LIVIVO - Search results -

Search results

Result 1 - 10 of total 99

Search options

Article ; Online: Innovations advancing our understanding of microglia in Alzheimer's disease: From in vitro to in vivo models.

Maksour, Simon / Ooi, Lezanne

2023 Volume 166, Issue 3, Page(s) 497–516

Abstract: Microglia have been implicated in Alzheimer's disease (AD) pathogenesis through the identification of risk factor genes that are specifically or predominantly expressed in this cell type. Additional evidence suggests that microglia undergo dramatic ... ...

Abstract	Microglia have been implicated in Alzheimer's disease (AD) pathogenesis through the identification of risk factor genes that are specifically or predominantly expressed in this cell type. Additional evidence suggests that microglia undergo dramatic morphological and phenotypic state changes during AD progression, as observed in human post-mortem tissue and animal model research. Although valuable, these studies are often hampered by either representing one time point in human tissue (end point) or because of the lack of conservation between species of microglial transcriptomes, proteomes and cell states. Thus, the development and application of novel human model systems have been beneficial in the study of microglia in neurodegeneration. Recent innovations include the use of human pluripotent stem cell (hPSC)-derived microglia in 2D or 3D culture systems, the transdifferentiation of microglia from patient monocytes and the xenotransplantation of hPSC-derived microglia into mouse brains. This review summarizes the recent innovations that have advanced our understanding of microglia in AD, through the use of single-cell RNA sequencing, hPSC-derived microglia culture within brain organoids and xenotransplantation into mouse brain. Through outlining the strengths and limitations of these approaches, we provide recommendations that will aid future endeavours in advancing our understanding of the complex role of microglia in AD onset and progression.
MeSH term(s)	Mice ; Animals ; Humans ; Alzheimer Disease/metabolism ; Microglia/metabolism ; Transcriptome ; Brain/metabolism ; Head ; Disease Models, Animal
Language	English
Publishing date	2023-06-15
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.15885
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

Ui II 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

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.

Details ▾

Article ; Online: How spatial omics approaches can be used to map the biological impacts of stress in psychiatric disorders: a perspective, overview and technical guide.

Curry, Amber R / Ooi, Lezanne / Matosin, Natalie

Stress (Amsterdam, Netherlands)

2024 Volume 27, Issue 1, Page(s) 2351394

Abstract: Exposure to significant levels of stress and trauma throughout life is a leading risk factor for the development of major psychiatric disorders. Despite this, we do not have a comprehensive understanding of the mechanisms that explain how stress raises ... ...

Abstract	Exposure to significant levels of stress and trauma throughout life is a leading risk factor for the development of major psychiatric disorders. Despite this, we do not have a comprehensive understanding of the mechanisms that explain how stress raises psychiatric disorder risk. Stress in humans is complex and produces variable molecular outcomes depending on the stress type, timing, and duration. Deciphering how stress increases disorder risk has consequently been challenging to address with the traditional single-target experimental approaches primarily utilized to date. Importantly, the molecular processes that occur following stress are not fully understood but are needed to find novel treatment targets. Sequencing-based omics technologies, allowing for an unbiased investigation of physiological changes induced by stress, are rapidly accelerating our knowledge of the molecular sequelae of stress at a single-cell resolution. Spatial multi-omics technologies are now also emerging, allowing for simultaneous analysis of functional molecular layers, from epigenome to proteome, with anatomical context. The technology has immense potential to transform our understanding of how disorders develop, which we believe will significantly propel our understanding of how specific risk factors, such as stress, contribute to disease course. Here, we provide our perspective of how we believe these technologies will transform our understanding of the neurobiology of stress, and also provided a technical guide to assist molecular psychiatry and stress researchers who wish to implement spatial omics approaches in their own research. Finally, we identify potential future directions using multi-omics technology in stress research.
MeSH term(s)	Humans ; Stress, Psychological ; Mental Disorders ; Proteomics ; Genomics
Language	English
Publishing date	2024-05-16
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1387706-9
ISSN	1607-8888 ; 1025-3890
ISSN (online)	1607-8888
ISSN	1025-3890
DOI	10.1080/10253890.2024.2351394
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5673: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Erratum: Update Notice: A Simple Microplate Assay for Reactive Oxygen Species Generation and Rapid Cellular Protein Normalization.

