Key molecule of ageing discovered!

Every cell and every organism ages sooner or later. But why is this so? Scientists at the German Cancer Research Center in Heidelberg have now discovered for the first time a protein that represents a central switching point in the aging process. It controls the life span of an individual – from the fly to the human being. This opens up new possibilities for developing therapies against age-related diseases.

Oxidative stress causes cells and entire organisms to age. If reactive oxygen species accumulate, this causes damage to the DNA as well as changes in the protein molecules and lipids in the cell. The cell ultimately loses its functionality and dies. Over time, the tissue suffers and the body ages. “The theory of oxidative stress or the accumulation of reactive oxygen species as the cause of aging has existed since the 1950s,” says Peter Krammer of the German Cancer Research Center (DKFZ). In fact, reactive oxygen species do more than just damage the body. For example, they are essential for the T-cells of the immune system to become active. DKFZ researchers led by Krammer and Karsten Gülow have now discovered the key regulator that is responsible for shifting the sensitive balance from vital to harmful amounts of reactive oxygen molecules and thus accelerating the aging process: A protein molecule called TXNIP (thiore doxin interacting protein).

One way in which the body disposes of harmful reactive oxygen species is their conversion by the enzyme thioredoxin-1 (TRX-1). TRX1 has been proven to play a role in protecting DNA from oxidative stress and slowing down aging processes. Its antagonist TXNIP inhibits thioredoxin-1 and thus ensures that the reactive oxygen molecules are retained.

The DKFZ researchers led by Krammer and Gülow now wanted to know whether more TXNIP is formed in the body with increasing age, thereby undermining the protective mechanism against oxidative stress. To this end, they first compared T cells from the blood of a group of over 55year-old volunteers with the T cells of younger blood donors, who were between 20 and 25 years old.

In fact, it turned out that the cells of older subjects produce significantly more TXNIP.