Tau Knockout and α- Synuclein A53T Synergy Modulated Parvalbumin-Positive Neurons Degeneration Staging in Substantia Nigra Pars Reticulata of Parkinson's Disease-Liked Model

The loss of parvalbumin-positive (PV ) neurons in the substantia nigra pars reticulata (SNR) was observed in patients with end-stage Parkinson's disease (PD) and our previously constructed old-aged α × triple transgenic mice model of PD. The aim of this study was to examine the progress of PV n...

Full description

Saved in:
Bibliographic Details
Published inFrontiers in aging neuroscience Vol. 13; p. 784665
Main Authors Zheng, Meige, Liu, Yanchang, Xiao, Zhaoming, Jiao, Luyan, Lin, Xian
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Research Foundation 11.01.2022
Frontiers Media S.A
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:The loss of parvalbumin-positive (PV ) neurons in the substantia nigra pars reticulata (SNR) was observed in patients with end-stage Parkinson's disease (PD) and our previously constructed old-aged α × triple transgenic mice model of PD. The aim of this study was to examine the progress of PV neurons loss. We demonstrated that, as compared with non-transgenic ( ) mice, the accumulation of α- in the SNR of aged α × mice was increased obviously, which was accompanied by the considerable degeneration of PV neurons and the massive generation of apoptotic NeuN TUNEL co-staining neurons. Interestingly, PV was not costained with TUNEL, a marker of apoptosis. PV neurons in the SNR may undergo a transitional stage from decreased expression of PV to increased expression of NeuN and then to TUNEL expression. In addition, the degeneration of PV neurons and the expression of NeuN were rarely observed in the SNR of and the other triple transgenic mice. Hence, we propose that knockout and α synergy modulate PV neurons degeneration staging in the SNR of aged PD-liked mice model, and NeuN may be suited for an indicator that suggests degeneration of SNR PV neurons. However, the molecular mechanism needs to be further investigated.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Edited by: Mario Sanhueza, Universidad Mayor, Chile
This article was submitted to Cellular and Molecular Mechanisms of Brain-aging, a section of the journal Frontiers in Aging Neuroscience
Reviewed by: Ichiro Kawahata, Tohoku University, Japan; Sachchida Nand Rai, University of Allahabad, India; Roberta Marongiu, Weill Cornell Medicine, United States
These authors have contributed equally to this work
ISSN:1663-4365
1663-4365
DOI:10.3389/fnagi.2021.784665