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

Normal brain ageing: models and mechanisms.

Emil C Toescu1

  • 1Division of Medical Sciences, University of Birmingham Department of Physiology Edgbaston, Birmingham B15 2TT, UK. e.c.toescu@bham.ac.uk

Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences
|December 3, 2005
PubMed
Summary
This summary is machine-generated.

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

Developmental exposure to ethanol increases the neuronal vulnerability to oxygen-glucose deprivation in cerebellar granule cell cultures.

Brain research·2015
Same author

Chronic NGF treatment induces somatic hyperexcitability in cultured dorsal root ganglion neurons of the rat.

Biomedical research (Tokyo, Japan)·2014
Same author

Vasopressin-induced intracellular Ca²⁺ concentration responses in non-neuronal cells of the rat dorsal root ganglion.

Brain research·2012
Same author

The effect of aging-associated impaired mitochondrial status on kainate-evoked hippocampal gamma oscillations.

Neurobiology of aging·2012
Same author

Neuroendocrine signalling: natural variations on a Ca2+ theme.

Cell calcium·2012
Same author

Segregation of calcium signalling mechanisms in magnocellular neurones and terminals.

Cell calcium·2012

Neuronal aging involves metabolic changes, particularly in mitochondria, reactive oxygen species (ROS), and intracellular calcium (Ca2+). This impacts neuron resilience, making them vulnerable to stress and neurodegeneration.

Area of Science:

  • Neuroscience
  • Cellular Biology
  • Metabolism

Background:

  • Normal aging leads to cognitive decline.
  • Understanding neuronal aging mechanisms is challenging.
  • Cellular aging is viewed as a metabolic state involving mitochondria, ROS, and Ca2+.

Purpose of the Study:

  • To review evidence of altered mitochondrial function in aging.
  • To discuss functional consequences of these alterations.

Main Methods:

  • Literature review focusing on mitochondrial function and aging.
  • Analysis of metabolic interactions within the mitochondria-ROS-Ca2+ triad.

Main Results:

  • Aging alters the mitochondria-ROS-Ca2+ metabolic triad.

Related Experiment Videos

  • This leads to decreased homeostatic reserve in neurons.
  • Aged neurons are vulnerable to metabolic stress, trauma, or ischemia.

    • Conclusions:

    • Altered mitochondrial function is a key aspect of neuronal aging.
    • Consequences include impaired Ca2+ homeostasis, ATP production, and increased ROS generation.