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M. J. Friedrich

JAMA. 2009;301(5):477.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

A cellular mechanism that involves the recycling of cell substances and protects cells against degeneration may, when it is disrupted, play a role in Parkinson disease, according to researchers at Emory University School of Medicine in Atlanta.

The presence of aggregates of a protein implicated in Parkinson disease, alpha-synuclein, in lesions called Lewy bodies in patients with the disorder has suggested that there is a problem with protein recycling and waste disposal in Parkinson disease. But until now a mechanism underlying this disruption hasn't been clear.

In studies using cell cultures and animal models of the disorder, the investigators showed that a process called chaperone-mediated autophagy controls the degradation and thereby regulates the activity of a neuronal survival factor, myocyte enhancer factor 2D (MEF2D), by shuttling it to lysosomes for degradation (Yang Q et al. Science. 2009;323[5910]:124-127). They observed that when chaperone-mediated autophagy was inhibited by . . . [Full Text of this Article]

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