Herpes Zoster and Dementia

Chen, Vincent Chin Hung; Wu, Shu‐I; Huang, Kuo You; Yang, Yao‐Hsu; Kuo, Ting Yu; Liang, Hsin Yi; Huang, Kuan Lun; Gossop, Michael

doi:10.4088/jcp.16m11312

Cited by 108 publications

(89 citation statements)

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“…In the second article, by Chen et al ( 2018 ), 39,205 patients with HZV, age range 54–90, were diagnosed during the period 1997–2013 and were followed over an average period of 6.2 years. The incidence of dementia was compared with that of 39,205 controls (mean age of both groups was 63.5 years).…”

Section: Evidence From Population Epidemiological Studies For a Role mentioning

confidence: 99%

Corroboration of a Major Role for Herpes Simplex Virus Type 1 in Alzheimer’s Disease

Itzhaki

2018

Front. Aging Neurosci.

199

153

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Strong evidence has emerged recently for the concept that herpes simplex virus type 1 (HSV1) is a major risk for Alzheimer’s disease (AD). This concept proposes that latent HSV1 in brain of carriers of the type 4 allele of the apolipoprotein E gene (APOE-ε4) is reactivated intermittently by events such as immunosuppression, peripheral infection, and inflammation, the consequent damage accumulating, and culminating eventually in the development of AD. Population data to investigate this epidemiologically, e.g., to find if subjects treated with antivirals might be protected from developing dementia—are available in Taiwan, from the National Health Insurance Research Database, in which 99.9% of the population has been enrolled. This is being extensively mined for information on microbial infections and disease. Three publications have now appeared describing data on the development of senile dementia (SD), and the treatment of those with marked overt signs of disease caused by varicella zoster virus (VZV), or by HSV. The striking results show that the risk of SD is much greater in those who are HSV-seropositive than in seronegative subjects, and that antiviral treatment causes a dramatic decrease in number of subjects who later develop SD. It should be stressed that these results apply only to those with severe cases of HSV1 or VZV infection, but when considered with the over 150 publications that strongly support an HSV1 role in AD, they greatly justify usage of antiherpes antivirals to treat AD. Three other studies are described which directly relate to HSV1 and AD: they deal respectively with lysosomal changes in HSV1-infected cell cultures, with evidence for a role of human herpes virus type 6 and 7 (HHV6 and HHV7) in AD, and viral effects on host gene expression, and with the antiviral characteristics of beta amyloid (Aβ). Three indirectly relevant studies deal respectively with schizophrenia, relating to antiviral treatment to target HSV1, with the likelihood that HSV1 is a cause of fibromyalgia (FM), and with FM being associated with later development of SD. Studies on the link between epilepsy, AD and herpes simplex encephalitis (HSE) are described also, as are the possible roles of APOE-ε4, HHV6 and HSV1 in epilepsy.

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Section: Evidence From Population Epidemiological Studies For a Role mentioning

confidence: 99%

Corroboration of a Major Role for Herpes Simplex Virus Type 1 in Alzheimer’s Disease

Itzhaki

2018

Front. Aging Neurosci.

199

153

View full text Add to dashboard Cite

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“…Subsequently, it was shown that HSV-1 infection of cultured neurons and glia and mouse brain can increase the production of Aβ [177], and induce cytoskeletal abnormalities in neurons that include tau hyperphosphorylation [178]. Recent works have indicated that Aβ has antimicrobial properties against bacteria and viruses [179,180], and have substantiated the associations of herpes virus infections and AD or dementia [181,182,183,184,185]. These findings suggest that Aβ and/or tau may be protective responses to CNS infections that would be more likely to occur with age-associated immunosenescence and a dysfunctional BBB.…”

Section: The Bbb In Age-associated Neurological Diseasesmentioning

confidence: 99%

Age-Associated Changes in the Immune System and Blood–Brain Barrier Functions

Erickson

Banks

2019

IJMS

141

107

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Age is associated with altered immune functions that may affect the brain. Brain barriers, including the blood–brain barrier (BBB) and blood–CSF barrier (BCSFB), are important interfaces for neuroimmune communication, and are affected by aging. In this review, we explore novel mechanisms by which the aging immune system alters central nervous system functions and neuroimmune responses, with a focus on brain barriers. Specific emphasis will be on recent works that have identified novel mechanisms by which BBB/BCSFB functions change with age, interactions of the BBB with age-associated immune factors, and contributions of the BBB to age-associated neurological disorders. Understanding how age alters BBB functions and responses to pathological insults could provide important insight on the role of the BBB in the progression of cognitive decline and neurodegenerative disease.

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“…Moreover, two retrospective cohort studies demonstrated that HSV infection significantly increased the risk of developing all-cause dementia. Of note is that this risk was almost eliminated in patients treated with antiherpetics ( Chen et al, 2018 ; Tzeng et al, 2018 ; Long and Holtzman, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

Potential Bidirectional Relationship Between Periodontitis and Alzheimer’s Disease

et al. 2020

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Alzheimer's disease (AD) is the most prevalent form of dementia in the elderly population, representing a global public health priority. Despite a large improvement in understanding the pathogenesis of AD, the etiology of this disorder remains still unclear, and no current treatment is able to prevent, slow, or stop its progression. Thus, there is a keen interest in the identification and modification of the risk factors and novel molecular mechanisms associated with the development and progression of AD. In this context, it is worth noting that several findings support the existence of a direct link between neuronal and non-neuronal inflammation/infection and AD progression. Importantly, recent studies are now supporting the existence of a direct relationship between periodontitis, a chronic inflammatory oral disease, and AD. The mechanisms underlying the association remain to be fully elucidated, however, it is generally accepted, although not confirmed, that oral pathogens can penetrate the bloodstream, inducing a low-grade systemic inflammation that negatively affects brain function. Indeed, a recent report demonstrated that oral pathogens and their toxic proteins infect the brain of AD patients. For instance, when AD progresses from the early to the more advanced stages, patients could no longer be able to adequately adhere to proper oral hygiene practices, thus leading to oral dysbiosis that, in turn, fuels infection, such as periodontitis. Therefore, in this review, we will provide an update on the emerging (preclinical and clinical) evidence that supports the relationship existing between periodontitis and AD. More in detail, we will discuss data attesting that periodontitis and AD share common risk factors and a similar hyper-inflammatory phenotype.

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Herpes Zoster and Dementia

Abstract: Herpes zoster was associated with an increased risk of dementia, independent of potential confounding factors. Antiviral treatment might be protective in preventing dementia in patients with herpes zoster.

Cited by 108 publications

References 0 publications

Corroboration of a Major Role for Herpes Simplex Virus Type 1 in Alzheimer’s Disease

Corroboration of a Major Role for Herpes Simplex Virus Type 1 in Alzheimer’s Disease

Age-Associated Changes in the Immune System and Blood–Brain Barrier Functions

Potential Bidirectional Relationship Between Periodontitis and Alzheimer’s Disease

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