BACKGROUND: Studies have demonstrated that trehalose possesses protective effects on cyropreserved sternum. But the mechanism of action remains poorly understood. OBJECTIVE: To investigate the effects of trehalose on bcl-2 and bax mRNA expression in cryopreserved sternum. METHODS: Four groups of freshly prepared solution were used: low-potassium dextran (LPD), LPD + dimethyl sulfoxide (DMSO), LPD + trehalose, LPD + DMSO + trehalose. Rat sternum was cut and then immediately cryopreserved in the tubes containing each group of solution. Fresh rat sternum tissue and 4 groups of samples cryopreserved for 120 days were taken and bcl-2 and bax mRNA expression in fresh and cryopreserved sternum was detected using reverse transcription-polymerase chain reaction.RESULTS AND CONCLUSION: bcl-2 mRNA expression in the LPD + trehalose group was significantly higher, but bax mRNA expression was significantly lower, than in the LPD, LPD + DMSO groups (both P < 0.01). LPD + DMSO + trehalose group showed highest bcl-2 mRNA expression and lowest bax mRNA expression, which were basically similar to fresh bone tissue (P > 0.05). These findings indicate that trehalose may protect cell activity in cryopreserved sternum by enhancing bcl-2 mRNA expression and inhibiting bax mRNA expression, and trehalose together with DMSO shows better protective effects.

Alzheimer's disease (AD) is a central neurodegenerative disease with still unclear pathogenesis. Recent studies have shown that axonal transport dysfuction of mitochondria may contribute to AD progression. Normal mitochondrial axonal transport mainly involves microtubules, molecular motors and connexins, while AD early pathological changes can damage mitochondrial axonal transport by interfering with these proteins: accumulated β-amyloid (Aβ) impairs the function of molecular motors; abnormally modified Tau protein reduces microtubule stability; mutant presenilin-1 (PS1) can induce phosphorylation of some related proteins by activating glycogen synthase kinase-3β (GSK-3β); all these processes can damage mitochondrial axonal transport, leading to synaptic dysfunction. This review aims to clarify the possible mechanisms of axonal transport dysfuction of mitochondria in AD and provides new ideas for AD treatment.

Microglia (MG) are resident immune cells in the central nervous system (CNS) and the first defense line of CNS damage. The maintenance of MG function requires abundant energy, and lipid can serve as an energy source for the brain when glucose utilization is limited, and lipid can also function as signaling molecule. Alzheimer's disease (AD) is the most common neurodegenerative disease, and MG lipid metabolism plays an important role in the development of this disease. Drugs targeting lipid metabolism provide a new direction for AD treatment. This review starts with the specific mechanism of lipid metabolism in MG, and briefly introduces the effect of lipid metabolism on MG function and its role in AD.