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

Venn diagrams and neuronal vulnerability.

R M Sapolsky1, E A Morrow, G C Tombaugh

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

Neurobiology of Aging
|September 1, 1989
PubMed
Summary

Alzheimer's disease (AD) brain damage doesn't perfectly correlate with NMDA receptor levels. Excitatory amino acids (EAAs) are necessary but not sufficient to cause AD neuronal damage, a common principle in neurodegeneration.

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

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

Molecular psychiatry·2011
Same author

SK2 potassium channel overexpression in basolateral amygdala reduces anxiety, stress-induced corticosterone secretion and dendritic arborization.

Molecular psychiatry·2009
Same author

Viral caspase inhibitor p35, but not crmA, is neuroprotective in the ischemic penumbra following experimental stroke.

Neuroscience·2007
Same author

The effects of toxoplasma infection on rodent behavior are dependent on dose of the stimulus.

Neuroscience·2007
Same author

Gene expression profiles associated with survival of individual rat dentate cells after endogenous corticosteroid deprivation.

The European journal of neuroscience·2004
Same author

Overexpression of calbindin D(28k) in dentate gyrus granule cells alters mossy fiber presynaptic function and impairs hippocampal-dependent memory.

Hippocampus·2004

Area of Science:

  • Neuroscience
  • Pathology
  • Alzheimer's Disease Research

Background:

  • Alzheimer's disease (AD) is characterized by progressive neurodegeneration, particularly in the hippocampus.
  • N-methyl-D-aspartate (NMDA) receptors are crucial for synaptic plasticity and excitotoxicity.
  • Previous research suggests a link between NMDA receptor function and neuronal damage in AD.

Purpose of the Study:

  • To investigate the correlation between hippocampal regions affected by Alzheimer's disease and NMDA receptor concentrations.
  • To evaluate the role of excitatory amino acids (EAAs) in explaining selective neuronal vulnerability in AD.

Main Methods:

  • Analysis of post-mortem brain tissue from Alzheimer's disease patients.
  • Quantification of NMDA receptor expression in different hippocampal subregions.
  • Correlation analysis between neuropathological findings and receptor density.

Main Results:

  • A poor correlation was observed between the extent of hippocampal damage in AD and the concentration of NMDA receptors.
  • This suggests that NMDA receptor levels alone do not fully account for the observed neuronal damage patterns.

Conclusions:

  • Excitatory amino acids (EAAs), including glutamate acting on NMDA receptors, are necessary but not sufficient to explain Alzheimer's-related neuronal damage.
  • Selective neuronal vulnerability in neurodegenerative diseases may be a general principle, where causative agents are necessary but not sufficient to explain cell death patterns.

Related Experiment Videos