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Lysosomal dysfunction reduces brain-derived neurotrophic factor expression

E Bednarski1, J C Lauterborn, C M Gall

  • 1Center for the Neurobiology of Learning and Memory, University of California, Irvine 92697-3800, USA.

Experimental Neurology
|March 26, 1998
PubMed
Summary
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Lysosomal dysfunction in aging brains reduces basal brain-derived neurotrophic factor (BDNF) but does not prevent its induction by physiological activity. This suggests a pathway to Alzheimer

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cellular Aging

Background:

  • Reduced brain-derived neurotrophic factor (BDNF) expression is a hallmark of Alzheimer's disease.
  • Lysosomal dysfunction is associated with brain aging and may impact neurotrophin levels.

Purpose of the Study:

  • To investigate whether lysosomal disturbances impair basal and/or induced expression of BDNF.
  • To examine the effect of cathepsin inhibition on BDNF mRNA levels in cultured hippocampal slices.

Main Methods:

  • Cultured hippocampal slices were treated with ZPAD, a cathepsin B and L inhibitor.
  • BDNF mRNA expression was quantified using in situ hybridization and densitometry.
  • The impact of kainate-induced glutamate receptor stimulation on BDNF mRNA was assessed.

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Main Results:

  • ZPAD treatment significantly reduced basal BDNF mRNA levels in hippocampal slices.
  • Kainate stimulation induced a significant increase in BDNF mRNA in the dentate gyrus.
  • ZPAD treatment did not block the percentage increase in BDNF mRNA following kainate stimulation.

Conclusions:

  • Lysosomal dysfunction in aging brains can disrupt constitutive BDNF production.
  • The neurotrophin response to intense physiological activity remains largely intact despite lysosomal impairment.
  • These findings suggest a potential aging-related mechanism contributing to Alzheimer's pathology and highlight therapeutic possibilities.