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The importance of disulphide bonds is readily demonstrated as these can be disrupted using reducing agents, with catastrophic effects on functionality

In various in-vivo and in-vitro studies, exogenous administration of IGF-1 mediated has been shown to increase glucose utilization, release acetylcholine from neurons, activate N-methyl-D-aspartate receptor (NMDA), protect the cerebromicrovascular environment, and maintenance of synaptic structure and function [36, 41,42,43,44,45]

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