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Tacrine, a Drug with Therapeutic Potential for Dementia: Post-Mortem Biochemical Evidence

Published online by Cambridge University Press:  18 September 2015

Paul T. Francis*
Affiliation:
Department of Neurochemistry, Institute of Neurology, The National Hospital for Nervous Diseases (Queen Square), University of London, GB
David M. Bowen
Affiliation:
Department of Neurochemistry, Institute of Neurology, The National Hospital for Nervous Diseases (Queen Square), University of London, GB
*
Institute of Neurology, 1 Wakefield Street, London WC1N 1PJ, UK
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Abstract:

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A review of biochemical findings is presented which support the idea that Alzheimer's disease represents a condition for which tetrahydroaminoacridine (tacrine) may have a beneficial effect. There is evidence that clinical and histopathologic hallmarks of the disease relate to cholinergic and serotonergic dysfunction, with less obvious abnormalities in other neurotransmitters (aspartate, dopamine, gamma-aminobutyrate, glutamate, noradrenaline and somatostatin). Clincially relevant concentrations of tacrine may ameliorate the above presynaptic deficits without producing harmful (neurotoxic) effects of aspartate and glutamate. The disease seems to be associated with an early and clinically relevant degeneration of some neurons with cortical perikarya that release these amino acid transmitters. Studies are now required on the effect of tacrine on postulated harmful peptide-bond hydrolase activity within and around such cells.

Type
Research Article
Copyright
Copyright © Canadian Neurological Sciences Federation 1989

References

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