Spherons are unique brain entities that are causally linked to the
amyloid plaques (SPs [
senile plaques]) of
Alzheimer's disease (AD). SPs are the quantitatively major tissue abnormality of AD.
Spherons increase in size (but not in number) gradually throughout life until they reach a size range where they burst and form SPs. Drugs targeted at attenuating the process of spheron transformation into SPs are a logical approach to AD
therapy. There are 20 criteria of validity for an SP causal entity that are satisfied by
spherons-and no more than a few of these 20 criteria are satisfied by any other known hypothesis. These criteria of validity are reviewed, in addition to common difficulties in understanding spheron theory and a number of common-sense considerations in AD therapeutic research. Spheron-based
drug therapy in AD potentially can retard the process of spheron bursting and subsequent plaque formation by: 1) blocking the formation of SPs; 2) reducing the size of SPs; 3) delaying spheron breakdown; and 4) retarding spheron growth. Isolated
spherons from human brain are intact human
drug targets and can be used as human in vitro or in vivo screening targets. The paramount importance of
spherons as a target for
drug therapy in AD is emphasized by considering that regardless of any other type of real or potential
therapy, there still already exists in every middle-aged adult a full population of
spherons in the brain, filled with more than enough
amyloid to bring about full-blown AD.