Lithium profoundly prevents brain damage associated with Parkinson disease

Jun 24, 2011

Lithium profoundly prevents the aggregation of toxic proteins and cell loss associated with Parkinson disease (PD) in a mouse model of the condition.

Preclinical research is now underway at the Buck Institute for Research on Aging to determine correct dosages for a drug that continues to be the gold standard for the treatment of bipolar disorder. The Buck is currently working toward initiating a Phase 2a clinical studies of lithium in humans in conjunction with standard Parkinson disease drug therapy. The research appears in the June 24 online edition of the Journal of Neuroscience Research.

"This is the first time lithium has been tested in an animal model of PD," said lead author and Buck Professor Julie Andersen PhD. "The fact that lithium's safety profile in humans is well understood greatly reduces trial risk and lowers a significant hurdle to getting it into the clinic."

According to Andersen, lithium has recently been suggested to be neuroprotective in relation to several neurodegenerative conditions including Alzheimer disease, Huntington disease, and amyotrophic lateral sclerosis and has been touted for its antiaging properties in simple animals. "We fed our mice levels of lithium that were at the low end of the therapeutic range," said Andersen. "The possibility that lithium could be effective in PD patients at subclinical levels is exciting, because it would avoid many side effects associated at the higher dose range." Overuse of lithium has been linked to hyperthyroidism and kidney toxicity.

The research was supported by a grant from the National Institutes of Health.

Source: News Release
Buck Institute for Age Research
June 24, 2011