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In experimental models of AF and in atrial appendage samples from patients with AF, cardiomyocyte autophagy was found to be activated by enhanced ER stress, which could be attenuated by treatment with the chemical chaperone 4-PBA 2+ levels increase, there is activation of calpain 1, a Ca 2+ -dependent neutral cysteine protease, in both paroxysmal and persistent AF, which, alongside autophagy, further enhances myolysis [177]

Critical Reviews in Clinical Laboratory Sciences

Recent findings suggest that pathological tau can spread trans-synaptically, accelerating neurodegeneration in a prion-like fashion (Meng et al., 2023)