We found previously, by using polymerase chain reaction (PCR) with stringen
t precautions against contamination, that herpes simplex virus type 1 (HSV1
) is present in certain regions of brain in a high proportion of elderly co
ntrols and patients with Alzheimer's disease (AD). Subsequent work by other
s (on non-AD brains) confirmed our findings. We have since found that the c
ombination of HSV1 in brain and carriage of the epsilon 4 allele of the gen
e for apolipoprotein E (apoE epsilon 4) is a strong risk factor for AD, and
that neither the virus nor apoE epsilon 4 alone is a risk. A study from an
other laboratory substantiated our findings. Our proposition that the effec
ts of the combination of virus and the genetic factor is harmful in the ner
vous system is strongly and independently supported by our finding that apo
E epsilon 4 is a risk factor for herpes labialis (cold sores), a disorder o
f the peripheral nervous system known to be caused by HSV1. We have now inv
estigated 'blind' (as before) further autopsy brain specimens from AD patie
nts and age-matched controls for the presence of HSV1 and for apoE genotype
, and further blood specimens from sufferers from herpes labialis, and non-
sufferers, for apoE genotyping. The results agree with our previous finding
s, thus supporting our contention that HSV1 in the brain of apoE epsilon 4
carriers is a strong risk factor for AD.