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A new brain-derived neurotrophic factor transcript and decrease in brain-derived neurotrophic factor transcripts 1, 2

Diego Garzon1, Guanhua Yu, Margaret Fahnestock

  • 1Department of Psychiatry and Behavioural Neurosciences, McMaster University, Hamilton, Ontario, Canada.

Journal of Neurochemistry
|October 3, 2002
PubMed
Summary
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Alzheimer's disease reduces specific brain-derived neurotrophic factor (BDNF) mRNA transcripts. This down-regulation may involve the cAMP response element binding protein, offering insights into Alzheimer's molecular mechanisms.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Brain-derived neurotrophic factor (BDNF) is crucial for neuronal survival and function, particularly in areas affected by Alzheimer's disease (AD).
  • Reduced BDNF mRNA levels are observed in AD brains, but the underlying molecular mechanisms remain unclear.
  • The human BDNF gene exhibits complex transcription patterns with multiple promoters and splice variants.

Purpose of the Study:

  • To investigate the specific molecular mechanisms causing down-regulation of BDNF mRNA in Alzheimer's disease.
  • To identify which BDNF transcripts are affected in AD and explore potential regulatory pathways.
  • To report a newly identified human BDNF splice variant.

Main Methods:

  • Utilized Reverse Transcription Polymerase Chain Reaction (RT-PCR) with primers specific to individual upstream exons of the BDNF gene.

Related Experiment Videos

  • Analyzed BDNF mRNA transcript levels in Alzheimer's disease and control brain tissues (hippocampus and parietal cortex).
  • Investigated the role of cAMP response element binding protein (CREB) phosphorylation in regulating specific BDNF transcripts in rat models.

    • Main Results:

    • A significant decrease was observed in three specific human BDNF mRNA transcripts (transcripts 1, 2, and 3) in Alzheimer's disease samples compared to controls.
    • Transcript 1 and 3 showed a two-fold decrease, while transcript 2 exhibited a five-fold decrease.
    • No significant differences were found for other transcripts, including a newly identified splice variant, between AD and control groups.
    • In rats, BDNF transcripts 1 and 3 are regulated by CREB, and CREB phosphorylation is reduced in the AD brain.

    Conclusions:

    • Specific BDNF mRNA transcripts are significantly down-regulated in Alzheimer's disease brains.
    • Reduced phosphorylation of CREB in AD brains may contribute to the specific down-regulation of BDNF transcripts 1 and 3.
    • These findings provide a molecular basis for reduced BDNF levels in AD and suggest potential therapeutic targets.