Therapeutic implications
There is a chance, however remote, that much of the clinical symptomatology in AD results from the impairment of neuronal function by intraneuronal Aß aggregates.
- If so, drugs that reduce the level of these aggregates (by reducing the production of intracellular Aß42 or otherwise adjusting conditions to prevent formation or hasten removal of intracellular aggregates) could have a highly beneficial effect even in seriously ill patients with large numbers of plaques and tangles.