S Ng, Neville / Ooi, Lezanne

Bio-protocol

2021 Volume 11, Issue 14

Abstract: This corrects the article .]. ...

Abstract	[This corrects the article .].
Language	English
Publishing date	2021-07-20
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2833269-6
ISSN	2331-8325 ; 2331-8325
ISSN (online)	2331-8325
ISSN	2331-8325
DOI	10.21769/BioProtoc.4164
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: A Simple Microplate Assay for Reactive Oxygen Species Generation and Rapid Cellular Protein Normalization.

Ng, Neville S / Ooi, Lezanne

Bio-protocol

2021 Volume 11, Issue 1, Page(s) e3877

Abstract: 2',7'-dichlorofluorescein (DCF) and derivatives are commonly used as fluorescent indicators of a broad spectrum of reactive oxygen species (ROS) generation in cell-based assays. However, there are numerous challenges inherent to the utilization of DCF ... ...

Abstract	2',7'-dichlorofluorescein (DCF) and derivatives are commonly used as fluorescent indicators of a broad spectrum of reactive oxygen species (ROS) generation in cell-based assays. However, there are numerous challenges inherent to the utilization of DCF probes for intracellular microscopic analysis, including photostability and probe efflux. Plate spectroscopy is comparatively simple and scalable compared to microscopy or flow cytometry-based acquisition, however is often subject to artefacts, including those introduced by thermal gradients and normalization methods. In this protocol we demonstrate a simple and sensitive plate spectrometry-based protocol utilizing the probes H
Language	English
Publishing date	2021-01-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2833269-6
ISSN	2331-8325 ; 2331-8325
ISSN (online)	2331-8325
ISSN	2331-8325
DOI	10.21769/BioProtoc.3877
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Neuronal hyperexcitability in Alzheimer's disease: what are the drivers behind this aberrant phenotype?

Targa Dias Anastacio, Helena / Matosin, Natalie / Ooi, Lezanne

Translational psychiatry

2022 Volume 12, Issue 1, Page(s) 257

Abstract: Alzheimer's disease (AD) is a progressive neurodegenerative disorder leading to loss of cognitive abilities and ultimately, death. With no cure available, limited treatments mostly focus on symptom management. Identifying early changes in the disease ... ...

Abstract	Alzheimer's disease (AD) is a progressive neurodegenerative disorder leading to loss of cognitive abilities and ultimately, death. With no cure available, limited treatments mostly focus on symptom management. Identifying early changes in the disease course may provide new therapeutic targets to halt or reverse disease progression. Clinical studies have shown that cortical and hippocampal hyperactivity are a feature shared by patients in the early stages of disease, progressing to hypoactivity during later stages of neurodegeneration. The exact mechanisms causing neuronal excitability changes are not fully characterized; however, animal and cell models have provided insights into some of the factors involved in this phenotype. In this review, we summarize the evidence for neuronal excitability changes over the course of AD onset and progression and the molecular mechanisms underpinning these differences. Specifically, we discuss contributors to aberrant neuronal excitability, including abnormal levels of intracellular Ca
MeSH term(s)	Alzheimer Disease/genetics ; Amyloid beta-Peptides/metabolism ; Animals ; Hippocampus/metabolism ; Humans ; Neurons/metabolism ; Phenotype
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2022-06-22
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2609311-X
ISSN	2158-3188 ; 2158-3188
ISSN (online)	2158-3188
ISSN	2158-3188
DOI	10.1038/s41398-022-02024-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: The P2X4 Receptor: Cellular and Molecular Characteristics of a Promising Neuroinflammatory Target.

Sophocleous, Reece Andrew / Ooi, Lezanne / Sluyter, Ronald

International journal of molecular sciences

2022 Volume 23, Issue 10

Abstract: The adenosine 5'-triphosphate-gated P2X4 receptor channel is a promising target in neuroinflammatory disorders, but the ability to effectively target these receptors in models of neuroinflammation has presented a constant challenge. As such, the exact ... ...

