[Alzheimer's disease and HSV-1 infection].
Neurol Neurochir Pol. 2006 Jan-Feb;40(1):57-61.
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AD is a common and complex disorder in which environmental and genetic factors are strongly involved. Major risk factors for the sporadic form include old age, family history of dementia, head injury, and apolipoprotein E ε4 (ApoE ε4). Recently, epidemiological data for a correlation between herpes infections and AD have been collected.
HSV-1 is neurotrophic and able to establish latency in humans. HSV-1 is latent in the peripheral nervous system of most populations. The first hypothesis that HSV-1 could be involved in the pathogenesis of AD was suggested by noting that the brain area damaged during HSV-1 encephalitis and affected early in AD is the temporal lobe. It was revealed that HSV-1 is present in latent form in the brains of a high proportion of elderly people and is a risk factor for ApoE ε4 positive AD cases.
HSV-1 was shown within amyloid deposits in the brains of patients with AD, but the role of HSV-1 in AD pathology remains a matter of controversy. The basic question concerns the mechanism of viral transport within CNS in the latency phase. The phenomenon of viral reactivation in neurons after trauma to the tissue they innervate, after systemic stimuli such as stress, hormonal, and nutritional factors is well-known, but the molecular mechanisms of HSV-1 reactivation in neurons and dissemination within CNS is unknown.
In the brains of patients with AD, a constant low level of HSV-1 replication may occur asymptomatically, but molecular mechanisms of HSV-1 transport within central nervous system in the latency are not known. The theory of the hematogenous dissemination of latent HSV-1 with involvement of ApoE or the transmission by promoting viral passage across the synapse has been discussed recently.
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