[The role of immunologic reactions in the pathogenesis in Binswanger's disease; a clue to therapeutic approach].
[The role of immunologic reactions in the pathogenesis in Binswanger's disease; a clue to therapeutic approach].
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Original abstract
We examined the alterations of glial cells in the brains with Binswanger's disease. In comparison to the brains with lacunar cerebral infarction and those from non-neurological controls, oligodendroglia was decreased in number, and microglia was increased and activated in the white matter lesions in Binswanger's disease. Astroglia occasionally showed a regressive change, termed clasmatodendrosis. In rodents, similar white matter lesions could be induced after chronic cerebral hypoperfusion along with a numerical decrease of oligodendroglia, an increase of astroglia and activation of microglia in the corresponding white matter. These white matter lesions were suppressed by injection of immunosuppressant, cyclosporin A or FK506, with a suppression of microglial activation. These findings indicate that the lesion development in the white matter may be mediated by an immunologic reaction. Unfortunately, these drugs may be inappropriate for a practical use in terms of their side effects. Alternatively, we tried the use of anti-thrombin drug, argatroban. In acute neurological exacerbation of Binswanger's disease, markers for coagulation-fibrinolysis pathway were elevated significantly, and this activation was suppressed along with a recovery of neurological symptoms such as parkinsonism and pseudobulbar palsy. Thrombin contributes to a microcirculatory disturbance and may also enhance an inflammatory response through the action of thrombin receptor.