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Book ; Online ; E-Book: Biometals in neurodegenerative diseases

White, Anthony R. / Aschner, Michael / Costa, Lucio / Bush, Ashley I.

mechanisms and therapeutics

2017

Author's details	edited by Anthony R. White, Michael Aschner, Lucio G. Costa, Ashley I. Bush
Language	English
Size	1 Online-Ressource (xiv, 451 Seiten), Illustrationen
Publisher	Elsevier AP
Publishing place	London
Publishing country	Great Britain
Document type	Book ; Online ; E-Book
Remark	Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
HBZ-ID	HT019403384
ISBN	978-0-12-804563-3 ; 9780128045626 ; 0-12-804563-9 ; 0128045620
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Book ; Online: The CB2 Cannabinoid System: A New Strategy in Neurodegenerative Disorder and Neuroinflammation

Colabufo, Nicola A. / Capparelli, Elena / Contino, Marialessandra / Bush, Ashley I.

2017

Abstract: The neurodegenerative disorders such as Parkinson's disease (PD) or Alzheimer's disease (AD) are the most common forms of dementia and no pharmacological treatments are to date available for these diseases. Indeed, the only used drugs are symptomatic and ...

Abstract	The neurodegenerative disorders such as Parkinson's disease (PD) or Alzheimer's disease (AD) are the most common forms of dementia and no pharmacological treatments are to date available for these diseases. Indeed, the only used drugs are symptomatic and no useful to block the progression of the diseases. The lack of a therapeutic approach is also due to a lack of an early diagnosis. This Research Topic describes a new target that is involved in the firs step of these disorders and that can be useful for the treatment and the diagnosis of such pathologies: the cannabinoid receptor subtype 2 or CB2R. Indeed, CB2R is overexpressed in reactive microglia and activated astrocytes during neuroinflammation and thus their detection by PET probes can be an easily strategy for an early diagnosis of neurodegeneration. Moreover, CB2 agonists and inverse agonists displayed neuroprotective effects and they so can be candidated as new therapeutich drugs for the treatment of these pathologies. Therefore, the aim of this Research Topic is to show the great potential of CB2R ligands for the development of new tools/drugs for both the therapy and the diagnosis of neurodegeneration
Keywords	Neurosciences. Biological psychiatry. Neuropsychiatry ; Science (General)
Size	1 electronic resource (100 p.)
Publisher	Frontiers Media SA
Document type	Book ; Online
Note	English ; Open Access
HBZ-ID	HT020095927
ISBN	9782889452231 ; 2889452239
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: How iron can drive neurodegeneration.

Kenkhuis, Boyd / Bush, Ashley I / Ayton, Scott

Trends in neurosciences

2023 Volume 46, Issue 5, Page(s) 333–335

Abstract: Iron overload in neurodegenerative diseases is well established but of uncertain significance. In a recent article, Ryan et al. reveal that microglia are especially vulnerable to iron overload-induced ferroptosis. Their evidence for microglial ... ...

Abstract	Iron overload in neurodegenerative diseases is well established but of uncertain significance. In a recent article, Ryan et al. reveal that microglia are especially vulnerable to iron overload-induced ferroptosis. Their evidence for microglial ferroptosis in clinical specimens indicates that ferroptosis inhibitors may hold therapeutic promise for these diseases.
MeSH term(s)	Humans ; Iron ; Neurodegenerative Diseases ; Iron Overload ; Microglia
Chemical Substances	Iron (E1UOL152H7)
Language	English
Publishing date	2023-02-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	282488-7
ISSN	1878-108X ; 0378-5912 ; 0166-2236
ISSN (online)	1878-108X
ISSN	0378-5912 ; 0166-2236
DOI	10.1016/j.tins.2023.02.003
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Zs.A 1442: 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)
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Article ; Online: Striking a NRF2: The Rusty and Rancid Vulnerabilities Toward Ferroptosis in Alzheimer's Disease.

Lane, Darius J R / Alves, Francesca / Ayton, Scott J / Bush, Ashley I

Antioxidants & redox signaling

2023 Volume 39, Issue 1-3, Page(s) 141–161

Abstract: Significance: ...

