已有研究发现cTnT在病变骨骼肌组织中表达明显升高，提示异常升高的cTnT是一种病理现象，很可能与慢性去神经导致的老年肌少症密切相关(II型肌纤维去神经发生更早更严重)，但是目前未见cTnT和骨骼肌慢性去神经萎缩的研究。前期工作发现：老年小鼠II型肌纤维NMJ部位cTnT信号较年轻小鼠显著增强，而维持NMJ稳定的PKA-RIα减弱、PKA-RIIα增强。cTnT是一种双向激酶锚定蛋白，我们提出假说：cTnT破坏了和NMJ稳定密切相关的PKA-RI/PKA-RII平衡，导致NMJ结构功能损伤，促进肌肉萎缩。我们采用AChR Pulldown、免疫荧光染色、激光共聚焦、免疫共沉淀、腺相关病毒感染、shRNA等方法，在不同年龄小鼠NMJ部位比较cTnT及PKA的差异，通过调控cTnT和PKA，明确cTnT在老年II型肌纤维慢性去神经时的作用及分子机制，为老年肌少症防治提供新的思路和潜在干预靶点。

cTnT was found to be expressed in some skeletal muscle myopathy, which indicates that abnormally elevated cTnT is potentially a pathological phenomena. cTnT is likely to be associated with sarcopenia which is caused mainly by muscle chronic denervation. Yet the research on cTnT and skeletal muscle chronic denervation in aging is rare. Our early stage work found that expression and enrichment of cTnT at NMJ is only found in elderly mice’s type II muscle fiber. Also we found PKA-RIα decreased, while PKA-RIIα increased. The former plays a key role in NMJ stability while the role of the latter is still unknown at NMJ. Given that cTnT is a known dual-AKAP, we propose the hypothesis: cTnT destroyed the dynamic balance of PKA-RI/PKA-RII which is closely related with NMJ stability, thus causing NMJ impairment and promoting muscle atrophy with aging. We plan to use qRT-PCR, Western blot, AChR pulldown, Immunofluorescence staining, confocal microscopy, and co-immunoprecipitation, to compare the level of cTnT and PKA in NMJ of type II muscle fiber in young, old, and very old mice. And by regulating cTnT expression with adeno-associated virus infection and shRNA, and by regulating PKA activity and expression, we expect to elucidate the role of cTnT in the chronic denervation of type II muscle fiber and the underlying molecular mechanism, which will provide new ideas and potential targets of intervention for sarcopenia.