TrkA immunoreactivity in reactive astrocytes in human neurodegenerative diseases and colchicine-treated rats

It has been shown that nerve growth factor (NGF) administration is capable of curbing tissue damage in several neurodegenerative disorders. As a first step to learning about the possible functional role of NGF in the astroglial response during neurodegeneration, we have analyzed the expression of the functional receptor for NGF, TrkA, in human neurodegenerative diseases which are accompanied by reactive astrocytosis, as well as in human astrocytomas. We have compared these results with those observed in reactive astrocytes following colchicine-induced cellular damage to adult rats. In the human brain, strong TrkA immunoreactivity is observed in reactive astrocytes in a number of unrelated diseases, including Alzheimer's disease, Huntington's disease, progressive supranuclear palsy, multiple sclerosis, Creutzfeldt-Jakob disease, multifocal leukoencephalopathy and residual hypoxic encephalopathy. Neoplastic astrocytes in grade II and III astrocytomas display strong TrkA immunoreactivity. In the rat brain, reactive astrocytes following mechanical needle injury and colchicine administration show strong TrkA immunoreactivity. The presence of TrkA receptors in reactive astrocytes from different human neurodegenerative diseases and experimentally induced models in rats, and in neoplastic astrocytes suggests that NGF may participate in the astroglial response to different types of injury and neoplastic proliferation. Since astroglial cells are capable of producing NGF, it is plausible that this neurotrophin may function as an autocrine or paracrine factor in TrkA-expressing reactive and neoplastic glial cells.