Abstract	Significance:
MeSH term(s)	Humans ; Ferroptosis ; Phospholipid Hydroperoxide Glutathione Peroxidase/genetics ; Phospholipid Hydroperoxide Glutathione Peroxidase/metabolism ; Alzheimer Disease ; NF-E2-Related Factor 2/metabolism ; Cell Death/genetics ; Lipid Peroxidation/genetics ; Iron/metabolism
Chemical Substances	Phospholipid Hydroperoxide Glutathione Peroxidase (EC 1.11.1.12) ; NF-E2-Related Factor 2 ; Iron (E1UOL152H7)
Language	English
Publishing date	2023-06-28
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2023.0318
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Zs.A 5488: Show issues

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Article ; Online: Does the FDA-approved Alzheimer drug aducanumab have a place in the Australian pharmacopoeia?

Gleason, Andrew / Ayton, Scott / Bush, Ashley I

The Medical journal of Australia

2022 Volume 216, Issue 4, Page(s) 172–174

MeSH term(s)	Alzheimer Disease/drug therapy ; Antibodies, Monoclonal, Humanized/therapeutic use ; Australia ; Drug Approval ; Humans ; United States ; United States Food and Drug Administration
Chemical Substances	Antibodies, Monoclonal, Humanized ; aducanumab (105J35OE21)
Language	English
Publishing date	2022-02-09
Publishing country	Australia
Document type	Journal Article
ZDB-ID	186082-3
ISSN	1326-5377 ; 0025-729X
ISSN (online)	1326-5377
ISSN	0025-729X
DOI	10.5694/mja2.51408
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Article ; Online: Single-session reproducibility of MR spectroscopy measures of glutathione in the mesial temporal lobe with MEGA-PRESS.

Vidyasagar, Rishma / Fazollahi, Amir / Desmond, Patricia / Moffat, Bradford / Bush, Ashley I / Ayton, Scott

Journal of neuroimaging : official journal of the American Society of Neuroimaging

2024 Volume 34, Issue 2, Page(s) 224–231

Abstract: Background and purpose: Magnetic resonance spectroscopy (MRS) measures neurochemicals in vivo. Glutathione (GSH) is a neuroprotective chemical shown to vary significantly in patients with Alzheimer's disease (AD). This work investigates the ... ...

Abstract	Background and purpose: Magnetic resonance spectroscopy (MRS) measures neurochemicals in vivo. Glutathione (GSH) is a neuroprotective chemical shown to vary significantly in patients with Alzheimer's disease (AD). This work investigates the reproducibility of GSH measures in the mesial temporal lobe (MTL) to identify its potential clinical utility. Methods: MRS data were acquired from eight healthy volunteers (31.1 ± 5.2 years; 4 male/female) using Mescher-Garwood-Point Resolved Spectroscopy (MEGA-PRESS) from the MTL in the left hemisphere across two scan sessions in the same visit. Total N-acetylaspartate (tNAA), choline (tCho), creatine (tCr), and GSH were quantified. Reproducibility of quantifications of these neurochemicals were tested using coefficient of variance (CV) between scan sessions. Reproducibility of voxel placement on the left MTL was calculated by measuring the tissue overlap and percent of hippocampus within that voxel. CV measured across different scan sessions in each individual, with a CV<15% was accepted as "good" reproducibility. Paired t-tests were carried out to establish the significant differences between the two scans across each individual with p<.05 as significant. Results: TNAA (%CV = 7.2; p = .5), tCr (%CV = 7.8; p = .6) and tCho (%CV = 9.3; p = .4), and GSH (%CV = 22; p = .1). The dice coefficient that reflects the level of overlap of hippocampal tissue in the voxel was shown to be 0.8 ± 0.1. Voxel tissue composition were: Scan 1 (cerebrospinal fluid [CSF]: 5 ± 1%, white matter [WM]: 52 ± 3%, gray matter [GM]: 43 ± 3%); Scan 2 (CSF: 5 ± 1%, WM: 52 ± 4%, GM: 44 ± 4%). Conclusion: The data suggest measures of abundant metabolites in the MTL using the MEGA-PRESS sequence has a high reproducibility. Reproducibility of GSH in this area was poorer requiring care when interpreting measures of GSH in the MTL for clinical translational purposes.
MeSH term(s)	Humans ; Male ; Female ; Reproducibility of Results ; Magnetic Resonance Spectroscopy/methods ; Temporal Lobe/diagnostic imaging ; Glutathione/metabolism ; Receptors, Antigen, T-Cell/metabolism
Chemical Substances	Glutathione (GAN16C9B8O) ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2024-01-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	1071724-9
ISSN	1552-6569 ; 1051-2284
ISSN (online)	1552-6569
ISSN	1051-2284
DOI	10.1111/jon.13179
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Zs.A 3211: Show issues

