Fig. 1

Inflammation and the neuroprogressive hypothesis. The graph above represents a theoretical model for clinical deterioration in BD. Of note, BD is a highly heterogeneous disease, which entails certain caveats to this model [12]. Notwithstanding, it appears that a significant portion of patients experience neuroprogression, that is, a progressive decline in neurocognitive function, associated with increasing frequency of mood (particularly manic) episodes. Notably, neurocognitive deficits (albeit less prominent) are evident, possibly as early as the prodromal phase [13]. Most patients experience a chronic, low-grade inflammatory state, which appears to be upregulated in concert with acute mood episodes. It is suggested that prolonged microglial activation compounds oxidative stresses, contributing to the progressive decline in neurocognitive function and neurostructural changes observed during the course of BD [12, 14]. Adapted with permission from Rosenblat and McIntyre, 2016 [15]