LIVIVO - Search results -

Search results

Result 1 - 10 of total 58

Search options

Article: Herpes Simplex Virus Type 1 Induces AD-like Neurodegeneration Markers in Human Progenitor and Differentiated ReNcell VM Cells.

Salgado, Blanca / Sastre, Isabel / Bullido, Maria J / Aldudo, Jesus

2023 Volume 11, Issue 5

Abstract: An increasing body of evidence strongly suggests that infections or reactivations of herpes simplex virus type 1 (HSV-1) may be closely linked to Alzheimer's disease (AD). Promising results have been obtained using cell and animal models of HSV-1 ... ...

Abstract	An increasing body of evidence strongly suggests that infections or reactivations of herpes simplex virus type 1 (HSV-1) may be closely linked to Alzheimer's disease (AD). Promising results have been obtained using cell and animal models of HSV-1 infection, contributing to the understanding of the molecular mechanisms linking HSV-1 infection and AD neurodegeneration. ReNcell VM is a human neural stem cell line that has been used as a model system to study the impact of various infectious agents on the central nervous system. In this study, we demonstrate the suitability of the ReNcell VM cell line for developing a new in vitro model of HSV-1 infection. By following standard differentiation protocols, we were able to derive various nervous cell types, including neurons, astrocytes, and oligodendrocytes, from neural precursors. Additionally, we demonstrated the susceptibility of ReNcell VM cells, including precursor and differentiated cells, to HSV-1 infection and subsequent viral-induced AD-like neurodegeneration. Our findings support the use of this cell line to generate a new research platform for investigating AD neuropathology and its most significant risk factors, which may lead to important discoveries in the context of this highly impactful disease.
Language	English
Publishing date	2023-05-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720891-6
ISSN	2076-2607
ISSN	2076-2607
DOI	10.3390/microorganisms11051205
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Article ; Online: Matrix metalloproteinase 14 regulates HSV-1 infection in neuroblastoma cells.

Llorente, Patricia / Mejías, Víctor / Sastre, Isabel / Recuero, María / Aldudo, Jesús / Bullido, Maria J

Antiviral research

2021 Volume 192, Page(s) 105116

Abstract: Growing evidence supports that chronic or latent infection of the central nervous system might be implicated in Alzheimer's disease (AD). Among them, Herpes simplex virus type 1 (HSV-1) has emerged as a major factor in the etiology of the disease. Our ... ...

Abstract	Growing evidence supports that chronic or latent infection of the central nervous system might be implicated in Alzheimer's disease (AD). Among them, Herpes simplex virus type 1 (HSV-1) has emerged as a major factor in the etiology of the disease. Our group is devoted to the study of the relationship among HSV-1, oxidative stress (OS) and neurodegeneration. We have found that HSV-1 induces the main neuropathological hallmarks of AD, including the accumulation of intracellular amyloid beta (Aβ), hyperphosphorylated tau protein and autophagic vesicles, that OS exacerbates these effects, and that matrix metalloproteinase 14 (MMP-14) participates in the alterations induced by OS. In this work, we focused on the role of MMP-14 in the degenerative markers raised by HSV-1 infection. Interestingly, we found that MMP-14 blockage is a potent inhibitor of HSV-1 infection efficiency, that also reduces the degeneration markers, accumulation of Aβ and hyperphosphorylated tau, induced by the virus. Our results point to MMP-14 as a potent antiviral target to control HSV-1 infection and its associated neurodegenerative effects.
MeSH term(s)	Alzheimer Disease/metabolism ; Alzheimer Disease/virology ; Amyloid beta-Peptides/metabolism ; Animals ; Antiviral Agents/pharmacology ; Autophagosomes/metabolism ; Biomarkers/metabolism ; Cell Line, Tumor ; Herpes Simplex/metabolism ; Herpes Simplex/virology ; Herpesvirus 1, Human/drug effects ; Herpesvirus 1, Human/physiology ; Humans ; Matrix Metalloproteinase 14/deficiency ; Matrix Metalloproteinase 14/metabolism ; Matrix Metalloproteinase Inhibitors/pharmacology ; Mice ; Neuroblastoma/pathology ; Oxidative Stress ; Phosphorylation ; tau Proteins/metabolism
Chemical Substances	Amyloid beta-Peptides ; Antiviral Agents ; Biomarkers ; MAPT protein, human ; Matrix Metalloproteinase Inhibitors ; tau Proteins ; MMP14 protein, human (EC 3.4.24.80) ; Matrix Metalloproteinase 14 (EC 3.4.24.80)
Language	English
Publishing date	2021-06-06
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	306628-9
ISSN	1872-9096 ; 0166-3542
ISSN (online)	1872-9096
ISSN	0166-3542
DOI	10.1016/j.antiviral.2021.105116
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1627: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Metabolic Overlap between Alzheimer's Disease and Metabolic Syndrome Identifies the

