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Reactivation of HSV-1 in the brain of patients with familial Alzheimer's disease

✍ Scribed by Isamu Mori; Yoshinobu Kimura; Hironobu Naiki; Rokuro Matsubara; Tohru Takeuchi; Takashi Yokochi; Yukihiro Nishiyama

Publisher
John Wiley and Sons
Year
2004
Tongue
English
Weight
345 KB
Volume
73
Category
Article
ISSN
0146-6615

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✦ Synopsis

Abstract

Herpes simplex virus type 1 (HSV‐1) has been proposed as an environmental risk factor for sporadic Alzheimer's disease, although this issue is still in dispute. The involvement of HSV‐1 in the pathogenesis of familial Alzheimer's disease, the uncommon type of Alzheimer's disease, has not been addressed yet. We investigated formalin‐fixed, paraffin‐embedded, postmortem brain tissue sections of three patients with familial Alzheimer's disease for the presence of HSV‐1 DNA. The nested polymerase chain reaction (PCR) detected the HSV‐1 glycoprotein D gene in the brain of all three patients with familial Alzheimer's disease preferentially in the frontal and temporal cortices, whereas only one case out of six age‐matched, non‐Alzheimer's disease individuals could disclose the presence of HSV‐1 gene. The PCR detected HSV‐1 DNA in the frontal cortex of the two patients with sporadic Alzheimer's disease. The presence of HSV‐1 was associated with β‐amyloid deposition in the cerebral cortex. To clarify the localization of HSV‐1 in the brain tissue of patients with familial Alzheimer's disease, the in situ hybridization of the tyramide signal amplification system was used. It detected the HSV‐1‐specific signals predominantly in the cytoplasm of cortical neurons in a dot‐like staining fashion. In addition, high‐sensitivity immunohistochemistry revealed the existence of HSV‐1 antigens in the cytoplasm of cortical neurons. This report provides the first evidence of reactivation of HSV‐1 in the brain of patients with familial Alzheimer's disease, associated with β‐amyloid deposition, and suggests the possible involvement of HSV‐1 together with genetic factors in the pathogenesis of familial Alzheimer's disease. J. Med. Virol. 73:605–611, 2004. © 2004 Wiley‐Liss, Inc.

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