UNDERSTANDING THE BIOLOGICAL BASIS OF BD IS CRUCIAL
FOR FINDING NEW TARGETED TREATMENTS AND IMPROVING
RISK ASSESSMENT, DIAGNOSIS, AND PROGRESSION.
Even though the pathophysiological pathways underlying BD remain elusive, there was a significant advance in BD’s pathophysiology in the last decades, suggesting that it is likely due to a multifactorial etiology involving interaction between multiple genetic, neurochemical, and environmental factors. Moreover, mechanisms underlying the impaired neuroplasticity and cellular resilience in BD could also explain the increased vulnerability to stressful events and episode recurrence among the patients.
Recent and ongoing studies have proposed that the pathophysiology of BD is orchestrated by the interaction of several mechanisms, including genetic load, epigenetic mechanisms, mitochondrial dysfunction, oxidative stress, inflammation, neurotrophic factors, circadian rhythm abnormalities, and biological aging acceleration.