Guardiola, Montse / Muntané, Gerard / Martínez, Iris / Martorell, Lourdes / Girona, Josefa / Ibarretxe, Daiana / Plana, Núria / Bullido, María J / Vilella, Elisabet / Ribalta, Josep

International journal of molecular sciences

2023 Volume 24, Issue 8

Abstract: Background: Alzheimer's disease (AD) and type 2 diabetes mellitus (T2DM) share metabolic alterations such as abnormal insulin and lipid metabolism and have some common genetic factors such as : Methodology: We first genotyped 48 single nucleotide ... ...

Abstract	Background: Alzheimer's disease (AD) and type 2 diabetes mellitus (T2DM) share metabolic alterations such as abnormal insulin and lipid metabolism and have some common genetic factors such as Methodology: We first genotyped 48 single nucleotide polymorphisms (SNPs) previously associated with AD in a cohort composed of 330 patients with cognitive impairment (CI) to assess their association with plasma lipids. Second, we conducted pleiotropy-informed conjunctional false discovery rate (FDR) analysis designed to identify shared variants between AD and plasma lipid levels. Finally, we used the SNPs to be found associated with lipid parameters and AD to search for associations with lipoprotein parameters in 281 patients with cardiometabolic risk. Results: Five SNPs were significantly associated with lower levels of cholesterol transported in remnant lipoprotein particles (RLPc) in subjects with CI; among these SNPs was the rs73572039 variant in Conclusions: We have identified three variants in
MeSH term(s)	Humans ; Alzheimer Disease/genetics ; Alzheimer Disease/complications ; Cardiovascular Diseases/genetics ; Cholesterol ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/genetics ; Dyslipidemias/genetics ; Dyslipidemias/complications ; Genome-Wide Association Study ; Metabolic Syndrome/genetics ; Metabolic Syndrome/complications ; Polymorphism, Single Nucleotide ; Triglycerides
Chemical Substances	Cholesterol (97C5T2UQ7J) ; Triglycerides ; NECTIN2 protein, human
Language	English
Publishing date	2023-04-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24087415
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Tetraspanin CD81 regulates HSV-1 infection.

Benayas, Beatriz / Sastre, Isabel / López-Martín, Soraya / Oo, Adrian / Kim, Baek / Bullido, Maria J / Aldudo, Jesús / Yáñez-Mó, María

Medical microbiology and immunology

2020 Volume 209, Issue 4, Page(s) 489–498

Abstract: Different members of the tetraspanin superfamily have been described to regulate different virus infectious cycles at several stages: viral entry, viral replication or virion exit or infectivity. In addition, tetraspanin CD81 regulates HIV reverse ... ...

