Posted by SLS on November 6, 2000, at 8:25:31
In reply to Re: Article: Lithium increases brain volume ?, posted by SLS on November 3, 2000, at 20:57:57
Hey Dan,
Check this out:
This abstract makes a good argument for continued inquiry to be made in the use of lithium in the treatment of neurodegenerative disorders like Parkinson's and Alzheimers Dementia. It also suggests that the neurotrophic and neuroprotective properties of lithium be used to treat mood disorders, regardless of the primary treatment. This abstract states that lithium is the most potent of available medications to increase the amount neurotrophic substances and decrease the amount of neurodegenerative substances.
A 3% increase in cortical volume may not be so far-fetched.
- Scott-------------------------------------------------------------
J Clin Psychiatry 2000;61 Suppl 9:82-96 Related Articles, Books,
Lithium up-regulates the cytoprotective protein Bcl-2 in the CNS in vivo: a role for neurotrophic and neuroprotective effects in manic depressive illness.Manji HK, Moore GJ, Chen G
Department of Psychiatry & Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, Mich 48201, USA. [email protected]
Although mood disorders have traditionally been conceptualized as "neurochemical disorders," considerable literature from a variety of sources demonstrates significant reductions in regional central nervous system (CNS) volume and cell numbers (both neurons and glia) in persons with mood disorders. It is noteworthy that recent advances in cellular and molecular biology have resulted in the identification of 2 novel, hitherto completely unexpected targets of lithium's actions, discoveries that may have a major impact on the future use of this unique cation in biology and medicine. Chronic lithium treatment has been demonstrated to markedly increase the levels of the major neuroprotective protein bc1-2 in rat frontal cortex, hippocampus, and striatum. Similar lithium-induced increases in bc1-2 are also observed in cells of human neuronal origin and are observed in rat frontal cortex at lithium levels as low as approximately 0.3 mM. Bc1-2 is widely regarded as a major neuroprotective protein, and genetic strategies that increase bc1-2 levels have demonstrated not only robust protection of neurons against diverse insults, but have also demonstrated an increase in the regeneration of mammalian CNS axons. Lithium has also been demonstrated to inhibit glycogen synthase kinase 3beta (GSK-3beta), an enzyme known to regulate the levels of phosphorylated tau and beta-catenin (both of which may play a role in the neurodegeneration observed in certain forms of Alzheimer's disease). Consistent with the increases in bc1-2 levels and inhibition of GSK-3beta, lithium has been demonstrated to exert robust protective effects against diverse insults both in vitro and in vivo. These findings suggest that lithium may exert some of its long-term beneficial effects in the treatment of mood disorders via underappreciated neurotrophic and neuroprotective effects. To date, lithium remains the only medication demonstrated to markedly increase bc1-2 levels in several brain areas; in the absence of other adequate treatments, an investigation of the potential efficacy of lithium in the long-term treatment of several neurodegenerative disorders is warranted. Additionally, we suggest that a reconceptualization of the use of lithium in mood disorders may be warranted-namely, that the use of lithium as a neurotrophic/neuroprotective agent should be considered in the long-term treatment of mood disorders, irrespective of the "primary" treatment modality being used for the condition.
Publication Types:
Review
Review, tutorialPMID: 10826666, UI: 20284917
poster:SLS
thread:47998
URL: http://www.dr-bob.org/babble/20001102/msgs/48250.html