Can ISRIB rescue memories in Alzheimer's by returning mitochondrial movement?

Previous posts linked mitochondrial dysfunction with Alzheimer's disease: the mother's of  Down syndrome, diacetyl , and Herpes Zoster.
http://angelabiggs.blogspot.com/2017/06/alzheimers-and-dysfunctional.html

If the mitochondria cannot move down the nerve's axon to the synapse is memory blocked? Does blocking growth and metabolism prevent mitochondrial movement?

When cells are under stress it would be beneficial to slow not just metabolism but the generation of new mitochondrias.  The SESN2 genes are involved in mitochondria generation and slows metabolism.  Thus SESN2 protects the mitochondria under stress.

ISRIB stops the expression of SESN2 without inducing apoptosis the way P53 does. 

mitochondrial dysfunction and integrated stress response ISRIB 
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4825760/

Under ER or mitochondrial stress ATF4 is expressed which increases SESN2 mitochondrial genes.

 ATF4 targets Nuclear genes involved in folding and assembly of proteins in the ER and ATF acts on mitochondrial genes involved with metabolism including protection against oxidative stress and regulation of apoptosis. 

Activation of p53 abolishes and reverses the earlier ATF4-mediated pro-survival stress response and induces apoptotic cell death.

SESN2 are  sestrins which hault growth under times of stress.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3858445/

ER stress, Memory loss,  and Alzheimer's:  the unfolded protein response (high ATF4)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3906588/

mice given ISRIB had reversed memory loss
https://www.ncbi.nlm.nih.gov/pubmed/23741617/

So my question is...can mitochondrias be visualized moving down axons in response to ISRIB.

2016 Alzheimer's and mitochondria review paper
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4746252/