Key points from article :
Blocking nutrient sensing by rapamycin treatment delays healthy mice ageing.
Tests if it could also extend the life of mice with short telomeres (ST).
Found that the opposite happens: they age up to 50% faster.
ST cause telomere syndrome, diseases such as dyskeratosis congenita, aplastic anaemia, etc.
In mice with ST, mTOR pathway is hyper-activated, cells are more sensitive to nutrients.
It is precisely because of this that allows these mice to survive.
mTOR, also hyper-activated in some organs of elderly mice.
Indicates that this phenomenon is associated not only with abnormally accelerated ageing.
But occurs also in natural physiological ageing.
Results are of clinical interest in human syndromes associated with critically ST.
Study by Telomeres and Telomerase Group of the Spanish National Cancer Research Center.
Published in Nature Communications.