Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Effects of Wheat Malt Extract on Molecular and Behavioral Markers in Aged APP/PS1 and Wild-Type Mice.

International journal of molecular sciences·2026
Same author

Sex Differences in Dietary-Induced Liver Steatosis and Insulin Receptor-Related Signaling in Aged Mice Lacking Serotonin Transporter.

International journal of molecular sciences·2026
Same author

Distinct Role of γ-Synuclein in the Regulation of Motor Performance and Behavioral Responses in Mice.

Biomedicines·2026
Same author

Retrospective Study of the Physiological and Molecular Features of the S-FUS (1-359) Mouse Transgenic Model with an ALS-like Phenotype: Lifespan, Body Weight Dynamics, Movement Disorders, and Dysregulation of the Dopaminergic System.

Journal of molecular neuroscience : MN·2026
Same author

Sex-Dependent Phenotypic and Histomorphometric Biomarkers in the APPswe/PS1dE9/Blg Mouse Model of Alzheimer's Disease.

Brain sciences·2025
Same author

Bolus MPTP Injection in Aged Mice to Mimic Parkinson Disease: Effects of Low-Dose Antioxidant Treatment with Fullerene (C<sub>60</sub>) and Fullerenol (C<sub>60</sub>(OH)<sub>24</sub>).

Biomedicines·2025
Same journal

Precision Proteomic Profiling of Systemic Lupus Erythematosus-Correlating Disease Activity and Complement Levels with Clinical Phenotypes.

Biomedicines·2026
Same journal

The Role of Salivary Microbiota in Pancreatic Cancer: From Screening to Tumor Progression and Treatment Response.

Biomedicines·2026
Same journal

Diagnostic Utility of Surface Electromyography for Identifying Muscles Affected by Myofascial Trigger Points: A Scoping Review.

Biomedicines·2026
Same journal

Performance Assessment of a Locally Semi-Automated NGS-Based Workflow for Homologous Recombination Deficiency Testing in High-Grade Serous Ovarian Carcinoma.

Biomedicines·2026
Same journal

Coupling and Uncoupling Pleiotropy Between Hypertension and Type 2 Diabetes Contribute to Exploring Potential Heterogeneity in Cardiovascular Risk in East Asian Population.

Biomedicines·2026
Same journal

Maternal Response to Therapeutic Plasma Exchange in Early Gestation: A Case Series of Thrombotic Microangiopathies and Neurological Disorders.

Biomedicines·2026
See all related articles

Related Experiment Video

Updated: Jan 7, 2026

Recombinant &#945;- &#946;- and &#947;-Synucleins Stimulate Protein Phosphatase 2A Catalytic Subunit Activity in Cell Free Assays
09:36

Recombinant α- β- and γ-Synucleins Stimulate Protein Phosphatase 2A Catalytic Subunit Activity in Cell Free Assays

Published on: August 13, 2017

7.0K

Synaptic Changes in Mice Lacking Alpha- and Gamma-Synucleins.

Anastasia M Krayushkina1, Olga Morozova1, Anastasia Khizeva1

  • 1Institute of Physiologically Active Compounds at Federal Research Center of Problems of Chemical Physics and Medicinal Chemistry, Russian Academy of Sciences, 142432 Chernogolovka, Russia.

Biomedicines
|December 30, 2025
PubMed
Summary
This summary is machine-generated.

In Parkinson disease (PD) models, beta-synuclein compensates for alpha-synuclein loss, suggesting potential therapeutic strategies for synapse repair.

Keywords:
Parkinson’s diseasealpha-synucleinbeta-synucleinconditional knock-outgamma-synucleinmouse modelstriatum

More Related Videos

Bioluminescence Imaging of Neuroinflammation in Transgenic Mice After Peripheral Inoculation of Alpha-Synuclein Fibrils
09:32

Bioluminescence Imaging of Neuroinflammation in Transgenic Mice After Peripheral Inoculation of Alpha-Synuclein Fibrils

Published on: April 13, 2017

8.9K
Evaluation of Synapse Density in Hippocampal Rodent Brain Slices
07:44

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Published on: October 6, 2017

17.9K

Related Experiment Videos

Last Updated: Jan 7, 2026

Recombinant &#945;- &#946;- and &#947;-Synucleins Stimulate Protein Phosphatase 2A Catalytic Subunit Activity in Cell Free Assays
09:36

Recombinant α- β- and γ-Synucleins Stimulate Protein Phosphatase 2A Catalytic Subunit Activity in Cell Free Assays

Published on: August 13, 2017

7.0K
Bioluminescence Imaging of Neuroinflammation in Transgenic Mice After Peripheral Inoculation of Alpha-Synuclein Fibrils
09:32

Bioluminescence Imaging of Neuroinflammation in Transgenic Mice After Peripheral Inoculation of Alpha-Synuclein Fibrils

Published on: April 13, 2017

8.9K
Evaluation of Synapse Density in Hippocampal Rodent Brain Slices
07:44

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Published on: October 6, 2017

17.9K

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Alpha-synuclein is central to Parkinson disease (PD) pathogenesis.
  • Aggregated alpha-synuclein impairs dopaminergic (DA) neuron function.
  • Synuclein family members (alpha, beta, gamma) may have overlapping presynaptic roles.

Purpose of the Study:

  • Investigate the functional interplay between synuclein proteins in PD.
  • Determine the consequences of alpha-synuclein loss in the absence of gamma-synuclein.
  • Explore potential compensatory mechanisms in early PD.

Main Methods:

  • Generated a novel mouse line with conditional knockout of alpha-synuclein on a gamma-synuclein knockout background.
  • Assessed behavioral changes (explorer activity).
  • Quantified gene expression (Mao-B) and protein levels (beta-synuclein) in specific brain regions (midbrain, striatum).

Main Results:

  • Early alpha-synuclein loss induced reduced explorer activity and decreased midbrain Mao-B expression.
  • Transient increase in striatal beta-synuclein protein levels observed post-alpha-synuclein inactivation.
  • Dopamine metabolism remained unaffected, with no significant changes in other dopamine-related enzyme expression or protein levels.

Conclusions:

  • Sudden alpha-synuclein depletion triggers a compensatory increase in beta-synuclein.
  • Beta-synuclein can functionally replace lost alpha-synuclein, particularly in the context of gamma-synuclein absence.
  • This compensatory mechanism may underlie synapse reconstruction in early PD and inform replacement therapies.