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

Glial Cells01:04

Glial Cells

85.7K
Overview
85.7K
Cross-bridge Cycle01:26

Cross-bridge Cycle

116.1K
As muscle contracts, the overlap between the thin and thick filaments increases, decreasing the length of the sarcomere—the contractile unit of the muscle—using energy in the form of ATP. At the molecular level, this is a cyclic, multistep process that involves binding and hydrolysis of ATP, and movement of actin by myosin.
116.1K
Neurogenesis and Regeneration of Nervous Tissue01:15

Neurogenesis and Regeneration of Nervous Tissue

680
In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...
680
Amyloid Fibrils03:03

Amyloid Fibrils

9.1K
Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining,...
9.1K
Parkinson's Disease: Overview01:15

Parkinson's Disease: Overview

342
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...
342
Neural Regulation01:37

Neural Regulation

39.0K
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.
39.0K

You might also read

Related Articles

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

Sort by
Same author

Mitochondrial NADK2-dependent NADPH controls tau oligomer uptake in human neurons.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2026
Same author

Microglial ITAM & ITIM Signaling in Neurodegenerative Disease and Brain Aging.

Journal of molecular biology·2026
Same author

The Genotoxic Stress Sensor ZBP1 Drives Tau Pathology.

Cells·2026
Same author

Accuracy of Sentinel Lymph Node Biopsy to Predict Nodal Metastasis in Head and Neck Merkel Cell Carcinoma.

JAMA otolaryngology-- head & neck surgery·2026
Same author

Wolf in sheep's clothing: leveraging sheep to study how maternal immune activation contributes to neurodevelopmental disorders.

Brain, behavior, and immunity·2026
Same author

Caspase-8 expression in CD8<sup>+</sup> T cells promotes pathogen restriction in the brain during <i>Toxoplasma gondii</i> infection.

Science advances·2025

Related Experiment Video

Updated: May 15, 2025

Primary Cultures of Rat Astrocytes and Microglia and Their Use in the Study of Amyotrophic Lateral Sclerosis
09:36

Primary Cultures of Rat Astrocytes and Microglia and Their Use in the Study of Amyotrophic Lateral Sclerosis

Published on: June 23, 2022

3.3K

Glia get RIPped in ALS.

Alexis M Johnson1, John R Lukens1

  • 1Center for Brain Immunology and Glia (BIG), Department of Neuroscience, University of Virginia, Charlottesville, VA, USA; Neuroscience Graduate Program, University of Virginia, Charlottesville, VA, USA; Brain Immunology and Glia Graduate Training Program, University of Virginia, Charlottesville, VA, USA.

Immunity
|April 9, 2025
PubMed
Summary

Researchers identified RIPK1 as a key regulator of glial cell-driven neuroinflammation in amyotrophic lateral sclerosis (ALS) models. This finding clarifies pathways coordinating neuroinflammation in ALS progression.

More Related Videos

Clinical Testing and Spinal Cord Removal in a Mouse Model for Amyotrophic Lateral Sclerosis ALS
12:35

Clinical Testing and Spinal Cord Removal in a Mouse Model for Amyotrophic Lateral Sclerosis ALS

Published on: March 17, 2012

28.0K
An In Vitro Model for the Study of Cellular Pathophysiology in Globoid Cell Leukodystrophy
07:45

An In Vitro Model for the Study of Cellular Pathophysiology in Globoid Cell Leukodystrophy

Published on: October 21, 2014

7.9K

Related Experiment Videos

Last Updated: May 15, 2025

Primary Cultures of Rat Astrocytes and Microglia and Their Use in the Study of Amyotrophic Lateral Sclerosis
09:36

Primary Cultures of Rat Astrocytes and Microglia and Their Use in the Study of Amyotrophic Lateral Sclerosis

Published on: June 23, 2022

3.3K
Clinical Testing and Spinal Cord Removal in a Mouse Model for Amyotrophic Lateral Sclerosis ALS
12:35

Clinical Testing and Spinal Cord Removal in a Mouse Model for Amyotrophic Lateral Sclerosis ALS

Published on: March 17, 2012

28.0K
An In Vitro Model for the Study of Cellular Pathophysiology in Globoid Cell Leukodystrophy
07:45

An In Vitro Model for the Study of Cellular Pathophysiology in Globoid Cell Leukodystrophy

Published on: October 21, 2014

7.9K

Area of Science:

  • Neuroscience
  • Immunology
  • Molecular Biology

Background:

  • Microglia and astrocytes are key glial cells involved in neuroinflammation.
  • Neuroinflammation contributes to neurodegenerative disease progression, notably in amyotrophic lateral sclerosis (ALS).
  • Specific molecular pathways coordinating glial cell-mediated neuroinflammation in ALS are not well understood.

Purpose of the Study:

  • To identify key regulators of glial cell-driven neuroinflammation in amyotrophic lateral sclerosis (ALS).
  • To elucidate the role of specific molecular pathways in coordinating glial responses in ALS.
  • To investigate potential therapeutic targets for ALS by understanding glial cell function.

Main Methods:

  • Utilized multiple mouse models of amyotrophic lateral sclerosis (ALS).
  • Investigated the role of Receptor-Interacting Protein Kinase 1 (RIPK1) in glial cells.
  • Analyzed neuroinflammatory responses mediated by microglia and astrocytes.

Main Results:

  • Receptor-Interacting Protein Kinase 1 (RIPK1) was identified as a pivotal regulator.
  • RIPK1 plays a crucial role in glial cell-driven neuroinflammation across different ALS models.
  • The study highlights RIPK1's involvement in pathways coordinating glial responses in ALS.

Conclusions:

  • Receptor-Interacting Protein Kinase 1 (RIPK1) is a critical mediator of glial cell-driven neuroinflammation in ALS.
  • Targeting RIPK1 may offer a therapeutic strategy for managing neuroinflammation in amyotrophic lateral sclerosis.
  • Further research into RIPK1 pathways can advance our understanding of ALS pathogenesis.