Abstract	Different members of the tetraspanin superfamily have been described to regulate different virus infectious cycles at several stages: viral entry, viral replication or virion exit or infectivity. In addition, tetraspanin CD81 regulates HIV reverse transcription through its association with the dNTP hydrolase SAMHD1. Here we aimed at analysing the role of CD81 in Herpes simplex virus 1 infectivity using a neuroblastoma cell model. For this purpose, we generated a CD81 KO cell line using the CRISPR/Cas9 technology. Despite being CD81 a plasma membrane protein, CD81 KO cells showed no defects in viral entry nor in the expression of early protein markers. In contrast, glycoprotein B and C, which require viral DNA replication for their expression, were significantly reduced in CD81 KO infected cells. Indeed, HSV-1 DNA replication and the formation of new infectious particles were severely compromised in CD81 KO cells. We could not detect significant changes in SAMHD1 total expression levels, but a relocalization into endosomal structures was observed in CD81 KO cells. In summary, CD81 KO cells showed impaired viral DNA replication and produced greatly diminished viral titers.
MeSH term(s)	CRISPR-Cas Systems ; Cell Line, Tumor ; Gene Knockout Techniques ; Herpesviridae Infections/virology ; Herpesvirus 1, Human/pathogenicity ; Herpesvirus 1, Human/physiology ; Humans ; SAM Domain and HD Domain-Containing Protein 1/metabolism ; Tetraspanin 28/genetics ; Tetraspanin 28/metabolism ; Viral Envelope Proteins/metabolism ; Virion/metabolism ; Virus Internalization ; Virus Replication
Chemical Substances	CD81 protein, human ; Tetraspanin 28 ; Viral Envelope Proteins ; glycoprotein B, human herpesvirus 1 ; glycoprotein gC, herpes simplex virus type 1 ; SAM Domain and HD Domain-Containing Protein 1 (EC 3.1.5.-) ; SAMHD1 protein, human (EC 3.1.5.-)
Keywords	covid19
Language	English
Publishing date	2020-06-04
Publishing country	Germany
Document type	Journal Article
ZDB-ID	120933-4
ISSN	1432-1831 ; 0300-8584
ISSN (online)	1432-1831
ISSN	0300-8584
DOI	10.1007/s00430-020-00684-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Un I Zs.170: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Matrix Metalloproteinase 14 Mediates APP Proteolysis and Lysosomal Alterations Induced by Oxidative Stress in Human Neuronal Cells.

Llorente, Patricia / Martins, Soraia / Sastre, Isabel / Aldudo, Jesús / Recuero, María / Adjaye, James / Bullido, Maria J

Oxidative medicine and cellular longevity

2020 Volume 2020, Page(s) 5917187

Abstract: The alteration of amyloid precursor protein (APP) proteolysis is a hallmark of Alzheimer's disease (AD). Recent studies have described noncanonical pathways of APP processing that seem partly executed by lysosomal enzymes. Our laboratory' ... ...

Abstract	The alteration of amyloid precursor protein (APP) proteolysis is a hallmark of Alzheimer's disease (AD). Recent studies have described noncanonical pathways of APP processing that seem partly executed by lysosomal enzymes. Our laboratory's
MeSH term(s)	Alzheimer Disease/metabolism ; Amyloid Precursor Protein Secretases/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Humans ; Lysosomes/metabolism ; Matrix Metalloproteinase 14/metabolism ; Neurons/metabolism ; Oxidative Stress/physiology ; Proteolysis
Chemical Substances	Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Amyloid Precursor Protein Secretases (EC 3.4.-) ; MMP14 protein, human (EC 3.4.24.80) ; Matrix Metalloproteinase 14 (EC 3.4.24.80)
Language	English
Publishing date	2020-11-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	2455981-7
ISSN	1942-0994 ; 1942-0994
ISSN (online)	1942-0994
ISSN	1942-0994
DOI	10.1155/2020/5917187
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: The lysosome system is severely impaired in a cellular model of neurodegeneration induced by HSV-1 and oxidative stress.

Kristen, Henrike / Sastre, Isabel / Muñoz-Galdeano, Teresa / Recuero, Maria / Aldudo, Jesus / Bullido, Maria J

Neurobiology of aging

2018 Volume 68, Page(s) 5–17

Abstract: The causal agent(s) and molecular mechanisms of Alzheimer's disease (AD) remain unclear. Mounting evidence suggests that herpes simplex virus type 1 (HSV-1) infection is involved in the AD pathogenesis. Oxidative stress (OS) may also be crucial in the AD ...

