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Accumulating evidence suggests that metabolic disturbances can promote the development of AF through structural and electrophysiological remodelling, but the underlying mechanisms that predispose an individual to AF are aetiology-dependent, thus emphasizing the need for tailored therapeutic strategies to treat AF that target an individuals metabolic profile

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Concurrently, to reverse neurological damage, innovative strategies should be explored including glial cell reprogramming (e.g., tamoxifen derivatives inducing neuroprotective astrocytes) and microbial-mitochondrial axis interventions, combined with high-throughput screening of BBB-protective agents using organoid models

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M., Stephenson, W., Rose, C