Targeting Alzheimer's disease neuronal mitochondria as a therapeutic approach

2021 ◽  
pp. 343-364
Author(s):  
Isaac G. Onyango ◽  
Gorazd B. Stokin
2006 ◽  
Vol 14 (7S_Part_26) ◽  
pp. P1391-P1392
Author(s):  
Eleanor Drummond ◽  
Fernando Goni ◽  
Frances Prelli ◽  
Henrieta Scholtzova ◽  
Thomas Wisniewski

1995 ◽  
Vol 10 (10) ◽  
pp. 871-874 ◽  
Author(s):  
Marcel Bahro ◽  
Earle Silber ◽  
Paulette Box ◽  
Trey Sunderland

2021 ◽  
Vol 17 (S9) ◽  
Author(s):  
Noah R Johnson ◽  
Athena Ching‐Jung Wang ◽  
Christina M Coughlan ◽  
Stefan H Sillau ◽  
Esteban M Lucero ◽  
...  

2014 ◽  
Vol 13 (3) ◽  
pp. 491-500 ◽  
Author(s):  
Sayed Sohrab ◽  
Sajjad Karim ◽  
Mohammad Kamal ◽  
Adel Abuzenadah ◽  
Adeel Chaudhary ◽  
...  

2021 ◽  
Vol 11 (2) ◽  
pp. 221-228
Author(s):  
Lijuan Huang ◽  
Hao Wang ◽  
Haijuan Sui ◽  
Yijie Shi ◽  
Liang Zhao

It was well known that circulating plasma exosomes (Pla-Exo) were enriched with multiple microRNAs (miRNAs) and participated in the regulation of biological and pathological process via exchanging information and transferring substance into targeted cells and organs. Therefore, clinical significance of Pla-Exo had been recognized and they functioned as biomarkers for the clinical diagnosis or therapeutic applications to treat diseases. We explored the possibility of using Pla-Exo as a novel therapeutic approach for ameliorating cognitive dysfunction in Alzheimer’s disease (AD) mice. Here we found that Pla-Exo freely crossed the blood-brain barrier (BBB) and was transferred into the hippocampus of mice. After following peritoneal injection (I.P.) of Pla-Exo, survival of neuron cells was enhanced and cognitive disorder was attenuated in okadaic acid (OA) treated mice via deactivating GSK-3β and down-regulating GSK-3β mediated hyperphosphorylation of Tau protein. Finally, some potential exosomal miRNAs were screened by bioinformatics analysis and confirmed their target of GSK-3β. Taken together, all data proved that Pla-Exo contributed to the amelioration of cognitive impairments.


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