A systematic review of evidence for the role of inflammatory biomarkers in bipolar patients

Alterations of the cerebellum and basal ganglia in bipolar disorder mood states detected by quantitative T1ρ mapping

“…Blood volume is another potential confound, although our findings of increased T1ρ signal in the cerebellum were inconsistent with prior reports of decreased blood volume in bipolar disorder . Additionally, neuroinflammation, which has been identified in bipolar disorder and may be mood‐state dependent, has been conjectured to potentially influence T1ρ relaxation times, but there is not yet evidence of this . It is of note that there are a number of variants of T1ρ mapping, such as dispersion imaging and adiabatic T1ρ and relaxation along a fictitious field (RAFF) mapping, as well as complementary techniques such as T2 mapping, that may provide increased sensitivity and/or specificity to particular disease processes in the future.…”

Adjunctive probiotic microorganisms to prevent rehospitalization in patients with acute mania: A randomized controlled trial

“…Immunological abnormalities have been identified in individuals with mania and may contribute to the pathophysiology of this acute mood state as well as to bipolar disorder more broadly . In a previous study performed by our group, individuals hospitalized for mania with increased levels of inflammation were more likely to be rehospitalized in the 6 months following discharge .…”

“…2,3 Immunological abnormalities have been identified in individuals with mania and may contribute to the pathophysiology of this acute mood state as well as to bipolar disorder more broadly. [4][5][6][7] In a previous study performed by our group, individuals hospitalized for mania with increased levels of inflammation were more likely to be rehospitalized in the 6 months following discharge. 8 In these studies, the levels of inflammation were determined by factor analysis of the levels of class-specific antibodies to auto-antigens, food-derived antigens, and infectious agents.…”

Neurobiology of bipolar disorders: a review of genetic components, signaling pathways, biochemical changes, and neuroimaging findings

“…Immune dysfunction in BD is supported by pre-clinical and clinical evidence showing elevated levels of proinflammatory cytokines, including interleukin-4 (IL-4), interleukin-1beta (IL-1b), interleukin-6 (IL-6), tumor necrosis factor (TNF)-alpha, soluble interleukin-2 receptor (sIL-2R), and soluble receptor of TNF-type 1 (STNFR1), among others, in patients compared to controls. [158][159][160][161][162][163][164] A recent systematic review has suggested an important role for acute inflammatory response during mania and depression, with the elevation in proinflammatory cytokines seemingly restored after remission of symptoms. 118 In addition, further findings in BD have also described significant negative associations between inflammatory markers and general cognitive abilities, as well as neuroanatomical alterations.…”