Aerobic exercise suppresses cognitive injury in patients with Alzheimer's disease by regulating long non-coding RNA TUG1

Copyright © 2024 Elsevier B.V. All rights reserved..

BACKGROUND: Alzheimer's disease (AD) is the primary reason for disability of the elderly. This article studied the diagnostic possibility of TUG1 and its potential mechanism in the regulation of aerobic exercise (AE) on AD.

METHODS: 77 AD patients undertook a three-month-long cycling exercise, and 77 healthy controls were recruited. Polymerase Chain Reaction amplification was applied to assess the expression of TUG1 and miR-129-5p. The diagnostic possibility was manifested by the receiver operating characteristic (ROC) curve. Spearman correlation analyzed the interrelationships between TUG1 and AD. In vivo, the APP/PS1 double transgenic mouse models of AD were included for rescue experiments. Morris water maze (MWM) was performed to assess cognitive function of AD mice.

RESULTS: The content of TUG1 was ascended in AD patients and was diminished after AE. The increase of TUG1 indicated the high risk of the occurrence of AD. TUG1 was closely connected to the cognitive assessment tools of AD patients. The TUG1/ miR-129-5p axis was the regulator of the regulation of AE in AD mice.

CONCLUSION: TUG1 was involved in AD development and targeted miR-129-5p to participate in the regulation of AE.

Medienart:

E-Artikel

Erscheinungsjahr:

2024

Erschienen:

2024

Enthalten in:

Zur Gesamtaufnahme - volume:826

Enthalten in:

Neuroscience letters - 826(2024) vom: 15. März, Seite 137732

Sprache:

Englisch

Beteiligte Personen:

Chen, Jiaojiao [VerfasserIn]
Su, Caixia [VerfasserIn]
Ma, Zhezhe [VerfasserIn]
Ou, Xiangling [VerfasserIn]
Zhan, Minmin [VerfasserIn]
Hu, Jiangbo [VerfasserIn]

Links:

Volltext

Themen:

Aerobic exercise
Alzheimer’s disease
Diagnosis
Journal Article
MiR-129-5p
MicroRNAs
Mirn129 microRNA, human
RNA, Long Noncoding
TUG1
TUG1 long noncoding RNA, human
TUG1 noncoding RNA, mouse

Anmerkungen:

Date Completed 01.04.2024

Date Revised 03.04.2024

published: Print-Electronic

Citation Status MEDLINE

doi:

10.1016/j.neulet.2024.137732

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM369803116