Abstract	The causal agent(s) and molecular mechanisms of Alzheimer's disease (AD) remain unclear. Mounting evidence suggests that herpes simplex virus type 1 (HSV-1) infection is involved in the AD pathogenesis. Oxidative stress (OS) may also be crucial in the AD development. Our group previously reported that both HSV-1 and OS trigger the appearance of AD-type neurodegeneration markers. The main aim of the present study was to identify the mechanisms involved in this triggering. Expression studies revealed the involvement of a set of OS-regulated genes in HSV-1-infected cells and in cells harboring the Swedish mutation of the amyloid beta precursor protein gene. Functional annotation of these genes revealed the lysosome system to be impaired, suggesting that the interaction of OS with both HSV-1 and amyloid beta precursor protein mutations affects lysosomal function. Functional studies revealed HSV-1 infection and OS to increase the lysosome load, reduce the activity of lysosomal hydrolases, affect cathepsin maturation, and inhibit the endocytosis-mediated degradation of the epidermal growth factor receptor. These findings suggest alterations in the lysosome system to be involved in different forms of AD.
MeSH term(s)	Alzheimer Disease/etiology ; Alzheimer Disease/pathology ; Amyloid beta-Protein Precursor/genetics ; Herpes Simplex/complications ; Herpes Simplex/genetics ; Herpesvirus 1, Human ; Humans ; Lysosomes/genetics ; Lysosomes/pathology ; Lysosomes/physiology ; Mutation ; Nerve Degeneration/etiology ; Neurodegenerative Diseases/etiology ; Neurodegenerative Diseases/pathology ; Oxidative Stress ; Tumor Cells, Cultured
Chemical Substances	Amyloid beta-Protein Precursor
Language	English
Publishing date	2018-03-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604505-4
ISSN	1558-1497 ; 0197-4580
ISSN (online)	1558-1497
ISSN	0197-4580
DOI	10.1016/j.neurobiolaging.2018.03.025
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1685: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 10: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: LAMP2 deficiency attenuates the neurodegeneration markers induced by HSV-1 infection.

Kristen, Henrike / Sastre, Isabel / Aljama, Sara / Fuentes, Maria / Recuero, Maria / Frank-García, Ana / Martin, Angel / Sanchez-Juan, Pascual / Lage, Carmen / Bullido, Maria J / Aldudo, Jesus

Neurochemistry international

2021 Volume 146, Page(s) 105032

Abstract: Mounting evidence suggests a major role of infectious agents in the pathogenesis of sporadic Alzheimer's disease (AD). Among them, herpes simplex virus type 1 (HSV-1) infection has emerged as a major factor in the etiology of AD. HSV-1 is able to induce ... ...