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Article ; Online: Vitamin A metabolites inhibit ferroptosis.

Jakaria, Md / Belaidi, Abdel A / Bush, Ashley I / Ayton, Scott

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2023 Volume 164, Page(s) 114930

Abstract: Vitamin A (retinol) is a lipid-soluble vitamin that acts as a precursor for several bioactive compounds, such as retinaldehyde (retinal) and isomers of retinoic acid. Retinol and all-trans-retinoic acid (atRA) penetrate the blood-brain barrier and are ... ...

Abstract	Vitamin A (retinol) is a lipid-soluble vitamin that acts as a precursor for several bioactive compounds, such as retinaldehyde (retinal) and isomers of retinoic acid. Retinol and all-trans-retinoic acid (atRA) penetrate the blood-brain barrier and are reported to be neuroprotective in several animal models. We characterised the impact of retinol and its metabolites, all-trans-retinal (atRAL) and atRA, on ferroptosis-a programmed cell death caused by iron-dependent phospholipid peroxidation. Ferroptosis was induced by erastin, buthionine sulfoximine or RSL3 in neuronal and non-neuronal cell lines. We found that retinol, atRAL and atRA inhibited ferroptosis with a potency superior to α-tocopherol, the canonical anti-ferroptotic vitamin. In contrast, we found that antagonism of endogenous retinol with anhydroretinol sensitises ferroptosis induced in neuronal and non-neuronal cell lines. Retinol and its metabolites atRAL and atRA directly interdict lipid radicals in ferroptosis since these compounds displayed radical trapping properties in a cell-free assay. Vitamin A, therefore, complements other anti-ferroptotic vitamins, E and K; metabolites of vitamin A, or agents that alter their levels, may be potential therapeutics for diseases where ferroptosis is implicated.
MeSH term(s)	Animals ; Vitamin A/pharmacology ; Ferroptosis ; Lipid Peroxidation/physiology ; Tretinoin/pharmacology ; Vitamins ; Retinaldehyde ; Lipids
Chemical Substances	Vitamin A (11103-57-4) ; Tretinoin (5688UTC01R) ; Vitamins ; Retinaldehyde (RR725D715M) ; Lipids
Language	English
Publishing date	2023-05-24
Publishing country	France
Document type	Journal Article
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2023.114930
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Article ; Online: Iron and Ferroptosis as Therapeutic Targets in Alzheimer's Disease.

Gleason, Andrew / Bush, Ashley I

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics

2020 Volume 18, Issue 1, Page(s) 252–264

Abstract: Alzheimer's disease (AD), one of the most common neurodegenerative diseases worldwide, has a devastating personal, familial, and societal impact. In spite of profound investment and effort, numerous clinical trials targeting amyloid-β, which is thought ... ...

Abstract	Alzheimer's disease (AD), one of the most common neurodegenerative diseases worldwide, has a devastating personal, familial, and societal impact. In spite of profound investment and effort, numerous clinical trials targeting amyloid-β, which is thought to have a causative role in the disease, have not yielded any clinically meaningful success to date. Iron is an essential cofactor in many physiological processes in the brain. An extensive body of work links iron dyshomeostasis with multiple aspects of the pathophysiology of AD. In particular, regional iron load appears to be a risk factor for more rapid cognitive decline. Existing iron-chelating agents have been in use for decades for other indications, and there are preliminary data that some of these could be effective in AD. Many novel iron-chelating compounds are under development, some with in vivo data showing potential Alzheimer's disease-modifying properties. This heretofore underexplored therapeutic class has considerable promise and could yield much-needed agents that slow neurodegeneration in AD.
MeSH term(s)	Alzheimer Disease/drug therapy ; Alzheimer Disease/metabolism ; Brain/metabolism ; Ferroptosis/physiology ; Humans ; Iron/metabolism ; Iron Chelating Agents/therapeutic use
Chemical Substances	Iron Chelating Agents ; Iron (E1UOL152H7)
Language	English
Publishing date	2020-10-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2316693-9
ISSN	1878-7479 ; 1933-7213
ISSN (online)	1878-7479
ISSN	1933-7213
DOI	10.1007/s13311-020-00954-y
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Article ; Online: β-amyloid: The known unknowns.

