Current drugs and future hopes in the treatment of Alzheimer’s disease

  • M. Windisch
  • B. Hutter-Paier
  • E. Schreiner
Part of the Journal of Neural Transmission. Supplementa book series (NEURAL SUPPL, volume 62)


In spite of several years of experience with the use of cholinesterase inhibitors for treatment of symptoms of Alzheimer’s disease their influence on disease progression remains still unclear. New cholinesterase inhibitors should provide an additional neuroprotective activity, because only substances which stop neuronal death can influence disease progression. New treatment strategies are focusing on amyloid processing, preventing the occurrence of toxic Aβ1–42 peptide. These procedures include the vaccination trials, but their clinical usefulness has to be proven. Also strategies focusing on neurofibrillary pathologies should be explored in detail. Drug development for Alzheimer’s disease should include all pathological events associated with neurodegeneration, like oxidative stress, neuroinflammation or disturbances in growth factor signaling. Abnormal protein aggregation as a common feature of different neurodegenerative diseases might also be a promising drug target. Beside β sheet breakers directed against β-amyloid deposition the endogenous protein β-synuclein or derivatives of it might be able to counteract aggregation of α-synuclein as well as of amyloid β protein. Interaction with a-synuclein deserves special attention because it might be an early step of synaptic degeneration. Due to the complexity of the disease combination of different drugs might be the most promising way to go. The parallel development of early biological markers should enable intervention in pre-symptomatic disease stages.


Alzheimer Disease Multiple System Atrophy Amyloid Precursor Protein Cholinesterase Inhibitor Alzheimer Disease Patient 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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Copyright information

© Springer-Verlag Wien 2002

Authors and Affiliations

  • M. Windisch
    • 1
  • B. Hutter-Paier
    • 1
  • E. Schreiner
    • 1
  1. 1.JSW-Research Forschungslabor GmbHGrazAustria

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