Herpes Viruses and Senile Dementia: First Population Evidence for a Causal Link

Abstract

Three articles have very recently appeared that are of especial relevance to the causes of dementia and its potential treatment. The first two (Tsai et al., published in PLoS One in November 2017; Chen et al., published in the January/February 2018 issue of Journal of Clinical Psychiatry) demonstrate an increased risk of subsequent senile dementia (SD) development in patients with acute varicella zoster (herpes zoster) infection. These articles present data highly relevant to the third, and most important, paper-by Tzeng et al., published online in the journal Neurotherapeutics at the end of February 2018. These authors report that infection with a different herpes virus, herpes simplex virus type 1 (HSV1), leads to a similarly increased risk of later developing SD. Further, when the authors looked at patients treated aggressively with antiherpetic medications at the time, the relative risk of SD was reduced by a factor of 10. It should be stressed that no investigations were made on subjects already suffering from SD, and that those treated were the few rare cases severely affected by HSV. Nonetheless, antiherpetic medication prevented later SD development in 90% of their study group. These articles provide the first population evidence for a causal link between herpes virus infection and senile dementia.

Is Alzheimer's disease linked to Herpes simplex virus type 1 infection? A mini‐review of the molecular correlation and the possible disease connections

“…Studies showed that a high proportion of the older people who were infected by AD had HSV1 in their brains that could be detected by polymerase chain reaction. 9 Further reviews stated that the HSV1 was predominantly absent in younger people and was mainly seen in older people. The main class of HSV1 with the presence of APOE e4 carriers was noticed to be found in older people with AD.…”

“…3 The unique character of AD is that it can be influenced by various molecular targets, such as acetylcholinesterase, N-methyl D-aspartate, beta-site amyloid precursor protein cleaving enzyme 1 and glycogen synthase kinase 3 beta. 9 Viral reactivation of HSV1 HSV1 is usually transmitted by oral-to-genital and oral-to-oral contact, causing genital herpes and oral herpes infection, respectively. The formation of plaques and tau phosphorylation is the key factor responsible for the pathogenesis of AD.…”

“…This led to a large-scale debate on how dementia, which is a symptom of AD, could be caused by the presence of underlying viruses. 9 Further reviews stated that the HSV1 was predominantly absent in younger people and was mainly seen in older people. 6 The neonatal infection by HSV type 1 (HSV1) has high mortality and significant morbidity.…”

“…8 Thought provoking studies have shown the potential link of HSV and AD. 9 Viral reactivation of HSV1 HSV1 is usually transmitted by oral-to-genital and oral-to-oral contact, causing genital herpes and oral herpes infection, respectively. The infection remains latent within neurons in sensory ganglia; however, when the host immunity becomes weak, HSV1 might become activated.…”

Gold Nanoparticles Crossing Blood-Brain Barrier Prevent HSV-1 Infection and Reduce Herpes Associated Amyloid-βsecretion

“…HSV-1 has been related to various neurodegenerative disorders in the last decade [7], and novel studies have contributed to new data and valuable approaches to understand the mechanisms of neurocognitive pathology. One of the most frequent HSV-1 infection-associated diseases is Alzheimer's disease (AD) [8][9][10][11][12][13]. Life expectancy after diagnosis varies between 7 and 15 years, depending on the severity at the time of diagnosis.…”