Absence of brain-derived neurotrophic factor and trkB receptor immunoreactivity in glia of Alzheimer's disease

Alterations in the neuronal expression of some neurotrophins have been show n in various neurodegenerative processes, particularly Alzheimer's disease (AD). Glia may up-regulate neurotrophins and their high-affinity tyrosine k inase (trk) receptors in response to neural injury. In human immunodeficien cy virus type 1 (HIV-1) encephalitis, activated microglia were shown to exp ress brain-derived neurotrophic factor (BDNF), while reactive astrocytes ex pressed trkB receptor. This observation has suggested the existence of loca l neurotrophic regulation between different glial populations. To character ize the glial cellular distribution of BDNF and trkB receptor proteins in,A D, we studied selected regions of postmortem brains from four AD and three age-matched control patients by double- immunofluorescence confocal microsc opy. In both groups, BDNF immunoreactivity was distributed in neuronal peri karya and neuritic processes in the neocortex and hippocampus. No BDNF immu noreactivity was observed in microglia or astrocytes within and between sen ile plaques of AD. Catalytic trkB receptor immunoreactivity was present in neuronal perikarya in the neocortex and hippocampus. Reactive astrocytes an d microglia were not immunoreactive for catalytic trkB. The absence of BDNF and trkB proteins in glia in AD patients is in contrast to the finding in patients with HIV-1 encephalitis. This difference suggests that glial expre ssion of BDNF and trkB proteins may be characteristic of particular disease processes, rather than merely representing a stereotyped response to any t ype of neural injury.