MbrlCatalogueTitleDetail

Do you wish to reserve the book?
Improvement Effect of Mitotherapy on the Cognitive Ability of Alzheimer’s Disease through NAD+/SIRT1-Mediated Autophagy
Improvement Effect of Mitotherapy on the Cognitive Ability of Alzheimer’s Disease through NAD+/SIRT1-Mediated Autophagy
Hey, we have placed the reservation for you!
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
You are currently in the queue to collect this book. You will be notified once it is your turn to collect the book.
Oops! Something went wrong.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Improvement Effect of Mitotherapy on the Cognitive Ability of Alzheimer’s Disease through NAD+/SIRT1-Mediated Autophagy
Oops! Something went wrong.
Oops! Something went wrong.
While trying to remove the title from your shelf something went wrong :( Kindly try again later!
Title added to your shelf!
Title added to your shelf!
View what I already have on My Shelf.
Oops! Something went wrong.
Oops! Something went wrong.
While trying to add the title to your shelf something went wrong :( Kindly try again later!
Do you wish to request the book?
Improvement Effect of Mitotherapy on the Cognitive Ability of Alzheimer’s Disease through NAD+/SIRT1-Mediated Autophagy
Improvement Effect of Mitotherapy on the Cognitive Ability of Alzheimer’s Disease through NAD+/SIRT1-Mediated Autophagy

Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
How would you like to get it?
We have requested the book for you! Sorry the robot delivery is not available at the moment
We have requested the book for you!
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Improvement Effect of Mitotherapy on the Cognitive Ability of Alzheimer’s Disease through NAD+/SIRT1-Mediated Autophagy
Improvement Effect of Mitotherapy on the Cognitive Ability of Alzheimer’s Disease through NAD+/SIRT1-Mediated Autophagy
Journal Article

Improvement Effect of Mitotherapy on the Cognitive Ability of Alzheimer’s Disease through NAD+/SIRT1-Mediated Autophagy

2023
Request Book From Autostore and Choose the Collection Method
Overview
To date, Alzheimer’s disease (AD) has grown to be a predominant health challenge that disturbs the elderly population. Studies have shown that mitochondrial dysfunction is one of the most significant features of AD. Transplantation therapy of healthy mitochondria (mitotherapy), as a novel therapeutic strategy to restore mitochondrial function, is proposed to treat the mitochondria−associated disease. Also, the molecular mechanism of mitotherapy remains unclear. Here, we applied the mitotherapy in AD model mice induced by amyloid−β (Aβ) plaque deposition and suggested that autophagy would be an important mechanism of the mitotherapy. After the healthy mitochondria entered the defective neuronal cells damaged by the misfolded Aβ protein, autophagy was activated through the NAD+−dependent deacetylase sirtuin 1 (SIRT1) signal. The damaged mitochondria and Aβ protein were eliminated by autophagy, which could also decrease the content of radical oxygen species (ROS). Moreover, the levels of brain−derived neurotrophic factor (BDNF) and extracellular−regulated protein kinases (ERK) phosphorylation increased after mitotherapy, which would be beneficial to repair neuronal function. As a result, the cognitive ability of AD animals was ameliorated in a water maze test after the healthy mitochondria were administrated to the mice. The study indicated that mitotherapy would be an effective approach to AD treatment through the mechanism of autophagy activation.