ABSTRACT
Over the past decade the study of Alzheimer’s disease has seen some of the most spectacular research in the field of neurology. Quite a clear, coherent explanation of the pathogenesis of the disease has emerged, although there is no explanation of the causes and mechanisms involved in the dementia that has met with unani mous acceptance. Clinical research has had to contend with major obstacles as, for example, the need for proper scales to assess the development of states of dementia for the purposes of accurate analysis, and the time lag, as diagnosis is only confirmed decades after pathogenesis has already started. However, recent progress has made it possible to conduct a number of clinical and epidemiological studies producing positive findings, proving that it is not totally unrealistic to consider ways of counteracting a neurodegenerative process, and to observe a coherent pattern in the pathogenesis of Alzheimer’s disease. While specialists may have differing opinions on the causal relationship of particular cellular events, a consensus on the usefulness of taking action on certain physiological processes is currently emerging (1-3). It is generally agreed, for example, that a substance that counteracts the effects of (3-amyloid peptide on the neurons (13amyloid peptide being the principal component of senile plaques, which are one of the hallmarks of Alzheimer’s disease) will be beneficial in treating the disease,
even if it could be proved at a later date that the actual deposit of the substance is not the primary causal event (4). For this reason, the coexistence of different etiopathogenic hypotheses does not invalidate the findings of pharmacological research.
