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1
ALS-associated TDP-43 induces endoplasmic reticulum stress, which drives cytoplasmic TDP-43 accumulation and stress granule formation
ALS-associated TDP-43 induces endoplasmic reticulum stress, which drives cytoplasmic TDP-43 accumulation and stress granule formation
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ALS-associated TDP-43 induces endoplasmic reticulum stress, which drives cytoplasmic TDP-43 accumulation and stress granule formation

PloS one, 2013-11, Vol.8 (11), p.e81170-e81170 [Peer Reviewed Journal]

COPYRIGHT 2013 Public Library of Science ;2013 Walker et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/3.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2013 Walker et al 2013 Walker et al ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0081170 ;PMID: 24312274

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2
Copper delivery to the CNS by CuATSM effectively treats motor neuron disease in SODG93A mice co-expressing the Copper-Chaperone-for-SOD
Copper delivery to the CNS by CuATSM effectively treats motor neuron disease in SODG93A mice co-expressing the Copper-Chaperone-for-SOD
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Copper delivery to the CNS by CuATSM effectively treats motor neuron disease in SODG93A mice co-expressing the Copper-Chaperone-for-SOD

Neurobiology of disease, 2016-05, Vol.89, p.1-9 [Peer Reviewed Journal]

EISSN: 1095-953X ;DOI: 10.1016/j.nbd.2016.01.020

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3
CuII(atsm) improves the neurological phenotype and survival of SOD1G93A mice and selectively increases enzymatically active SOD1 in the spinal cord
CuII(atsm) improves the neurological phenotype and survival of SOD1G93A mice and selectively increases enzymatically active SOD1 in the spinal cord
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CuII(atsm) improves the neurological phenotype and survival of SOD1G93A mice and selectively increases enzymatically active SOD1 in the spinal cord

Scientific reports, 2017-02, Vol.7 (1), p.42292-42292, Article 42292 [Peer Reviewed Journal]

Copyright Nature Publishing Group Feb 2017 ;Copyright © 2017, The Author(s) 2017 The Author(s) ;ISSN: 2045-2322 ;EISSN: 2045-2322 ;DOI: 10.1038/srep42292 ;PMID: 28205575

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4
Regular Physical Exercise Modulates Iron Homeostasis in the 5xFAD Mouse Model of Alzheimer’s Disease
Regular Physical Exercise Modulates Iron Homeostasis in the 5xFAD Mouse Model of Alzheimer’s Disease
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Regular Physical Exercise Modulates Iron Homeostasis in the 5xFAD Mouse Model of Alzheimer’s Disease

International journal of molecular sciences, 2021-08, Vol.22 (16), p.8715 [Peer Reviewed Journal]

2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2021 by the authors. 2021 ;ISSN: 1422-0067 ;ISSN: 1661-6596 ;EISSN: 1422-0067 ;DOI: 10.3390/ijms22168715 ;PMID: 34445419

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5
Metal ionophore treatment restores dendritic spine density and synaptic protein levels in a mouse model of Alzheimer's disease
Metal ionophore treatment restores dendritic spine density and synaptic protein levels in a mouse model of Alzheimer's disease
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Metal ionophore treatment restores dendritic spine density and synaptic protein levels in a mouse model of Alzheimer's disease

PloS one, 2011-03, Vol.6 (3), p.e17669 [Peer Reviewed Journal]

COPYRIGHT 2011 Public Library of Science ;COPYRIGHT 2011 Public Library of Science ;2011 Adlard et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;Adlard et al. 2011 ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0017669 ;PMID: 21412423

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6
Copper-ATSM as a Treatment for ALS: Support from Mutant SOD1 Models and Beyond
Copper-ATSM as a Treatment for ALS: Support from Mutant SOD1 Models and Beyond
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Copper-ATSM as a Treatment for ALS: Support from Mutant SOD1 Models and Beyond

Life (Basel, Switzerland), 2020-11, Vol.10 (11), p.271 [Peer Reviewed Journal]

2020 by the authors. 2020 ;ISSN: 2075-1729 ;EISSN: 2075-1729 ;DOI: 10.3390/life10110271 ;PMID: 33158182

