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Decreased brain energy metabolism is correlated with cognitive impairment in Alzheimer's disease (AD). Accumulating evidence indicates that lactate and monocarboxylate transporters (MCTs) participate in brain energy metabolism. To date, changes in lactate level and expression of MCTs in AD remain unclear. This study was conducted to detect the changes in lactate content and expression of MCT2 in Aβ25-35-treated rat model of AD. Sprague-Dawley rats were randomly divided into control and model groups, which received bilateral intrahippocampal injections of saline and Aβ25-35, respectively. Cognitive functions were detected by Morris water-maze test. Lactate content in the cerebral cortex and hippocampus was measured by absorbance assay. The MCT2 level in the brain was examined by immunohistochemistry and Western blot. Morris water-maze test showed that the model group exhibited impaired learning and memory compared with the control group. Lactate content in the cerebral cortex and hippocampus was decreased in the model group compared with that in the control group. Immunohistochemistry and Western blot showed that the expression of MCT2 in the model group significantly decreased compared with that in the control group. Results indicate that decreased lactate content and downregulated MCT2 expression in the cerebral cortex and hippocampus reflected impaired energy metabolism in the brain, which may participate in the pathologic progression of AD.

Electroacupuncture (EA) has been used worldwide to treat demyelinating diseases, but its therapeutic mechanism is poorly understood. In this study, a custom-designed model of compressed spinal cord injury (CSCI) was used to induce demyelination. Zusanli (ST36) and Taixi (KI3) acupoints of adult rats were stimulated by EA to demonstrate its protective effect. At 14 days after EA, both locomotor skills and ultrastructural features of myelin sheath were significantly improved. Phenotypes of proliferating cells were identified by double immunolabeling of 5-ethynyl-2'-deoxyuridine with antibodies to cell markers: NG2 [oligodendrocyte precursor cell (OPC) marker], 2',3'-cyclic-nucleotide 3'-phosphodiesterase (CNPase) (oligodendrocyte marker), and glial fibrillary acidic protein (GFAP) (astrocyte marker). EA enhanced the proliferation of OPCs and CNPase, as well as the differentiation of OPCs by promoting Olig2 (the basic helix-loop-helix protein) and attenuating Id2 (the inhibitor of DNA binding 2). EA could also improve myelin basic protein (MBP) and protect existing oligodendrocytes from apoptosis by inhibiting caspase-12 (a representative of endoplasmic reticulum stress) and cytochrome c (an apoptotic factor and hallmark of mitochondria). Therefore, our results indicate that the protective effect of EA on neural myelin sheaths is mediated via promotion of oligodendrocyte proliferation and inhibition of oligodendrocyte death after CSCI.

Demyelination occurred after CSCI and might be partly caused by oligodendrocyte apoptosis, which was positively correlated with ER-mitochondria interactions and enhanced Id2 expression after CSCI in rats.

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