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It could be hypothesized that greater increases in circulating BA may be due to lower transamination and, thus, may result in larger increases in muscle carnosine content
It is widely recognized that diabetes affects hippocampal synaptic plasticity, and this disruption in synaptic plasticity is related to cognition.118 Reisi et al reported that both presynaptic and postsynaptic components are involved in diabetes-induced damage to synaptic plasticity.119 In animal models of diabetes with cognitive impairment, synaptic plasticity was impaired in the two experimental forms of long-term enhancement (LTP)120124 and long-term depression (LTD).125,126 Moreover, the ultrastructure of hippocampal synapses is destroyed,127 thereby reducing the hippocampal dendritic spine density.123 Besides, synaptic plasticity-related proteins, including CREB, pCREB, brain-derived neurotrophic factor (BDNF), and activity-regulated cytoskeleton (Arc) proteins, are significantly reduced.128 Our previous data showed that central IR may significantly affect the expression of synaptic plasticity proteins, such as postsynaptic density protein-95 (PSD95), Arc, synapsin1, BDNF, resulting in the impaired synaptic plasticity of neurons and decreased learning and memory ability (data not shown)
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