The pathogenesis of Alzheimer's disease is far from clear since it is still
undetermined whether and how extracellular beta-protein and cytoskeletal d
egeneration of neurons, which are colocalised in the association neocortex
of Alzheimer patients, are related to one another. By using beta-protein an
d other derivatives of the precursor protein, efforts to cause cell lesions
comparable to neurofibrillary degeneration have been fruitless. However, t
he view that the amyloid issued from the polymerisation of beta-protein is
neurotoxic, remains the most attractive. To fully explore this hypothesis,
attention should be paid to neurons that participate in neocortical circuit
s and to factors that may influence their vulnerability, whether selective
or not, to beta-protein and associated proteins.