The brains of people suffering from diseases of old age, such as Alzheimer’s and Parkinson’s, often present with an accumulation and clotting of misfolded proteins. While searching for the cause of this phenomenon, UMCG researcher and geneticist Prof. Ellen Nollen stumbled across the gene that regulates the breakdown of the essential amino acid tryptophan. Disabling this gene in worm models greatly increases the protective effect against Alzheimer’s and Parkinson’s. The results seem to indicate that raising tryptophan levels may be important for these protective effects. The researchers’ findings will be published this week in the leading American journal Proceedings of the National Academy of Sciences.
The researchers focused their studies on the tryptophan 2,3-dioxygenase (TDO-2) gene. This gene is responsible for regulating the enzyme TDO-2, which breaks down the essential amino acid tryptophan. Nollen’s studies showed that repressing the TDO-2 enzyme blocked the breakdown of tryptophan and increased the lifespan of the worm, also known as C. elegans. Adding extra tryptophan to the worms’ diet gave the same protective effect. The worm, C. elegans, is a widely accepted model organism for studying diseases of old age such as Alzheimer’s and Parkinson’s.
The TDO-2 gene has been well preserved during evolution. In other words, there are many similarities in the TDO-2 enzyme, and its role in tryptophan metabolism, between the worm and humans. The researchers are very interested in studying how the tryptophan metabolism in humans can be linked to the development of diseases of old age like Alzheimer’s and Parkinson’s. This may provide clues in the search for new treatments.
Please contact the UMCG Press Office for more information, tel. (050) 361 22 00.
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