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Gareth W. Roberts, PhD
Division of Psychiatry Clinical Research Center Watford Rd Harrow, HA1 3UJ England

Arch Neurol. 1987;44(1):12.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—It has been suggested that "repeated reactivation of latent or dormant herpesvirus... may well represent an etiological infrastructure for the clinical syndrome of Alzheimer's dementia."^1,2 This is proposed on the basis of two types of evidence: (1) that herpes simplex virus has a predilection for the temporal lobe (the main site of the pathology in Alzheimer's disease); and (2) that recovered encephalitis cases display amnesiac syndromes (similar to those found in Alzheimer's disease). This is an intriguing hypothesis that has been investigated experimentally. Results of hybridization studies designed to detect the presence of herpes simplex DNA in cases of Alzheimer's disease have been negative.^3,4,5 These types of studies have the ability to detect active and latent viral infections.^6,7 Immunocytochemical studies have failed to detect expression of the herpes simplex antigen in the vast majority of Alzheimer's disease cases.^8,9,10 Neuropathologic studies uu not show . . . [Full Text PDF of this Article]

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