What a normal 90’s kid thinks after he/she hears the “Lithium”
What a 90’s kid in neurochemistry thinks when he/she hears “Lithium”
During the week of November 3rd, we reviewed an article concerning the efficacy of lithium in neurological diseases. As much of the public is aware, lithium has been used in the treatment of bipolar disorder for decades. When patients suffering from Major Depressive Disorder are unresponsive to all other popular treatments, lithium is actually one of the first “alternative” treatments considered. Lithium’s mood-altering effects come from its ability to inhibit GSK3. GSK3 activates serotonin autoreceptors, which prevent serotonergic action by facilitating its reuptake into the neuron. GSK3 is involved in many other pathways, especially those involved in neurodegeneration. Because of its actions on the normal constituents of a common pathway, lithium has been studied and shown to be effective in many other disorders and diseases. Lithium has also been shown to be neuroprotective when given as pretreatment before stroke through its prevention of excitotoxicity. After stroke, lithium treatment can even have benefits due to its ability to induce transcription and proliferation, leading to neuronal recovery. In Parkinson’s, lithium has been shown prevent apoptotic (programmed) cell death. In Huntington’s disease, lithium treatment prevents excitotoxicity and increases the expression of neuroprotective factors leading to improved mood and also some improvement in motor function. Lithium has also been effective in amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease) for similar reasons, though it is most effective when supplemented with antioxidants as oxidative stress has been implicated in ALS onset. Lithium has been shown to be effective in slowing the progression of multiple sclerosis (MS) by reducing inflammatory responses. Lithium’s neuroprotective role in MS was shown to be greatest when used before the disease’s onset. Lithium even has been shown to curb alcohol-induced degeneration in utero and greatly diminishes the symptoms of fetal alcohol syndrome; this protection was even seen when lithium was administered after alcohol consumption. Lithium can also be used to counteract some of the adverse effects of antipsychotics without decreasing their efficacy. Lithium also has been shown to be effective in preventing the hyper-phosphorylation of tau proteins and amyloid-β aggregation.
As we can plainly see, lithium has numerous benefits in neurological treatment and also can be used to prevent many adverse effects. On paper, it appears to be a neuroprotective wonder-drug. Why is the public not taking lithium supplements? In the lab, lithium also shows promise; clinical trials are another story. Some studies show great effect, while others are inconclusive at best. Also, a simple WebMD search shows that side effects include nausea, diarrhea, dizziness, muscle weakness, and fatigue. There also are some potential interactions with many commonly-prescribed and over-the-counter medications. Members of the general public should not jump to conclusions and buy lithium supplements with a 30-day supply in one pill like they do with vitamin C. Because of its many routes of action, lithium has the potential to cause a slew of adverse effects if not dosed properly. When used to treat bipolar disorder, lithium levels are monitored very carefully to prevent toxicity. As human studies on neurodegeneration attenuation show conflicting results, more research should be done with consistent methods and longitudinal designs to evaluate the long-term efficacy of lithium treatment in degenerative diseases.
Just a Hit by a Grunge Band?