Abstract	The adenosine 5'-triphosphate-gated P2X4 receptor channel is a promising target in neuroinflammatory disorders, but the ability to effectively target these receptors in models of neuroinflammation has presented a constant challenge. As such, the exact role of P2X4 receptors and their cell signalling mechanisms in human physiology and pathophysiology still requires further elucidation. To this end, research into the molecular mechanisms of P2X4 receptor activation, modulation, and inhibition has continued to gain momentum in an attempt to further describe the role of P2X4 receptors in neuroinflammation and other disease settings. Here we provide an overview of the current understanding of the P2X4 receptor, including its expression and function in cells involved in neuroinflammatory signalling. We discuss the pharmacology of P2X4 receptors and provide an overview of P2X4-targeting molecules, including agonists, positive allosteric modulators, and antagonists. Finally, we discuss the use of P2X4 receptor modulators and antagonists in models of neuroinflammatory cell signalling and disease.
MeSH term(s)	Adenosine Triphosphate/metabolism ; Humans ; Receptors, Purinergic P2X4/genetics ; Receptors, Purinergic P2X4/metabolism ; Signal Transduction
Chemical Substances	Receptors, Purinergic P2X4 ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2022-05-20
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23105739
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Generation of APOE knock-down SK-N-SH human neuroblastoma cells using CRISPR/Cas9: a novel cellular model relevant to Alzheimer's disease research.

Muñoz, Sonia Sanz / Garner, Brett / Ooi, Lezanne

Bioscience reports

2021 Volume 41, Issue 2

Abstract: APOE ε4 is the major genetic risk factor for Alzheimer's disease (AD). A precise role for apolipoprotein E (apoE) in the pathogenesis of the disease remains unclear in part due to its expression in multiple cell types of the brain. APOE is highly ... ...

Abstract	APOE ε4 is the major genetic risk factor for Alzheimer's disease (AD). A precise role for apolipoprotein E (apoE) in the pathogenesis of the disease remains unclear in part due to its expression in multiple cell types of the brain. APOE is highly expressed in astrocytes and microglia, however its expression can also be induced in neurons under various conditions. The neuron-like cell line SK-N-SH is a useful model in the study of the cellular and molecular effects of apoE as it can be differentiated with retinoic acid to express and secrete high levels of apoE and it also shows the same apoE fragmentation patterns observed in the human brain. We previously found that apoE is cleaved into a 25-kDa fragment by high temperature-requirement serine protease A1 (HtrA1) in SK-N-SH cells. To further understand the endogenous functions of apoE, we used CRISPR/Cas9 to generate SK-N-SH cell lines with APOE expression knocked-down (KD). APOE KD cells showed lower APOE and HTRA1 expression than parental SK-N-SH cells but no overt differences in neuritogenesis or cell proliferation compared with the CRISPR/Cas9 control cells. This research shows that the loss of apoE and HtrA1 has a negligible effect on neuritogenesis and cell survival in SK-N-SH neuron-like cells.
MeSH term(s)	Alzheimer Disease/genetics ; Apolipoproteins E/genetics ; CRISPR-Cas Systems ; Cell Differentiation ; Cell Line, Tumor ; Humans ; Neuroblastoma/pathology
Chemical Substances	ApoE protein, human ; Apolipoproteins E
Language	English
Publishing date	2021-02-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	764946-0
ISSN	1573-4935 ; 0144-8463
ISSN (online)	1573-4935
ISSN	0144-8463
DOI	10.1042/BSR20204243
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1676: 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: The role of amyloid oligomers in neurodegenerative pathologies.

Wells, Cameron / Brennan, Samuel / Keon, Matt / Ooi, Lezanne

International journal of biological macromolecules

2021 Volume 181, Page(s) 582–604

Abstract: Many neurodegenerative diseases are rooted in the activities of amyloid-like proteins which possess conformations that spread to healthy proteins. These include Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD) and amyotrophic ...

