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Fibroblasts from Alzheimer's disease donors do not differ from controls in response to heat shock

B Arosio1, G Annoni, C Vergani

  • 1Department of Internal Medicine, University of Milan and Ospedale Maggiore, Italy.

Neuroscience Letters
|December 1, 1998
PubMed

Insights

Heat shock (HS) response in Alzheimer's disease (AD) fibroblasts is preserved. Both control and AD cells showed similar increases in heat shock proteins (HSPs) mRNA and sAPP release after HS, indicating intact defensive cellular mechanisms.

Area of Science:

  • Cellular biology
  • Neuroscience
  • Genetics

Background:

  • Alzheimer's disease (AD) is a neurodegenerative disorder.
  • Heat shock proteins (HSPs) are involved in cellular defense mechanisms.
  • Previous research suggests potential alterations in cellular responses in AD.

Purpose of the Study:

  • To investigate heat shock proteins (HSPs) mRNA expression in cultured fibroblasts from control and AD patients.
  • To assess the cellular response to heat shock (HS) in AD.

Main Methods:

  • Fibroblast cultures from control and AD patients.
  • Northern blot analysis to quantify HSP70 and HSC73 mRNA levels.
  • Measurement of soluble amyloid precursor protein (sAPP) release.

Main Results:

  • Heat shock (HS) induced a several-fold increase in HSP70 and HSC73 mRNA in both control and AD fibroblasts.
  • The magnitude of mRNA increase was similar between control and AD cells.
  • HS also elicited a modest, comparable increase in sAPP release in both groups.

Conclusions:

  • AD fibroblasts exhibit a preserved ability to mount a defensive response to heat shock.
  • Cellular stress response mechanisms appear intact in fibroblasts from AD patients.
  • These findings suggest that the cellular defensive capacity against heat shock is not compromised in AD.

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