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 Experiment Videos

Modelling neuroinflammatory phenotypes in vivo.

Marion S Buckwalter1, Tony Wyss-Coray

  • 1Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, 94305-5235, USA. twc@stanford.edu

Journal of Neuroinflammation
|August 3, 2004
PubMed
Summary

Central nervous system inflammation is key to neurological disease. Studies using transforming growth factor beta-1 (TGF-beta1) mutant mice reveal its role in neuroinflammation and Alzheimer

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

Biological aging clocks in health and disease.

Nature medicine·2026
Same author

Targeting immune cells in the aged brain reveals that engineered cytokine IL-10 enhances neurogenesis and improves cognition.

Immunity·2026
Same author

Plasma proteomic signatures of cellular aging predict human disease.

Nature medicine·2026
Same author

Infarct-associated oligoclonal T cell expansion in chronic experimental stroke across age, sex, and models.

Experimental neurology·2026
Same author

Plasma proteomics reveals divergent sex-specific senescence and bone biology signatures across neurodegenerative diseases.

bioRxiv : the preprint server for biology·2026
Same author

Juvenile Mice Develop Infarct-Induced Neurodegeneration and Emerging Cognitive Decline in a Model of Pediatric Stroke.

Stroke·2026

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Central nervous system (CNS) inflammation is a critical, yet poorly understood, aspect of neurological disorders.
  • Acute brain injury or infection triggers a complex inflammatory response involving microglia, astrocytes, cytokines, chemokines, acute phase proteins, and complement factors.
  • Neurodegenerative diseases feature a continuous inflammatory response, with unclear beneficial or detrimental roles.

Purpose of the Study:

  • To investigate the role of inflammation in neurological diseases, particularly Alzheimer's disease (AD).
  • To utilize animal models to dissect the specific functions of inflammatory mediators.
  • To examine the impact of transforming growth factor beta-1 (TGF-beta1) on neuroinflammation.

Main Methods:

Related Experiment Videos

  • Employing mutant mice with varying levels of the cytokine TGF-beta1 to study neuroinflammatory phenotypes.
  • Crossbreeding TGF-beta1 mutant mice with established mouse models of Alzheimer's disease.
  • Analyzing neuropathological phenotypes characteristic of AD in the resulting crossbred mice.

    • Main Results:

    • Mutant mice expressing different levels of TGF-beta1 exhibited distinct neuroinflammatory phenotypes.
    • Crossbreeding provided novel insights into the contribution of inflammation to AD pathogenesis.
    • Specific neuropathological features of AD were modulated by TGF-beta1 levels and genetic background.

    Conclusions:

    • TGF-beta1 is a significant modulator of neuroinflammation with implications for neurological disease.
    • Animal models are valuable tools for dissecting complex inflammatory processes in the CNS.
    • Inflammation plays a crucial role in the development and progression of Alzheimer's disease phenotypes.