and may have broader implication for targeting other neurological disorders whose distinct hallmark is also amyloid formation. (C) 2017 Elsevier B.V. All rights reserved.