17Î²-trenbolone, an anabolic-androgenic steroid as well as an environmental hormone, contributes to neurodegeneration.
Both genetic and environmental factors contribute to neurodegenerative disorders. In a large number of neurodegenerative diseases (for example, Alzheimer's disease (AD)), patients do not carry the mutant genes. Other risk factors, for example the environmental factors, should be evaluated. 17Î²-trenbolone is a kind of environmental hormone as well as an anabolic-androgenic steroid. 17Î²-trenbolone is used as a growth promoter for livestock in the USA. Also, a large portion of recreational exercisers inject 17Î²-trenbolone in large doses and for very long time to increase muscle and strength. 17Î²-trenbolone is stable in the environment after being excreted. In the present study, 17Î²-trenbolone was administered to adult and pregnant rats and the primary hippocampal neurons. 17Î²-trenbolone's distribution and its effects on serum hormone levels and AÎ²42 accumulation in vivo and its effects on AD related parameters in vitro were assessed. 17Î²-trenbolone accumulated in adult rat brain, especially in hippocampus, and in the fetus brain. It altered AÎ²42 accumulation. 17Î²-trenbolone induced apoptosis of primary hippocampal neurons in vitro and resisted neuroprotective function of testosterone. Presenilin-1 protein expression was down-regulated while Î²-amyloid peptide 42 (AÎ²42) production and caspase-3 activities were increased. Both androgen and estrogen receptors mediated the processes. 17Î²-trenbolone played critical roles in neurodegeneration. Exercisers who inject large doses of trenbolone and common people who are exposed to 17Î²-trenbolone by various ways are all influenced chronically and continually. Identification of such environmental risk factors will help us take early prevention measure to slow down onset of neurodegenerative disorders
I've searched high and low and cant find get a link to the full article. Correct me if im wrong, but the way I interpret this is that they administered tren directly into the hippocampus which resulted in the resistance and down regulation, not the actual drug circulating through the system as it normally would if it were to be administered IM? Ive gone through my university portal to try and get the full article however it was only published less than a month ago in china, if i could have a read through the actual results could clear a few things up.