Abstract
Currently, the important part played by the senile plaque and neurofibrillary tangles puts amyloid protein and tau hyperphosphorylation at the centre of a new direction in the investigation of the molecular biology and treatment of Alzheimer s disease. OBJECTIVE. To consider the scientific evidence regarding the limitations of anticholinesterase treatment. DEVELOPMENT. Most of the clinical trials with anticholinesterase inhibitor drugs have been too short (3-6 months in a disease lasting an average of 8.5 years). There is slight clinical improvement with a definite therapeutic ceiling. A small proportion of patients respond, but there is no way of knowing who these will be. Improvement occurs during the early stages of the illness. This means that when the illness is advanced or does not respond initially, treatment should be reconsidered. It is necessary for consensus to be reached to obtain uniformity of objectives and methodology in clinical trials, which have been heterogeneous until now, incorporating the results of epidemiological studies. CONCLUSION. Initial expectations of an analogy between the cholinergic deficit of Alzheimer s disease and the dopaminergic deficit of Parkinson s disease, with the effects on treatment implied by this, has been proved false with the passage of time and clinical, therapeutic and scientific experience.
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