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7
Diacetylbis(N(4)-methylthiosemicarbazonato) Copper(II) (CuII(atsm)) Protects against Peroxynitrite-induced Nitrosative Damage and Prolongs Survival in Amyotrophic Lateral Sclerosis Mouse Model
Diacetylbis(N(4)-methylthiosemicarbazonato) Copper(II) (CuII(atsm)) Protects against Peroxynitrite-induced Nitrosative Damage and Prolongs Survival in Amyotrophic Lateral Sclerosis Mouse Model
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Diacetylbis(N(4)-methylthiosemicarbazonato) Copper(II) (CuII(atsm)) Protects against Peroxynitrite-induced Nitrosative Damage and Prolongs Survival in Amyotrophic Lateral Sclerosis Mouse Model

The Journal of biological chemistry, 2011-12, Vol.286 (51), p.44035-44044 [Peer Reviewed Journal]

2011 © 2011 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology. ;2011 by The American Society for Biochemistry and Molecular Biology, Inc. 2011 ;ISSN: 0021-9258 ;EISSN: 1083-351X ;DOI: 10.1074/jbc.M111.274407 ;PMID: 22033929

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8
Iron accumulation in skeletal muscles of old mice is associated with impaired regeneration after ischaemia–reperfusion damage
Iron accumulation in skeletal muscles of old mice is associated with impaired regeneration after ischaemia–reperfusion damage
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Iron accumulation in skeletal muscles of old mice is associated with impaired regeneration after ischaemia–reperfusion damage

Journal of cachexia, sarcopenia and muscle, 2021-04, Vol.12 (2), p.476-492 [Peer Reviewed Journal]

2021 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders ;2021 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders. ;2021. This work is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;ISSN: 2190-5991 ;EISSN: 2190-6009 ;DOI: 10.1002/jcsm.12685 ;PMID: 33665974

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9
Proteome-wide systems genetics identifies UFMylation as a regulator of skeletal muscle function
Proteome-wide systems genetics identifies UFMylation as a regulator of skeletal muscle function
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Proteome-wide systems genetics identifies UFMylation as a regulator of skeletal muscle function

eLife, 2022-12, Vol.11 [Peer Reviewed Journal]

2022, Molendijk et al. ;2022, Molendijk et al. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2022, Molendijk et al 2022 Molendijk et al ;ISSN: 2050-084X ;EISSN: 2050-084X ;DOI: 10.7554/ELIFE.82951 ;PMID: 36472367

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10
Microglial ferroptotic stress causes non-cell autonomous neuronal death
Microglial ferroptotic stress causes non-cell autonomous neuronal death
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Microglial ferroptotic stress causes non-cell autonomous neuronal death

Molecular neurodegeneration, 2024-02, Vol.19 (1), p.14-14, Article 14 [Peer Reviewed Journal]

2024. The Author(s). ;COPYRIGHT 2024 BioMed Central Ltd. ;2024. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2024 ;ISSN: 1750-1326 ;EISSN: 1750-1326 ;DOI: 10.1186/s13024-023-00691-8 ;PMID: 38317225

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11
Neuroprotective copper bis(thiosemicarbazonato) complexes promote neurite elongation
Neuroprotective copper bis(thiosemicarbazonato) complexes promote neurite elongation
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Neuroprotective copper bis(thiosemicarbazonato) complexes promote neurite elongation

PloS one, 2014-02, Vol.9 (2), p.e90070-e90070 [Peer Reviewed Journal]

COPYRIGHT 2014 Public Library of Science ;COPYRIGHT 2014 Public Library of Science ;2014 Bica et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2014 Bica et al 2014 Bica et al ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0090070 ;PMID: 24587210

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12
ZnII(atsm) is protective in amyotrophic lateral sclerosis model mice via a copper delivery mechanism
ZnII(atsm) is protective in amyotrophic lateral sclerosis model mice via a copper delivery mechanism
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ZnII(atsm) is protective in amyotrophic lateral sclerosis model mice via a copper delivery mechanism

Neurobiology of disease, 2015-09, Vol.81, p.20-24 [Peer Reviewed Journal]

EISSN: 1095-953X ;DOI: 10.1016/j.nbd.2015.02.023

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13
Inhibition of TDP-43 accumulation by bis(thiosemicarbazonato)-copper complexes
Inhibition of TDP-43 accumulation by bis(thiosemicarbazonato)-copper complexes
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Inhibition of TDP-43 accumulation by bis(thiosemicarbazonato)-copper complexes

PloS one, 2012-08, Vol.7 (8), p.e42277 [Peer Reviewed Journal]

COPYRIGHT 2012 Public Library of Science ;Parker et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2012 Parker et al 2012 Parker et al ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0042277 ;PMID: 22879928

