Bipolar disorder with Marfan syndrome: a case illustration based on possible involvement of TGF-β1 in the common etiopathogenesis

Marfan syndrome (MFS) is mainly characterized by the pathological connective tissue. The mutant fibrillin protein in MFS misleads the constitutive pathways of various tissues through inappropriate transforming growth factor beta (TGF-β) signalling. Bipolar disorder (BPD) is believed to arise as a result of impaired synaptic modulation and neural plasticity in crucial pathways that mediate cognition and affection. TGF-β was linked with neurogenesis and developmental neural remodelling. Altered TGF-β functions with pleiotropic effects to the brain could increase susceptibility to psychiatric disorders such as BPD. Disrupted circuits of molecular signalling chains cause improper synapse formation, synaptic transmission, and synaptic plasticity that ultimately may end up with BPD. Here, we report a 26-year-old male who was diagnosed with MFS and BPD. This case report aimed to argue probable impaired neuroprotective mechanisms which may lead to such comorbidity. We may inspire later studies on possible shared etiopathogenesis via defective microfibrillar proteins of both disorders.