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The Journal of Neuroscience, March 10, 2004, 24(10):2421-2430; doi:10.1523/JNEUROSCI.5599-03.2004

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Cellular/Molecular
Induction of Brain-Derived Neurotrophic Factor in Plaque-Associated Glial Cells of Aged APP23 Transgenic Mice

Guido J. Burbach,¹ Rainer Hellweg,² Carola A. Haas,³ Domenico Del Turco,¹ Uwe Deicke,² Dorothee Abramowski,⁴ Mathias Jucker,⁵ Matthias Staufenbiel,⁴ and Thomas Deller¹

¹Institute of Clinical Neuroanatomy, J. W. Goethe University, D-60590 Frankfurt, Germany, ²Department of Psychiatry and Psychotherapy, Charité-University Medicine, Campus Benjamin Franklin, D-14050 Berlin, Germany, ³Institute of Anatomy and Cell Biology, University of Freiburg, D-79001 Freiburg, ⁴Novartis Institutes of BioMedical Research Basel, Nervous System Department, CH-4002 Basel, Switzerland, and ⁵Department of Cellular Neurology, Hertie-Institute for Clinical Brain Research, University of Tübingen, D-72076 Tübingen, Germany

Brain-derived neurotrophic factor (BDNF) is a versatile neurotrophic factor that has been implicated in cell survival, cell differentiation, axonal growth, and activity-dependent synaptic plasticity. Changes in BDNF expression have also been reported during the course of several neurological disorders, including Alzheimer's disease (AD). The role of BDNF in AD, however, has remained elusive. To learn more about this neurotrophic factor, we investigated BDNF expression in brain of amyloid precursor protein overexpressing mice (APP23 transgenic mice). In situ hybridization revealed BDNF mRNA signals associated with amyloid plaques. Laser microdissection in combination with quantitative RT-PCR demonstrated a sixfold increase of BDNF mRNA in the immediate plaque vicinity, a threefold increase in a tissue ring surrounding the plaque, and control levels in interplaque areas comparable with those measured in age-matched nontransgenic mice. Double immunofluorescence localized BDNF to microglial cells and astrocytes surrounding the plaque. Cortical BDNF protein levels were quantified by ELISA demonstrating a >10-fold increase compared with age-matched controls. This upregulation of BDNF protein significantly correlated with the -amyloid load in the transgenic animals. Taken together, our data demonstrate a plaque-associated upregulation of BDNF in APP23 transgenic mice and implicate this neurotrophin in the regulation of inflammatory and axonal growth processes in the plaque vicinity.

Key words: Alzheimer's disease; axonal sprouting; neurotrophins; laser microdissection; amyloid precursor protein

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Received Sep 10, 2003; revised January 26, 2004; accepted January 26, 2004.

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