Abstract	Mounting evidence suggests a major role of infectious agents in the pathogenesis of sporadic Alzheimer's disease (AD). Among them, herpes simplex virus type 1 (HSV-1) infection has emerged as a major factor in the etiology of AD. HSV-1 is able to induce some of the main alterations of the disease such as hyperphosphorylation of tau protein and accumulation of amyloid-β peptide. Functional genomic analysis of a cell model of HSV-1 infection and oxidative stress developed in our laboratory revealed lysosomal system to be the main pathway altered, and the lysosome-associated membrane protein 2 (LAMP2) gene one of the most strongly modulated genes. The aim of this work is to study LAMP2 as an AD candidate gene and to investigate its role in the neurodegeneration induced by HSV-1 using a LAMP2 knockdown cell model. LAMP2 deficiency led to a significant reduction of viral DNA replication and formation of infectious particles. In addition, tau hyperphosphorylation and inhibition of Aβ secretion induced by the virus were attenuated by the absence of LAMP2. Finally, genetic association studies revealed LAMP2 genetic variants to be associated with AD risk. In summary, our data indicate that LAMP2 could be a suitable candidate to mediate the AD-like phenotype caused by HSV-1.
MeSH term(s)	Aged ; Aged, 80 and over ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/virology ; Animals ; Cell Line, Tumor ; Female ; Gene Knockdown Techniques/methods ; Herpes Simplex/genetics ; Herpes Simplex/metabolism ; Herpes Simplex/prevention & control ; Herpesvirus 1, Human/metabolism ; Humans ; Lysosomal-Associated Membrane Protein 2/antagonists & inhibitors ; Lysosomal-Associated Membrane Protein 2/genetics ; Lysosomal-Associated Membrane Protein 2/metabolism ; Male ; Mice ; Middle Aged ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/virology
Chemical Substances	Lysosomal-Associated Membrane Protein 2
Language	English
Publishing date	2021-03-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	283190-9
ISSN	1872-9754 ; 0197-0186
ISSN (online)	1872-9754
ISSN	0197-0186
DOI	10.1016/j.neuint.2021.105032
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1610: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: A Free Radical-Generating System Regulates Amyloid Oligomers: Involvement of Cathepsin B.

Llorente, Patricia / Kristen, Henrike / Sastre, Isabel / Toledano-Zaragoza, Ana / Aldudo, Jesús / Recuero, María / Bullido, María J

Journal of Alzheimer's disease : JAD

2018 Volume 66, Issue 4, Page(s) 1397–1408

Abstract: Amyloid-β (Aβ), a major component of senile plaques, is generated via the proteolysis of amyloid-β protein precursor (AβPP). This cleavage also produces AβPP fragment-derived oligomers which can be highly neurotoxic. AβPP metabolism/processing is ... ...

Abstract	Amyloid-β (Aβ), a major component of senile plaques, is generated via the proteolysis of amyloid-β protein precursor (AβPP). This cleavage also produces AβPP fragment-derived oligomers which can be highly neurotoxic. AβPP metabolism/processing is affected by many factors, one of which is oxidative stress (OS). Associated with aging, OS is an important risk factor for Alzheimer's disease. In addition, the protein degradation systems, especially those involving cathepsins, are impaired in aging brains. Moreover, cathepsin B (CTSB) is a cysteine protease with potentially specific roles in AβPP proteolysis (β-secretase activity) and Aβ clearance (Aβ degradative activity). The present work examines the effect of OS and the involvement of CTSB in amyloid oligomer formation. The xanthine/xanthine oxidase (X-XOD) free radical generating system induced the partial inhibition of CTSB activity, which was accompanied by an increase in large amyloid oligomers. These were located throughout the cytosol and in endo-lysosomal vesicles. Cells treated with the CTSB inhibitor CA-074Me also showed increased amyloid oligomer levels, whereas those subjected to OS in the presence of the inhibitor showed no such increase. However, CTSB inhibition clearly modulated the AβPP metabolism/processing induced by X-XOD, as revealed by the increase in intracellular AβPP and secreted α-secretase-cleaved soluble AβPP. The present results suggest that CTSB participates in the changes of amyloid oligomer induced by mild OS.
MeSH term(s)	Aging/metabolism ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Brain/drug effects ; Brain/metabolism ; Cathepsin B/antagonists & inhibitors ; Cathepsin B/metabolism ; Cell Line, Tumor ; Dipeptides/pharmacology ; Free Radicals/metabolism ; Humans ; Lysosomes/metabolism ; Neurons/drug effects ; Neurons/metabolism ; Oxidative Stress/drug effects ; Oxidative Stress/physiology
Chemical Substances	Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; CA 074 methyl ester ; Dipeptides ; Free Radicals ; Cathepsin B (EC 3.4.22.1)
Language	English
Publishing date	2018-11-03
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-170159
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6084: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Tetraspanin CD81 regulates HSV-1 infection

