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

Gene therapy effectiveness differs for neuronal survival and behavioral performance.

R G Phillips1, M L Monje, L C Giuli

  • 1Department of Biological Sciences, Stanford University, Stanford, CA 94305-5020 USA.

Gene Therapy
|April 26, 2001
PubMed
Summary

Gene therapy using calbindin D(28K) shows neuroprotection against excitotoxic insults when administered up to 1 hour post-injury. However, delayed treatment impacts behavioral recovery, highlighting the critical timing for effective neuronal gene therapy.

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

Migraine and vertebrobasilar dissection: Case reports.

Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association·2015
Same author

Regulation of inflammatory transcription factors by heat shock protein 70 in primary cultured astrocytes exposed to oxygen-glucose deprivation.

Neuroscience·2014
Same author

Pharmacological induction of the 70-kDa heat shock protein protects against brain injury.

Neuroscience·2014
Same author

Innate inflammatory responses in stroke: mechanisms and potential therapeutic targets.

Current medicinal chemistry·2013
Same author

Influence of therapeutic hypothermia on regeneration after cerebral ischemia.

Frontiers of neurology and neuroscience·2013
Same author

Basolateral amygdala regulation of adult hippocampal neurogenesis and fear-related activation of newborn neurons.

Molecular psychiatry·2011

Area of Science:

  • Neuroscience
  • Gene Therapy
  • Neuroprotection

Background:

  • Clinical utility of neuronal gene therapy requires demonstrating neuroprotection after injury.
  • Calbindin D(28K) is a protein relevant to neuronal function and survival.

Purpose of the Study:

  • To investigate the efficacy of calbindin D(28K) gene transfer via herpes simplex virus amplicon vector for neuroprotection when administered at different time points after an excitotoxic insult.
  • To evaluate the impact of delayed gene therapy on behavioral recovery in a hippocampal-dependent task.

Main Methods:

  • Excitotoxic insult model in neurons.
  • Herpes simplex virus amplicon vector for calbindin D(28K) gene transfer.
  • Administration of gene therapy at immediate, 30 min, 1 h, and 4 h post-insult time points.

Related Experiment Videos

  • Assessment of neuronal survival and hippocampal-dependent behavioral performance.
  • Main Results:

    • Equivalent neuronal protection was observed when gene transfer occurred immediately, 30 min, or 1 h after the excitotoxic insult.
    • No significant neuroprotection was achieved with gene transfer 4 hours after the insult.
    • Despite similar neuronal sparing in immediate and 1-hour delay groups, behavioral recovery was significantly slower in the delayed treatment group.

    Conclusions:

    • Calbindin D(28K) gene transfer demonstrates neuroprotective effects against excitotoxic injury if initiated within 1 hour post-insult.
    • While neuronal survival can be maintained with delayed gene therapy, functional recovery may be compromised, underscoring the importance of timely intervention for optimal outcomes in neuronal gene therapy.