Ayton, Scott / Bush, Ashley I

Ageing research reviews

2020 Volume 65, Page(s) 101212

Abstract: Alzheimer's disease (AD) stands out as a major disease without any form of preventative or disease modifying therapy. This is not for lack of trying. 33 phase 3 clinical trials of drugs targeting amyloid beta (Aβ) have failed to slow cognitive decline in ...

Abstract	Alzheimer's disease (AD) stands out as a major disease without any form of preventative or disease modifying therapy. This is not for lack of trying. 33 phase 3 clinical trials of drugs targeting amyloid beta (Aβ) have failed to slow cognitive decline in AD. The field is at a cross-roads about whether to continue anti-Aβ therapy or more actively pursue alternative targets. With the burden of this disease to patients, families, and healthcare budgets growing yearly, the need for disease modifying AD therapies has become one of the highest priorities in all of medicine. While pathology, genetic and biochemical data offer a popular narrative for the causative role of Aβ, there are alternative explanations, and dissenting findings that, now more than ever, warrant thorough reanalysis. This review questions the major assumptions about Aβ on which therapies for AD were premised, and invites renewed interrogation into AD pathogenesis.
MeSH term(s)	Alzheimer Disease/drug therapy ; Amyloid beta-Peptides ; Cognitive Dysfunction ; Humans
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2020-11-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2075672-0
ISSN	1872-9649 ; 1568-1637
ISSN (online)	1872-9649
ISSN	1568-1637
DOI	10.1016/j.arr.2020.101212
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Article ; Online: Bioactive poly(2-oxazoline)-based nanomaterials bearing arylalkylamine and benzamide motifs possess intrinsic radical trapping and anti-ferroptosis properties.

Morrow, Joshua P / Pizzi, David / Mazrad, Zihnil A I / Bush, Ashley I / Kempe, Kristian

Biomaterials science

2023 Volume 11, Issue 9, Page(s) 3159–3171

Abstract: Radical trapping agents such as Ferrostatin-1 (Fer-1) are capable of rescuing cells from ferroptosis, an iron-dependent form of cell death. Previously, poly(2-oxazoline)-Fer-1 (POx-Fer-1) conjugates were reported, which possess increased water-solubility ...

Abstract	Radical trapping agents such as Ferrostatin-1 (Fer-1) are capable of rescuing cells from ferroptosis, an iron-dependent form of cell death. Previously, poly(2-oxazoline)-Fer-1 (POx-Fer-1) conjugates were reported, which possess increased water-solubility and remain active after covalent conjugation of Fer-1. In this study, we break down the structural and functional layers of POx-Fer-1 conjugates and reveal that drug-free POx containing arylalkylamine and benzamide motifs show anti-ferroptosis properties. Intriguingly, even the basic construct poly(2-methyl-2-oxazoline-grad-2-phenyl-2-oxazoline) P(MeOx-grad-PhOx) was found to be active. Therefore, P(MeOx-grad-PhOx) of varying compositions were prepared, characterized by
MeSH term(s)	Ferroptosis ; Oxazoles/pharmacology ; Oxazoles/chemistry ; Lipid Peroxidation ; Cell Death
Chemical Substances	poly(2-oxazoline) ; Oxazoles
Language	English
Publishing date	2023-05-02
Publishing country	England
Document type	Journal Article
ZDB-ID	2693928-9
ISSN	2047-4849 ; 2047-4830
ISSN (online)	2047-4849
ISSN	2047-4830
DOI	10.1039/d2bm02087d
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