Benayas, Beatriz / Sastre, Isabel / López-Martín, Soraya / Oo, Adrian / Kim, Baek / Bullido, Maria J / Aldudo, Jesús / Yáñez-Mó, María

Med Microbiol Immunol

Abstract	Different members of the tetraspanin superfamily have been described to regulate different virus infectious cycles at several stages: viral entry, viral replication or virion exit or infectivity. In addition, tetraspanin CD81 regulates HIV reverse transcription through its association with the dNTP hydrolase SAMHD1. Here we aimed at analysing the role of CD81 in Herpes simplex virus 1 infectivity using a neuroblastoma cell model. For this purpose, we generated a CD81 KO cell line using the CRISPR/Cas9 technology. Despite being CD81 a plasma membrane protein, CD81 KO cells showed no defects in viral entry nor in the expression of early protein markers. In contrast, glycoprotein B and C, which require viral DNA replication for their expression, were significantly reduced in CD81 KO infected cells. Indeed, HSV-1 DNA replication and the formation of new infectious particles were severely compromised in CD81 KO cells. We could not detect significant changes in SAMHD1 total expression levels, but a relocalization into endosomal structures was observed in CD81 KO cells. In summary, CD81 KO cells showed impaired viral DNA replication and produced greatly diminished viral titers.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #710745
Database	COVID19

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾

Article ; Online: Herpes simplex virus type 2 infection induces AD-like neurodegeneration markers in human neuroblastoma cells.

Kristen, Henrike / Santana, Soraya / Sastre, Isabel / Recuero, Maria / Bullido, Maria J / Aldudo, Jesus

Neurobiology of aging

2015 Volume 36, Issue 10, Page(s) 2737–2747

Abstract: Herpes simplex virus (HSV) types 1 and 2 are neurotropic viruses that establish lifelong latent infections in neurons. Mounting evidence suggests that HSV-1 infection is involved in the pathogenesis of Alzheimer's disease (AD). The relationships between ... ...

Abstract	Herpes simplex virus (HSV) types 1 and 2 are neurotropic viruses that establish lifelong latent infections in neurons. Mounting evidence suggests that HSV-1 infection is involved in the pathogenesis of Alzheimer's disease (AD). The relationships between other herpesvirus infections and events associated with neurodegeneration have not, however, been extensively studied. The present work reports that HSV-2 infection leads to the strong accumulation of hyperphosphorylated tau and the amyloid-β peptides Aβ40 and Aβ42 (all major pathological hallmarks of AD) in human SK-N-MC neuroblastoma cells. Infection is also associated with a marked reduction in the amount of Aβ40 secreted and in the proteolytic fragments of the amyloid-β precursor protein (APP) (secreted APPα and the α-C-terminal fragment). These results indicate that HSV-2 infection inhibits the nonamyloidogenic pathway of APP processing and impairs Aβ secretion in these cells. In addition, HSV-2 induces the accumulation of intracellular autophagic compartments containing Aβ due to a failure in the late stages of autophagy. To our knowledge, this is the first report to show that HSV-2 infection strongly alters the tau phosphorylation state, APP processing, and autophagic process in human neuroblastoma cells, leading to the appearance of AD-like neurodegeneration markers.
MeSH term(s)	Alzheimer Disease/virology ; Amyloid beta-Peptides/metabolism ; Autophagy ; Cell Line, Tumor ; Herpes Simplex/metabolism ; Herpesvirus 2, Human ; Humans ; Neuroblastoma/metabolism ; Peptide Fragments/metabolism ; Phosphorylation ; tau Proteins/metabolism
Chemical Substances	Amyloid beta-Peptides ; Peptide Fragments ; amyloid beta-protein (1-40) ; amyloid beta-protein (1-42) ; tau Proteins
Language	English
Publishing date	2015-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604505-4
ISSN	1558-1497 ; 0197-4580
ISSN (online)	1558-1497
ISSN	0197-4580
DOI	10.1016/j.neurobiolaging.2015.06.014
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1685: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 10: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito