17β-trenbolone was administered to adult and pregnant rats and the primary hippocampal neurons
Administered directly to the campus?
Alzheimer Treatments have failed, so its not as simple as you state. Secondly its linked, strongly to diabetes.
The most promising treatment was a drug Squalmine that targeted PTP1B - which funnily enough is a strong target for help with obesity and treatment of diabetes.
But it didnt cross the blood brain barrier, until they found trodusquemine did. Which now may be a treatment for alzheimers, and diabetes. (and incidientally clearly out atherosclerosis plaque with a single dose and capable of repairing/regenerating heart tissue for heart attack patients).
The study says 48 hours, some of the tests are in vitro.
Three secretases are involved
in proteolysis of APP, α-secretase, β-secretase, and γ-secretase. Cleavage of APP by β- and γ-secretases will produce Aβ. On the contrast,
Aβ production will be avoided if APP is cleaved first by α-secretase instead by β-secretase
What that is stating is that there is an increase in those β and γ in that 48 hour window after tren administration in those rats, or at least in the in vitro tests, you need to see how the production of the enzyme in that window is being increase, and it needs to be done over a long period of time not 48 hours.
From your study
17βtrenbolone accumulated predominantly in brain, especially in the hippocampus
Most of the tren dose ends up in the brain? Somehow I dont think this is particularly accurate in humans. In their graph they are showing that the ratio of tren in the male hippocampus is 14x higher than the plasma level in blood after 12 hours of administration. They also measured T levels, and it barely changed over the 48 hours with male rats, and that estrogen went up.