Vitamin B12 metabolism and its relation for neural and cognitive functions

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K07770
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Integrative animal science
• Research Institution: Osaka Prefecture University
• Principal Investigator: Takenaka Shigeo 大阪府立大学, 総合リハビリテーション学研究科, 教授 (10280067)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: ビタミンB12 / 神経細胞 / 認知機能 / 欠乏

Outline of Final Research Achievements

It has been reported that vitamin B12 (Cobalamin, B12) might be a risk factor for cognitive function in elderly people, but its biochemical and molecular mechanisms are remained unclear. Here I examined the mechanism with a neural stem cells which knockdown or knockout its B12 metabolize enzymes and with a B12 and/or folate-deficient mice model.
The cbl genes which are B12-metabolizing protein coding genes, in SH-SY5Y cell, a model cell of neurite formation, were down-regulated with a RNAi plasmid or edited CRISR/CAS9 system. The dendrites formation induced by all trans retinoic acid were inhibited and the formation of actin filaments under the dendrites were reduced in the cells. The learning ability was significantly reduced in the B12 and folate-deficient mice.
In conclusion, B12-deficiency might reduce the learning ability in mice and might be involved in the neural cell differentiation and their viability.

Free Research Field

食品栄養学