Why the study?
Genetic studies implicate cytoskeletal dysfunction and regulatory proteins like MACF1 in BPAD pathogenesis, but its nervous system functions and role in lithium therapeutic action require review.
This review highlights the functions of MACF1 in the nervous system, its role in bipolar disorder pathogenesis, and its potential involvement in lithium's mechanism of action.
MACF1 implicated in BPAD cytoskeletal dysfunction; leaves open validation as lithium target or therapeutic node.
Bipolar affective disorder (BPAD) are life-long disorders that account for significant morbidity in afflicted patients. The etiology of BPAD is complex, combining genetic and environmental factors to increase the risk of disease. Genetic studies have pointed toward cytoskeletal dysfunction as a potential molecular mechanism through which BPAD may arise and have implicated proteins that regulate the cytoskeleton as risk factors. Microtubule actin crosslinking factor 1 (MACF1) is a giant cytoskeletal crosslinking protein that can coordinate the different aspects of the mammalian cytoskeleton with a wide variety of actions. In this review, we seek to highlight the functions of MACF1 in the nervous system and the molecular mechanisms leading to BPAD pathogenesis. We also offer a brief perspective on MACF1 and the role it may be playing in lithium's mechanism of action in treating BPAD.
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Salem et al. (2023) studied this question.
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