Disrupting Neurons and Glial Cells Oneness in the Brain—The Possible Causal Role of Herpes Simplex Virus Type 1 (HSV-1) in Alzheimer’s Disease

Mielcarska, Matylda Barbara; Skowrońska, Katarzyna; Wyżewski, Zbigniew; Toka, Felix N.

doi:10.3390/ijms23010242

Cited by 12 publications

(15 citation statements)

References 299 publications

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“…Furthermore, it is well established that the autophagy reduction and the increased production of oxidant species promote inflammation. The release of inflammatory agents stimulates Aβ production in astrocytes, while soluble tau oligomers may be secreted into the extracellular environment and contribute, independently or combined with Aβ, to synaptic dysfunction [ 162 ]. Glial cells play either a protective or restorative role in neurons, and thus impairment of their function by HHVs infection could contribute to AD progression.…”

Section: Discussionmentioning

confidence: 99%

New Insights into the Molecular Interplay between Human Herpesviruses and Alzheimer’s Disease—A Narrative Review

Athanasiou¹,

Gargalionis

Anastassopoulou

et al. 2022

Brain Sciences

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Human herpesviruses (HHVs) have been implicated as possible risk factors in Alzheimer’s disease (AD) pathogenesis. Persistent lifelong HHVs infections may directly or indirectly contribute to the generation of AD hallmarks: amyloid beta (Aβ) plaques, neurofibrillary tangles composed of hyperphosphorylated tau proteins, and synaptic loss. The present review focuses on summarizing current knowledge on the molecular mechanistic links between HHVs and AD that include processes involved in Aβ accumulation, tau protein hyperphosphorylation, autophagy, oxidative stress, and neuroinflammation. A PubMed search was performed to collect all the available research data regarding the above mentioned mechanistic links between HHVs and AD pathology. The vast majority of research articles referred to the different pathways exploited by Herpes Simplex Virus 1 that could lead to AD pathology, while a few studies highlighted the emerging role of HHV 6, cytomegalovirus, and Epstein–Barr Virus. The elucidation of such potential links may guide the development of novel diagnostics and therapeutics to counter this devastating neurological disorder that until now remains incurable.

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Section: Discussionmentioning

confidence: 99%

New Insights into the Molecular Interplay between Human Herpesviruses and Alzheimer’s Disease—A Narrative Review

Athanasiou¹,

Gargalionis

Anastassopoulou

et al. 2022

Brain Sciences

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“…Three articles from the 2021 Special Issue report data and discuss the role of viral infection in AD [ 5 , 6 , 7 ]. Mielcarska and coauthors describe changes in neurons, astrocytes, microglia, and oligodendrocytes related to the production of inflammatory factors, transition of glial cells into a reactive state, along with oxidative damage, Aβ secretion, tau hyperphosphorylation, apoptosis, and autophagy after infection by human herpes simplex virus-1 (HSV-1) [ 5 ].…”

Section: Alzheimer Disease Cell Senescence Chronic Inflammation and V...mentioning

confidence: 99%

Special Issue Editorial: “Infections, Inflammation and Neurodegeneration in Alzheimer Disease” Infections, Neuronal Senescence, and Dementia

Licastro

2022

IJMS

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Alzheimer’s disease (AD) is a complex chronic disease of the brain characterized by several neurodegenerative mechanisms and is responsible for most dementia cases in the elderly. Declining immunity during ageing is often associated with peripheral chronic inflammation, and chronic neuroinflammation is a constant component of AD brain pathology. In the Special Issue published in 2021 eight papers were collected regarding different aspects of neurodegeneration associated with AD. Five papers presented and discussed infectious agents involved in brain AD pathology and three discussed data regarding receptors regulation and possible treatment of the disease. Below I will discuss and further elaborate on topics related to infections, inflammation, and neurodegenerative pathways in AD and brain senescence. The topic presented here may contribute to early intervention protocols for preventing or slowing the progression of cognitive deterioration in the elderly.

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“…The virus sits dormant in the dorsal root ganglia and occasionally reactivates under stress. HSV-1 occasionally spreads to the central nervous system causing viral encephalitis [89]. In recent data, HSV-1 has shown a possible connection to AD, specifically sporadic AD.…”

Section: Herpes Simplex Virus-1 (Hsv-1)mentioning

confidence: 99%

“…HSV-1 has been shown to damage neurons and glial cells, through inflammation and subsequent alpha-beta deposition and tau phosphorylation [89]. In regions of the inflammation found in the brain from HSV-1, it was observed to have phosphorylated tau immunopositively neurons in the medial temporal lobe [89].…”

Section: Herpes Simplex Virus-1 (Hsv-1)mentioning

confidence: 99%

Transactivation Response DNA-Binding Protein of 43 (TDP-43) and Glial Cell Roles in Neurological Disorders

Hussain¹,

Djurin²,

Rodríguez³

et al. 2022

Cureus

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The trans-activation response DNA-binding protein of 43kDa (TDP-43) is involved in the pathogenesis of multiple brain disorders. As scientists are unraveling TDP-43 function and its impact on various diseases, we have begun to subcategorize them into TDP-43 proteinopathies. Furthermore, glial cell dysfunction contributes to various disorders, and TDP-43 is involved with glial cells via multiple pathways (direct or indirect) that aggravate the pathophysiology of such disorders. We are only now discovering and understanding the vast and diverse roles TDP-43 plays on neuronal cells and its effects on gliosis and neurodegenerative pathologies. It has multiple roles: mRNA maturation and splicing, transporting and maintaining mRNA stability, a component of stress granules and ubiquitination of dysfunctional or misfolded proteins, transcription of microtubule "Futsch" protein, and a role in maintaining synapse integrity and possibly more as we continue to research and uncover the labyrinth of the neuronal network. TDP-43 could also have a detrimental impact on glial cell activation and pathophysiology in diseases where TDP-43 is associated with its pathogenesis. We will review the pathophysiology of various neurological disorders that are associated with the alteration of the TDP-43 levels along with glial cell activation. Further, multiple diseases have glial cell participation in the pathogenesis, and the role of TDP-43 has not yet been investigated. We, therefore, explore those disorders in the context of both TDP-43 and glial cells involvement. This step will enhance the understanding of neurodegeneration where further research could prompt curative modalities with the advancement of technology.

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Disrupting Neurons and Glial Cells Oneness in the Brain—The Possible Causal Role of Herpes Simplex Virus Type 1 (HSV-1) in Alzheimer’s Disease

Cited by 12 publications

References 299 publications

New Insights into the Molecular Interplay between Human Herpesviruses and Alzheimer’s Disease—A Narrative Review

New Insights into the Molecular Interplay between Human Herpesviruses and Alzheimer’s Disease—A Narrative Review

Special Issue Editorial: “Infections, Inflammation and Neurodegeneration in Alzheimer Disease” Infections, Neuronal Senescence, and Dementia

Transactivation Response DNA-Binding Protein of 43 (TDP-43) and Glial Cell Roles in Neurological Disorders

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