Persistent Infection with Herpes Simplex Virus 1 and Alzheimer’s Disease—A Call to Study How Variability in Both Virus and Host may Impact Disease

Mangold, Colleen A.; Szpara, Moriah L.

doi:10.3390/v11100966

Cited by 34 publications

(40 citation statements)

References 195 publications

(271 reference statements)

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“…The reason may be that HSV can cause Aβ accumulation and the phosphorylation of tau peptide, which then induces AD. Importantly, HSV was also found in the brain areas seriously affected by AD, which substantiates the above hypothesis (Mangold and Szpara, 2019). The inhibitory effect of MYR on HSV (Lyu et al, 2005) will help patients reduce the risk of AD and help control the status of Aβ and tau peptide.…”

Section: Myr and Dmy Play An Anti-ad Role By Inhibiting Bacteria Andsupporting

confidence: 79%

Molecular Level Insight Into the Benefit of Myricetin and Dihydromyricetin Uptake in Patients With Alzheimer’s Diseases

Liu

Guo

et al. 2020

Front. Aging Neurosci.

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Alzheimer's disease (AD) is a neurodegenerative disease with a high incidence rate and complicated pathogenesis. Currently, all anti-AD drugs treat the symptoms of the disease, and with currently no cure for AD. Flavonoid containing natural products, Myricetin (MYR) and Dihydromyricetin (DMY), are abundant in fruits and vegetables, and have been approved as food supplements in some countries. Interestingly, MYR and DMY have been reported to have anti-AD effects. However, the underlying anti-AD mechanism of action of MYR and DMY is complex with many facets being identified. In this review, we explore the benefit of MYR and DMY in AD patients from a molecular level. Their mechanism of action are discussed from various aspects including amyloid β-protein (Aβ) imbalance, neuroinflammation, dyshomeostasis of metal ions, autophagy disorder, and oxidative stress.

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Section: Myr and Dmy Play An Anti-ad Role By Inhibiting Bacteria Andsupporting

confidence: 79%

Molecular Level Insight Into the Benefit of Myricetin and Dihydromyricetin Uptake in Patients With Alzheimer’s Diseases

Liu

Guo

et al. 2020

Front. Aging Neurosci.

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“…Epstein–Barr virus (EBV), human herpesvirus 6 (HH6), and HSV-1 have been linked to demyelinating diseases, although their role in these pathologies, and particularly in MS, is difficult to determine given their almost ubiquitous nature [ 11 ]. HSV-1 has also been involved in neurodegenerative disorders of the CNS [ 14 , 15 , 16 , 17 ].…”

Section: Introductionmentioning

confidence: 99%

The Role of Herpes Simplex Virus Type 1 Infection in Demyelination of the Central Nervous System

Bello-Morales

Andreu

Löpez‐Guerrero

2020

IJMS

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Herpes simplex type 1 (HSV-1) is a neurotropic virus that infects the peripheral and central nervous systems. After primary infection in epithelial cells, HSV-1 spreads retrogradely to the peripheral nervous system (PNS), where it establishes a latent infection in the trigeminal ganglia (TG). The virus can reactivate from the latent state, traveling anterogradely along the axon and replicating in the local surrounding tissue. Occasionally, HSV-1 may spread trans-synaptically from the TG to the brainstem, from where it may disseminate to higher areas of the central nervous system (CNS). It is not completely understood how HSV-1 reaches the CNS, although the most accepted idea is retrograde transport through the trigeminal or olfactory tracts. Once in the CNS, HSV-1 may induce demyelination, either as a direct trigger or as a risk factor, modulating processes such as remyelination, regulation of endogenous retroviruses, or molecular mimicry. In this review, we describe the current knowledge about the involvement of HSV-1 in demyelination, describing the pathways used by this herpesvirus to spread throughout the CNS and discussing the data that suggest its implication in demyelinating processes.

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“…Alzheimer's disease (AD) is the most common neurodegenerative disease, with 46.8 million people currently suffering from AD worldwide, and the number is expected to reach 131.5 million by 2050 [1]. AD is generally characterized by reduced cognitive function, including memory loss, but it is also characterized by behavioral or psychological symptoms such as anxiety, depression and delusions [2].…”

Section: Introductionmentioning

confidence: 99%

K284-6111 Alleviates Memory Impairment and Neuroinflammation in Tg2576 Mice by Inhibition of Chitinase-3-like 1 Regulating ERK Dependent PTX3 Pathway

Ham

Lee

Yun

et al. 2020

Preprint

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Background Alzheimer's disease (AD) is one of the most prevalent neurodegenerative disorders characterized by gradual memory loss and neuropsychiatric symptoms. We have previously demonstrated that the 2-({3-[2-(1-Cyclohexen-1-yl)ethyl]-6,7-dimethoxy-4-oxo-3,4-dihydro-2-quinazolinyl}sulfanyl)-N-(4-ethylphenyl)butanamide (K284-6111), the inhibitor of CHI3L1, has an inhibitory effect on memory impairment in Αβ infusion mouse model and on LPS-induced neuroinflammation in the murine BV-2 microglia and primary cultured astrocyte. Methods In the present study, we investigated that the inhibitory effect of K284-6111 on memory dysfunction and neuroinflammation in Tg2576 transgenic mice, and more detailed correlation of CHI3L1 and AD. To investigate the effects of K284-6111 on memory dysfunction, we administered K284-6111 (3 mg/kg, p.o.) daily for four weeks to Tg2576, followed by behavioral tests of water maze test, probe test, and passive avoidance test.Results Administration of K284-6111 alleviated memory impairment in Tg2576 mice and had the effect of reducing accumulation of Aβ and neuroinflammatory responses in the mouse brain. K284-6111 treatment also selectively inactivated ERK and NF-κB pathways, which were activated when CHI3L1 was overexpressed, in mouse brain and in BV-2 cells. Web-based gene network analysis and our results of gene expression level in BV-2 cells showed that CHI3L1 is closely correlated with PTX3. Our result revealed that knockdown of PTX3 has inhibitory effect on the production of inflammatory proteins and cytokines, and on the phosphorylation of ERK and IκBα.Conclusion These results suggest that K284-6111 could improve memory dysfunction by alleviating neuroinflammation through inhibiting CHI3L1 through blocking ERK dependent PTX3 pathway.

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Persistent Infection with Herpes Simplex Virus 1 and Alzheimer’s Disease—A Call to Study How Variability in Both Virus and Host may Impact Disease

Cited by 34 publications

References 195 publications

Molecular Level Insight Into the Benefit of Myricetin and Dihydromyricetin Uptake in Patients With Alzheimer’s Diseases

Molecular Level Insight Into the Benefit of Myricetin and Dihydromyricetin Uptake in Patients With Alzheimer’s Diseases

The Role of Herpes Simplex Virus Type 1 Infection in Demyelination of the Central Nervous System

K284-6111 Alleviates Memory Impairment and Neuroinflammation in Tg2576 Mice by Inhibition of Chitinase-3-like 1 Regulating ERK Dependent PTX3 Pathway

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