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

Aging01:26

Aging

Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
The Effect of Aging on Tissues01:19

The Effect of Aging on Tissues

Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...

You might also read

Related Articles

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

Sort by
Same author

Increased expression of aromatase after focal cerebral ischemia: Relevance to neuroprotection and functional recovery.

Neuroprotection (Chichester, England)·2026
Same author

Diabetes increases SCO-spondin secretion but reduces Wnt5a interaction with ependymal cells, inducing ciliary stiffness and Frizzled-2 downregulation.

Neurobiology of disease·2025
Same author

Role of early life adversities in inflammation-related neuropsychiatric comorbidity in obesity.

Brain, behavior, and immunity·2025
Same author

Elevation of ghrelin by B-adrenergic activation is independent of glucose variations and feeding regimen in the rat.

Endocrine·2025
Same author

Early movement restriction impairs the development of sensorimotor integration, motor skills and memory in rats: Towards a preclinical model of developmental coordination disorder?

The European journal of neuroscience·2024
Same author

Tibolone treatment after traumatic brain injury exerts a sex-specific and Y chromosome-dependent regulation of methylation and demethylation enzymes and estrogen receptors in the cerebral cortex.

Biochimica et biophysica acta. Molecular basis of disease·2024

Related Experiment Video

Updated: Jul 13, 2026

Precise Visualization of Insulin Receptors A and B in Murine Brain with an RNA In Situ Hybridization Assay
08:34

Precise Visualization of Insulin Receptors A and B in Murine Brain with an RNA In Situ Hybridization Assay

Published on: July 15, 2025

Estradiol, insulin-like growth factor-I and brain aging.

Luis M Garcia-Segura1, Yolanda Diz-Chaves, Margarita Perez-Martin

  • 1Instituto Cajal, CSIC, E-28002 Madrid, Spain. lmgs@cajal.csic.es

Psychoneuroendocrinology
|July 10, 2007
PubMed
Summary

Aging decreases key hormones like estradiol and insulin-like growth factor-I (IGF-I), potentially harming brain function. Their interaction promotes neuroprotection by activating survival pathways and inhibiting damaging processes in the brain.

More Related Videos

Ovariectomy and 17β-estradiol Replacement in Rats and Mice: A Visual Demonstration
06:51

Ovariectomy and 17β-estradiol Replacement in Rats and Mice: A Visual Demonstration

Published on: June 7, 2012

Related Experiment Videos

Last Updated: Jul 13, 2026

Precise Visualization of Insulin Receptors A and B in Murine Brain with an RNA In Situ Hybridization Assay
08:34

Precise Visualization of Insulin Receptors A and B in Murine Brain with an RNA In Situ Hybridization Assay

Published on: July 15, 2025

Ovariectomy and 17β-estradiol Replacement in Rats and Mice: A Visual Demonstration
06:51

Ovariectomy and 17β-estradiol Replacement in Rats and Mice: A Visual Demonstration

Published on: June 7, 2012

Area of Science:

  • Neuroscience
  • Endocrinology
  • Molecular Biology

Background:

  • Hormonal changes with aging, specifically decreases in estradiol and insulin-like growth factor-I (IGF-I), may negatively affect brain function.
  • Estradiol and IGF-I exhibit neuroprotective properties, potentially counteracting brain deterioration caused by adrenal steroids and other factors.

Purpose of the Study:

  • To investigate the interaction between estradiol and IGF-I signaling pathways in promoting neuroprotection.
  • To elucidate the molecular mechanisms underlying the synergistic neuroprotective effects of estradiol and IGF-I.
  • To explore the potential impact of aging on these crucial neuroprotective signaling pathways in the brain.

Main Methods:

  • Investigated the physical interaction between estrogen receptor alpha, IGF-I receptor, and downstream signaling molecules (PI3K/Akt/GSK3 pathway).
  • Assessed the synergistic activation of Akt by estradiol and IGF-I.
  • Examined the modulation of GSK3 activity and Tau phosphorylation by estradiol through estrogen receptor alpha interactions.

Main Results:

  • Estradiol and IGF-I signaling synergistically activate Akt, leading to decreased GSK3 activity, a key mechanism for neuronal survival.
  • Estradiol influences Tau phosphorylation by modulating interactions between estrogen receptor alpha, GSK3, and beta-catenin.
  • These molecular interactions highlight a significant role for estradiol and IGF-I in neuronal survival and cytoskeletal regulation.

Conclusions:

  • The interaction between estradiol and IGF-I signaling pathways is crucial for neuroprotection, involving the PI3K/Akt/GSK3 pathway and modulation of Tau phosphorylation.
  • Aging may alter the expression or activity of these signaling molecules, potentially diminishing the neuroprotective effects of estradiol.
  • Further research is warranted to determine how aging impacts estradiol and IGF-I signaling in the brain to understand age-related cognitive decline.