Preservation of testosterone may be an important step in preventing development of Parkinson’s disease, suggest the findings of a mouse study published in The Journal of Biological Chemistry (2013;288:20843-20855).

Compared with normal young male mice, young male mice that had been castrated produced dramatically higher levels of inducible nitric oxide synthase (iNOS) in the nigra of the midbrain, which causes neurons to die. 

The study, led by biochemist Kalipada Pahan, PhD, of Rush University Medical Center in Chicago, found that subcutaneous implantation of 5α-dihydrotestosterone pellets reversed the nigrostriatal Parkinson’s pathology in the castrated mice. The fact that castration does not cause Parkinson’s-like symptoms in male mice deficient in the iNOS gene indicates that testosterone loss causes those symptoms by means of increased nitric oxide production.

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