Aspirin for Bipolar Patients?

April 29, 2010 · Posted in Potential Treatments 

Bipolar patients treated with acetylsalicylic acid (aspirin) in conjunction with lithium prophylaxis needed fewer other adjunctive treatments, compared to patients treated with lithium alone, reports Stanley Rapoport of the National Institutes of Health. These retrospective epidemiological data are of considerable interest in relationship to evidence of an inflammatory component in the affective disorders, as reviewed in Vol. 13(2), 2009 of the BNN, but because the data is preliminary, more study is required.

EDITOR’S NOTE: Several measures of inflammation are higher in children and adults with bipolar disorder compared with controls. These include the ratio of inflammatory to anti-inflammatory cytokines, higher levels of TNF-alpha, and the inflammatory marker c-reactive protein. These peripheral markers measured in blood have been confirmed with direct measurements in postmortem brain autopsy specimens of people who had a history of bipolar disorder.

It is unclear how this information about inflammation in bipolar disorder may eventually inform treatment.  In past BNNs, we have noted the positive effects of the anti-inflammatory antibiotic minocycline on schizophrenia, and stressed the need for studies of this compound in bipolar disorder. TNF-alpha inhibitors have also been associated with improvement in depression when used in the treatment of patients with rheumatoid arthritis and other autoimmune disorders.


This preliminary epidemiological analysis of those treated with lithium with and without aspirin also must be replicated in order to document whether aspirin augmentation is indeed useful.  Eventually, after further study, the data on inflammatory processes in the affective disorders may provide new treatment approaches.
In addition to providing hope of new treatments, new information about inflammation’s role in bipolar disorder contributes to the understanding of how potential pathophysiological mechanisms could endanger neurons and glia, and thus may help explain how cognitive dysfunction emerges in the unipolar and bipolar disorders as a function of the number of affective episodes experienced. The new data emphasize the importance of long-term prophylactic treatment, not only to prevent episodes and their associated increases in inflammation, but also to prevent manic and depressive episode-related decreases in brain-derived neurotrophic factor (BDNF) and other neuroprotective factors.

A number of mood-stabilizing treatments either increase BDNF directly or prevent episode-related decrements in BDNF that can endanger neuronal and glial function. Without mood stabilization, the mechanisms of episode-related increases in inflammation and oxidative stress and decreases in neuroprotective factors may interact, making the brain especially vulnerable to functional deterioration.  It is noteworthy that lithium, in addition to its ability to increase BDNF, also exerts some anti-inflammatory effects. How other approaches to inflammation in the affective disorders may ultimately improve therapeutic efficacy remains to be further studied.

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