Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Neural Regulation

Neural Regulation

Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.

You might also read

Related Articles

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

Sort by

Same author

Relative increase of memory B-cell subsets under s.c. B-cell-depleting therapies in multiple sclerosis.

Frontiers in immunology·2026

Same author

Exploratory crossover field study indicates efficacy and feasibility of light therapy glasses to mitigate fatigue in multiple sclerosis.

Scientific reports·2026

Same author

Sex-Dependent Effects of CSF1R-Mediated Myeloid Cell Depletion in a Mouse Model of Multiple System Atrophy.

The European journal of neuroscience·2026

Same author

Reply to: "Mathematical Comments on Linking Neurofilament Light Chain Levels to Disease Severity in HSP Subtypes SPG11 and SPG15".

Movement disorders : official journal of the Movement Disorder Society·2026

Same author

<sup>68</sup>Ga-FAPI-PET/CT in extra-cervical CUP: Head-to-Head Comparison of <sup>68</sup>Ga-FAPI-46 with <sup>18</sup>F-FDG in 13 patients.

European journal of nuclear medicine and molecular imaging·2026

Same author

Photon-counting CT in cardiac imaging: multi-institutional guidance on technical principles, clinical evidence, and practical protocols.

European journal of radiology·2026

Search research articles

Related Experiment Video

Updated: Dec 25, 2025

Analyzing the Parkinson's Disease Mouse Model Induced by Adeno-associated Viral Vectors Encoding Human α-Synuclein

Analyzing the Parkinson's Disease Mouse Model Induced by Adeno-associated Viral Vectors Encoding Human α-Synuclein

Published on: July 29, 2022

alpha-Synuclein: a Modulator During Inflammatory CNS Demyelination.

Kristina Kuhbandner^1,2, Alana Hoffmann¹, María Nazareth González Alvarado^2,3

¹Department of Molecular Neurology, University Hospital Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Schwabachanlage 6, 91054, Erlangen, Germany.

Journal of Molecular Neuroscience : MN

|March 25, 2020

Summary

Alpha-Synuclein (aSyn) deficiency reduces central nervous system inflammation and myelin loss in experimental autoimmune encephalomyelitis. However, aSyn does not impact demyelination or remyelination in the cuprizone model.

Keywords:

Cuprizone Demyelination Experimental autoimmune encephalomyelitis Neuroinflammation alpha-Synuclein

More Related Videos

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

Published on: June 26, 2018

A Method to Study α-Synuclein Toxicity and Aggregation Using a Humanized Yeast Model

A Method to Study α-Synuclein Toxicity and Aggregation Using a Humanized Yeast Model

Published on: November 25, 2022

Related Experiment Videos

Last Updated: Dec 25, 2025

Analyzing the Parkinson's Disease Mouse Model Induced by Adeno-associated Viral Vectors Encoding Human α-Synuclein

Analyzing the Parkinson's Disease Mouse Model Induced by Adeno-associated Viral Vectors Encoding Human α-Synuclein

Published on: July 29, 2022

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

Published on: June 26, 2018

A Method to Study α-Synuclein Toxicity and Aggregation Using a Humanized Yeast Model

A Method to Study α-Synuclein Toxicity and Aggregation Using a Humanized Yeast Model

Published on: November 25, 2022

Area of Science:

Neuroscience
Immunology
Pathology

Background:

Neuroinflammation and demyelination are key features of neurological disorders like multiple sclerosis.
Understanding factors that modulate de- and regeneration is crucial for disease research.
Alpha-Synuclein (aSyn) is implicated in neurodegenerative disease pathology and modulates peripheral immune responses.

Purpose of the Study:

To investigate the role of alpha-Synuclein (aSyn) deficiency in central nervous system (CNS) de- and regenerative processes.
To analyze the impact of aSyn deficiency on experimental autoimmune encephalomyelitis (EAE) and cuprizone-induced demyelination models.

Main Methods:

Utilized two distinct animal models: chronic MOG35-55-induced experimental autoimmune encephalomyelitis (EAE) and the cuprizone model.
Conducted histopathological analysis of spinal cord cross-sections at 8 weeks post-EAE induction.
Assessed myelination and neuroinflammatory patterns following cuprizone-induced demyelination and subsequent remyelination.

Main Results:

aSyn-deficient mice showed significantly reduced CNS inflammation and myelin loss in late-stage EAE.
aSyn deficiency did not affect myelination or neuroinflammation in the cuprizone model.
Remyelination following cuprizone withdrawal was also unaffected by aSyn deficiency.

Conclusions:

Alpha-Synuclein (aSyn) plays a role in regulating peripheral immune responses during neuroinflammation, impacting degenerative events in demyelinating diseases like EAE.
The findings suggest a specific role for aSyn in inflammatory demyelination rather than direct modulation of myelin repair or non-inflammatory demyelination.