Mitochondrial dysfunction is a critical factor in the pathogenesis of Alzheimer's disease (AD). The mitochondrial contact site and cristae organizing system (MICOS) plays a pivotal role in shaping the inner mitochondrial membrane, forming cristae junctions and establishing interaction sites between the inner and outer mitochondrial membranes and thereby serving as a cornerstone of mitochondrial structure and function. In the past decade, MICOS abnormalities have been extensively linked to AD pathogenesis. In particular, dysregulated expression of MICOS subunits and mutations in MICOS-related genes have been identified in AD, often in association with hallmark pathological features such as amyloid-β plaque accumulation, neurofibrillary tangle formation, and neuronal apoptosis. Furthermore, MICOS subunits interact with several etiologically relevant proteins, significantly influencing AD progression. The intricate crosstalk between these proteins and MICOS subunits underscores the relevance of MICOS dysfunction in AD. Therapeutic strategies targeting MICOS subunits or their interacting proteins may offer novel approaches for AD treatment. In the present review, we introduce current understanding of MICOS structures and functions, highlight MICOS pathogenesis in AD, and summarize the available MICOS-targeting drugs potentially useful for AD.

Objective to study the effect of curcumin on tumor necrosis factor α(tNF-α)-induced osteoblast apoptosis. Methods Primary osteo-blast cells were divided into three groups:control group(no treated),group treated with tNF-α(treated with tNF-α for 24 h),and group pretreated with curcumin(treated with curcumin for 2 h,and then treated with tNF-α for 24 h). Western blot analysis was carried out with primary antibodies against caspase-2,caspase-3,caspase-8,Bcl-2,Fas,and tRAIL. Apoptosis cells were observed by immunofluorescence microscope. Results In group treated with tNF-α,the protein levels of caspase-2,caspase-3,caspase-8,Fas,and tRAIL increased(P < 0.01),whereas the protein level of Bcl-2 remained unchanged(P > 0.05). In group pretreated with curcumin,the protein levels of caspase-2,caspase-3,caspase-8,Fas,and tRAIL were lower than those in group treated with tNF-α(P < 0.01). the number of apoptotic cells was dramatically increased after the administration of tNF-α. While the number of apoptotic cells decreased in the presence of curcumin. Conclusion the present study clearly demonstrated that cur-cumin can suppress osteoblast apoptosis induced by tNF-α.