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      Free radical mechanisms in dementia of Alzheimer type and the potential for antioxidative treatment.

      1 ,
      Arzneimittel-Forschung

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          Abstract

          Neurodegenerative diseases, e.g. dementia of Alzheimer type and Parkinson's disease, are characterized neurochemically by a transmitter-specific loss of neurons, which progresses and extends to several neuronal systems over the course of the disease. At present, no single specific pathomechanism may explain the heterogeneous disorder of familial and sporadic dementia of Alzheimer type, both with early and late onset of the disease. The hypothesis has been proposed that cellular events involving "oxidative stress" may be one basic pathway leading to neurodegeneration in e.g. dementia of Alzheimer type and Parkinson's disease. There are indications for an increased activity or impaired defense mechanisms of free oxygen radicals in dementia of Alzheimer type, although less clear than in Parkinson's disease. Primary and secondary factors interact and may result in a self-propagating cascade of neurodegenerative events. Since these mechanisms of neuronal death involve different areas of cell metabolism, therapeutic strategies for "neuroprotection" also have to encompass different approaches. Since a specificity of oxygen radical toxicity in dementia of Alzheimer type has not been proven, "partial" neuroprotective drugs might be more beneficial in clinical practice than specific drugs affecting only one selective pathomechanism.

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          Author and article information

          Journal
          Arzneimittelforschung
          Arzneimittel-Forschung
          0004-4172
          0004-4172
          Mar 1995
          : 45
          : 3A
          Affiliations
          [1 ] Department of Psychiatry I, University of Frankfurt am Main, Fed. Rep. of Germany.
          Article
          7763342
          21f4bffb-72ce-4fc4-998f-1300c957a9e4
          History

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