In the absence of any naturally occurring animal model of Alzheimer's disease (AD), the British conviction in the 1970's that clinico-pathological investigations of human cases offered the best approach to unraveling the pathogenesis of AD rapidly influenced clinical neuroscientists, neuropathologists and funding agencies in Canada and the USA. But as with my confreres, years of our quantifying AD lesions in autopsy brains have yet to yield definitive conclusions about what is the most important neuronal abnormality. However, during my elusive search, evidence has been slowly gathered that reactivation of latent Herpes simplex virus, traveling from trigeminal ganglia into neighbouring mesial temporal cortex, might best explain the limbic predilection for and earliest site of neurofibrillary tangle formation. This maturing hypothesis may serendipitously prove to have been a more essential byproduct of generating the voluminous data than all the publications from our laboratory that reflected endless hours of quantitative morphometry.