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Behavioral deficits without motor neuron loss in mice fed cycad : implications for ALS

University of British Columbia

Amyotrophic lateral sclerosis-parkinsonism dementia complex (ALS-PDC) is a neurodegenerative disease characterized by features of ALS, parkinsonism, and Alzheimer's disease (AD). Occurring primarily in Guam, it has been linked epidemiologically to the consumption of cycad. Similarly, mice fed cycad develop a neurological disorder that mimics ALS-PDC both behaviorally and neuropathologically. In previous studies employing this model, mice were fed cycad for the entire duration of the experiment. However, many human cases of ALS-PDC arise after a period in which little or no cycad is consumed. We therefore hypothesize that feeding cycad to mice for a limited amount of time will lead to the persistence and even worsening of symptoms despite the cessation of cycad exposure. In contrast, we found that the mice may recover from significant behavioral deficits (Experiment 1). In Experiment 2, we sought to extend these findings to older animals that were fed cycad for a longer time. These mice displayed no symptoms through most of the experiment but developed a severe behavioral syndrome months after the cessation of cycad feeding. Both groups of mice had no significant loss of motor neurons in the lumbar spinal cord. These data suggest the possibility of a "window of opportunity" in which symptoms are detectable but neurons are yet rescuable. This highlights the importance of early detection and treatment of ALS.

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2009-12-11

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http://hdl.handle.net/2429/16565

Neuroscience

University of British Columbia

UBCV

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