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

Parkinson's Disease: Treatment01:24

Parkinson's Disease: Treatment

371
Neurodegenerative disorders, such as Parkinson's Disease (PD), involve the gradual and irreversible destruction of neurons in particular brain areas. These disorders exhibit standard features like proteinopathies, selective vulnerability of some neurons, and an interaction of intrinsic properties, genetics, and environmental influences in neural injury.
Parkinson's Disease is primarily a result of the loss of dopaminergic neurons in the substantia nigra pars compacta. The cornerstone of...
371
Parkinson's Disease: Overview01:15

Parkinson's Disease: Overview

700
Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is...
700
Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein01:20

Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein

432
Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
432
Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

260
Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
260

You might also read

Related Articles

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

Sort by
Same author

SUMOylation In Cerebral Ischaemia: A Dynamic, Isoform-Specific Regulator of Neuroprotection and Injury.

Journal of neurochemistry·2026
Same author

Adolescent Vitamin D Supplementation Reverses Neuroplasticity and Motivational Deficits Induced by Developmental Alcohol Exposure and Early-Life Stress.

International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience·2026
Same author

Autophagy-NAD<sup>+</sup> axis: emerging insights into neuronal homeostasis and neurodegenerative diseases.

Frontiers in molecular biosciences·2025
Same author

Intranasal 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) Administration Hampered Contractile Response of Dopamine in Isolated Rat Ileum.

Biomedicines·2025
Same author

RNA dysfunction in age-related macular degeneration: the role of U1 snRNP complex and neurodegenerative diseases.

International journal of retina and vitreous·2025
Same author

Role of the U1 snRNP Complex in Human Health and Disease.

Wiley interdisciplinary reviews. RNA·2025

Related Experiment Video

Updated: Sep 6, 2025

Fractionation for Resolution of Soluble and Insoluble Huntingtin Species
07:08

Fractionation for Resolution of Soluble and Insoluble Huntingtin Species

Published on: February 27, 2018

9.7K

SUMO-modifying Huntington's disease.

Ericks S Soares1, Rui D Prediger1,2, Patricia S Brocardo2

  • 1Post-graduate Program in Pharmacology, Federal University of Santa Catarina (UFSC), Florianópolis, Santa Catarina, Brazil.

IBRO Neuroscience Reports
|June 24, 2022
PubMed
Summary

Small ubiquitin-like modifiers (SUMOylation) impact neurodegenerative diseases like Huntington's disease (HD). This review explores how Htt SUMOylation contributes to HD pathogenesis.

Keywords:
HuntingtinHuntington’s diseaseNeurodegenerationPost-translational modificationSUMOSUMOylation

More Related Videos

Generation of Native, Untagged Huntingtin Exon1 Monomer and Fibrils Using a SUMO Fusion Strategy
11:22

Generation of Native, Untagged Huntingtin Exon1 Monomer and Fibrils Using a SUMO Fusion Strategy

Published on: June 27, 2018

8.1K
Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice
08:27

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice

Published on: March 11, 2020

6.3K

Related Experiment Videos

Last Updated: Sep 6, 2025

Fractionation for Resolution of Soluble and Insoluble Huntingtin Species
07:08

Fractionation for Resolution of Soluble and Insoluble Huntingtin Species

Published on: February 27, 2018

9.7K
Generation of Native, Untagged Huntingtin Exon1 Monomer and Fibrils Using a SUMO Fusion Strategy
11:22

Generation of Native, Untagged Huntingtin Exon1 Monomer and Fibrils Using a SUMO Fusion Strategy

Published on: June 27, 2018

8.1K
Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice
08:27

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice

Published on: March 11, 2020

6.3K

Area of Science:

  • Biochemistry
  • Neuroscience
  • Genetics

Background:

  • Small ubiquitin-like modifiers (SUMOs) regulate protein function via SUMOylation, a key post-translational modification.
  • SUMOylation is increasingly linked to neurodegenerative disorders, including Alzheimer's, Parkinson's, and Huntington's diseases (HD).
  • Huntington's disease (HD) is caused by a CAG repeat expansion in the huntingtin (HTT) gene, leading to toxic mutant Htt protein aggregation.

Purpose of the Study:

  • To review the critical role of huntingtin (Htt) SUMOylation in the cellular mechanisms underlying Huntington's disease (HD) pathogenesis.
  • To highlight the involvement of SUMOylation pathways, SUMO ligases, and cellular components in HD progression.

Main Methods:

  • Literature review focusing on SUMOylation, huntingtin protein, and Huntington's disease.
  • Analysis of existing research on post-translational modifications in neurodegeneration.

Main Results:

  • SUMOylation of huntingtin (Htt) influences its aggregation and toxicity, key factors in HD.
  • Dysregulation of SUMOylation pathways and associated proteins (SUMO ligases, mitochondrial, and autophagic components) are implicated in HD progression.

Conclusions:

  • Htt SUMOylation is a significant factor in the pathogenesis of Huntington's disease.
  • Understanding Htt SUMOylation offers potential therapeutic targets for HD treatment.