Thumbnail Image
Item

Infusion of plasma from exercised mice ameliorates cognitive dysfunction by increasing hippocampal neuroplasticity and mitochondrial functions in 3xtg-ad mice

Kim, TW
; 
Park, SS
; 
Park, JY
; 
Park, HS
Citations
Altmetric:
Genre
Journal Article
Date
2020-05-01
Advisor
Committee member
Group
Department
Subject
Alzheimer’s disease
 cognitive function
 exercise
 hippocampus
 mitochondria
 neuroplasticity
 young plasma
Permanent link to this record
http://hdl.handle.net/20.500.12613/4483
Collections
Faculty/Researcher Works
Show all metadata
Files
Thumbnail Image
Infusion of Plasma from Exercised Mice Ameliorates Cognitive Dysfunction by Increasing Hippocampal Neuroplasticity and Mitoc.pdf
Adobe PDF, 3.64 MB
Research Projects
Organizational Units
Journal Issue
DOI
10.3390/ijms21093291
Abstract
© 2020, MDPI AG. All rights reserved. Alzheimer’s disease is the most common neurodegenerative brain disease causing dementia. It is characterized by slow onset and gradual worsening of memory and other cognitive functions. Recently, parabiosis and infusion of plasma from young mice have been proposed to have positive effects in aging and Alzheimer’s disease. Therefore, this study examined whether infusion of plasma from exercised mice improved cognitive functions related to the hippocampus in a 3xTg-Alzheimer’s disease (AD) model. We collected plasma from young mice that had exercised for 3 months and injected 100 µL of plasma into the tail vein of 12-month-old 3xTg-AD mice 10 times at 3-day intervals. We then analyzed spatial learning and memory, long-term memory, hippocampal GSK3β/tau proteins, synaptic proteins, mitochondrial function, apoptosis, and neurogenesis. In the hippocampus of 3xTg-AD mice, infusion of plasma from exercised mice improved neuroplasticity and mitochondrial function and suppressed apoptosis, ultimately improving cognitive function. However, there was no improvement in tau hyperphosphorylation. This study showed that plasma from exercised mice could have a protective effect on cognitive dysfunction and neural circuits associated with AD via a tau-independent mechanism involving elevated brain-derived neurotrophic factor due to exercise.
Description
Citation
Citation to related work
MDPI AG
Has part
International Journal of Molecular Sciences
ADA compliance
For Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu
Embedded videos