Abstract	Many neurodegenerative diseases are rooted in the activities of amyloid-like proteins which possess conformations that spread to healthy proteins. These include Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD) and amyotrophic lateral sclerosis (ALS). While their clinical manifestations vary, their protein-level mechanisms are remarkably similar. Aberrant monomeric proteins undergo conformational shifts, facilitating aggregation and formation of solid fibrils. However, there is growing evidence that intermediate oligomeric stages are key drivers of neuronal toxicity. Analysis of protein dynamics is complicated by the fact that nucleation and growth of amyloid-like proteins is not a linear pathway. Feedback within this pathway results in exponential acceleration of aggregation, but activities exerted by oligomers and fibrils can alter cellular interactions and the cellular environment as a whole. The resulting cascade of effects likely contributes to the late onset and accelerating progression of amyloid-like protein disorders and the widespread effects they have on the body. In this review we explore the amyloid-like proteins associated with AD, PD, HD and ALS, as well as the common mechanisms of amyloid-like protein nucleation and aggregation. From this, we identify core elements of pathological progression which have been targeted for therapies, and which may become future therapeutic targets.
MeSH term(s)	Amyloid/metabolism ; Animals ; Drug Delivery Systems ; Humans ; Nerve Degeneration/metabolism ; Nerve Degeneration/pathology ; Nerve Degeneration/therapy ; Protein Aggregates ; Protein Multimerization
Chemical Substances	Amyloid ; Protein Aggregates
Language	English
Publishing date	2021-03-23
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	282732-3
ISSN	1879-0003 ; 0141-8130
ISSN (online)	1879-0003
ISSN	0141-8130
DOI	10.1016/j.ijbiomac.2021.03.113
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

Zs.B 2374: 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: Increased Neuronal Nitric Oxide Synthase in Alzheimer's Disease Mediates Spontaneous Calcium Signaling and Divergent Glutamatergic Calcium Responses.

Balez, Rachelle / Stevens, Claire H / Lenk, Kerstin / Maksour, Simon / Sidhu, Kuldip / Sutherland, Greg / Ooi, Lezanne

Antioxidants & redox signaling

2024

Abstract: Nitrosative stress is a feature of Alzheimer's disease (AD). ...

Abstract	Nitrosative stress is a feature of Alzheimer's disease (AD).
Language	English
Publishing date	2024-03-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2023.0395
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

Zs.A 5488: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Wnt is here! Could Wnt signalling be promoted to protect against Alzheimer disease?: An Editorial for 'Wnt signaling loss accelerates the appearance of neuropathological hallmarks of Alzheimer's disease in J20- APP transgenic and wild-type mice' on doi:10.1111/jnc.14278.

Garner, Brett / Ooi, Lezanne

Journal of neurochemistry

2018 Volume 144, Issue 4, Page(s) 356–359

Abstract: This Editorial highlights an article in the current issue by Tapia-Rojas and Inestrosa suggesting that attenuation of Wnt signalling may be a triggering factor for the pathogenesis of Alzheimer disease (AD) in the J20 mouse model of AD. Their study ... ...

Abstract	This Editorial highlights an article in the current issue by Tapia-Rojas and Inestrosa suggesting that attenuation of Wnt signalling may be a triggering factor for the pathogenesis of Alzheimer disease (AD) in the J20 mouse model of AD. Their study utilises Wnt signalling inhibitors that operate at different points in the signalling pathway. The molecular changes of several key Wnt signaling components are examined, along with a thorough analysis of both the amyloid and tau based pathologies in the mouse brain. Studies focusing on inhibition of Wnt signalling in AD mice have the potential to provide much needed information regarding the pathological mechanisms by which attenuated Wnt signalling impacts on AD.
MeSH term(s)	Alzheimer Disease ; Animals ; Disease Models, Animal ; Mice ; Mice, Transgenic ; Wnt Signaling Pathway
Language	English
Publishing date	2018-01-26
Publishing country	England
Document type	Editorial ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.14276
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

Ui II 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 ▾

To top

Full text online

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

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito