Reports of altered cation transport genes and their transmembrane protein transcripts in cultured cell lines from bipolar patients were judged as irreproducable by other research groups, and the original report was eventually withdrawn by Gershon and colleagues. In the 15-25 years since, have there been in vitro studies that either support or further debunk the theory that hereditary differences in Na+ Li+ countertransport levels in peripheral blood or cultured cell lines from patients might be useful surrogate markers for the clinical diagnosis of affective disorders or clues to their pathophysiology?
Haven't kept up on this target. All our focus for the last few years has been on PGC positive risk SNPs and their association with the transcriptome or epigenome.
Hi,
This is a really great question!
Unfortunately, there has not been a lot of new research into Na+-K+ ATPase and its role in bipolar disorder. Even after decades of research, the mechanism of action of lithium (a commonly prescribed first-line drug for bipolar disorder) remains only partially understood, but its efficacy in the treatment of bipolar disorder is unquestioned in the psychiatric community. The Li+-Na+ countertransport appears to be inhibited during lithium treatment.
Perhaps others in the community may have more information to share.
Best regards,
Qin Xiang
Article The Na, K-ATPase hypothesis for bipolar illness
Article Lithium in the treatment of bipolar disorder: Pharmacology a...
A very interesting question. I know that a lot of work now around identification of biomarkers for bipolar disorder focus more around inflammatory cytokines; some of these studies reference Na-Li counter transport. You may be able to track down more recent research by searching for this type of inflammatory biomarker research as a backdoor to answering your question. Good luck!
Thank you all for your responses. The article by Martin Alda is quite comprehensive and helpful.
Just now returning to the responses to this question I first posted in 2017. So much has changed since the RBC membrane was considered a useful and accessible model for neuronal membrane function in areas involved in the pathophysiology of mental and nervous disorders. As Dr Kleinman correctly points out, the astonishing progress in understanding the human genome and development of ways to find and even correct genetic mutations that underly brain disorders has advanced the field of psychiatric disorders diagnosis and treatment by giant leaps. While the development of sophisticated functional imaging has given insights into the anatomical and functional connections underlying human brain in both healthy and mentally challenged persons.
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