http://www.checkbiotech.org/orphan_N...px?infoId=2824
"To gain insight into the cellular processes that play a role in protein misfolding, the research group, led by Ellen Nollen, looked for genes in the round worm Caenorhabditis elegans that, if switched off, cause the number of inclusions to increase. During the course of their research, the scientists individually switched off 17,000 of the 19,000 genes and studied the effect on protein formation.

The study findings indicate that the gene sir-2.1 has a considerable effect on protein formation. In humans, this gene, called SIRT1, is evolutionarily conserved and is involved in the aging of yeast, flies, and worms and probably also in mammals. It lengthens the lifespan of worms by the activation of various routes through which signals are transmitted (stress response and insulin signal transduction). These findings suggest that sir 2.1 may represent a possible mechanistic relationship between aging and Parkinson's disease.

The accumulation of proteins has been shown to be strongly age-dependent and to occur in clearly distinguishable phases. From RNA-interference screening, it appears that the manner in which proteins accumulate in the roundworm model can be clearly differentiated from that of other diseases in which the aggregation of proteins occurs. Moreover, it shows a clear link with the aging process, in which the membranes of the endoplasmatic reticulum/Golgi system of the cell probably play a role.

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