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14
Lithium administered to pregnant, lactating and neonatal rats: entry into developing brain
Lithium administered to pregnant, lactating and neonatal rats: entry into developing brain
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Lithium administered to pregnant, lactating and neonatal rats: entry into developing brain

Fluids and barriers of the CNS, 2021-12, Vol.18 (1), p.57-57, Article 57 [Peer Reviewed Journal]

2021. The Author(s). ;COPYRIGHT 2021 BioMed Central Ltd. ;2021. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2021 ;ISSN: 2045-8118 ;EISSN: 2045-8118 ;DOI: 10.1186/s12987-021-00285-w ;PMID: 34876168

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15
C-Jun N-terminal kinase controls TDP-43 accumulation in stress granules induced by oxidative stress
C-Jun N-terminal kinase controls TDP-43 accumulation in stress granules induced by oxidative stress
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C-Jun N-terminal kinase controls TDP-43 accumulation in stress granules induced by oxidative stress

Molecular neurodegeneration, 2011-08, Vol.6 (1), p.57-57, Article 57 [Peer Reviewed Journal]

COPYRIGHT 2011 BioMed Central Ltd. ;Copyright ©2011 Meyerowitz et al; licensee BioMed Central Ltd. 2011 Meyerowitz et al; licensee BioMed Central Ltd. ;ISSN: 1750-1326 ;EISSN: 1750-1326 ;DOI: 10.1186/1750-1326-6-57 ;PMID: 21819629

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16
Iron overload and impaired iron handling contribute to the dystrophic pathology in models of Duchenne muscular dystrophy
Iron overload and impaired iron handling contribute to the dystrophic pathology in models of Duchenne muscular dystrophy
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Iron overload and impaired iron handling contribute to the dystrophic pathology in models of Duchenne muscular dystrophy

Journal of cachexia, sarcopenia and muscle, 2022-06, Vol.13 (3), p.1541-1553 [Peer Reviewed Journal]

2022 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders. ;2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;ISSN: 2190-5991 ;EISSN: 2190-6009 ;DOI: 10.1002/jcsm.12950 ;PMID: 35249268

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17
Effects of paracetamol (acetaminophen) on gene expression and permeability properties of the rat placenta and fetal brain [version 2; peer review: 2 approved]
Effects of paracetamol (acetaminophen) on gene expression and permeability properties of the rat placenta and fetal brain [version 2; peer review: 2 approved]
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Effects of paracetamol (acetaminophen) on gene expression and permeability properties of the rat placenta and fetal brain [version 2; peer review: 2 approved]

F1000 research, 2020, Vol.9, p.573 [Peer Reviewed Journal]

Copyright: © 2020 Koehn LM et al. ;Copyright: © 2020 Koehn LM et al. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;Copyright: © 2020 Koehn LM et al. 2020 ;ISSN: 2046-1402 ;EISSN: 2046-1402 ;DOI: 10.12688/f1000research.24119.2 ;PMID: 32934805

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18
Evidence for disrupted copper availability in human spinal cord supports CuII(atsm) as a treatment option for sporadic cases of ALS
Evidence for disrupted copper availability in human spinal cord supports CuII(atsm) as a treatment option for sporadic cases of ALS
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Evidence for disrupted copper availability in human spinal cord supports CuII(atsm) as a treatment option for sporadic cases of ALS

Scientific reports, 2024-03, Vol.14 (1), p.5929-5929 [Peer Reviewed Journal]

The Author(s) 2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2024 ;EISSN: 2045-2322 ;DOI: 10.1038/s41598-024-55832-w

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19
Increased zinc and manganese in parallel with neurodegeneration, synaptic protein changes and activation of Akt/GSK3 signaling in ovine CLN6 neuronal ceroid lipofuscinosis
Increased zinc and manganese in parallel with neurodegeneration, synaptic protein changes and activation of Akt/GSK3 signaling in ovine CLN6 neuronal ceroid lipofuscinosis
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Increased zinc and manganese in parallel with neurodegeneration, synaptic protein changes and activation of Akt/GSK3 signaling in ovine CLN6 neuronal ceroid lipofuscinosis

PloS one, 2013-03, Vol.8 (3), p.e58644-e58644 [Peer Reviewed Journal]

COPYRIGHT 2013 Public Library of Science ;COPYRIGHT 2013 Public Library of Science ;2013 Kanninen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2013 Kanninen et al 2013 Kanninen et al ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0058644 ;PMID: 23516525

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20
Deregulation of subcellular biometal homeostasis through loss of the metal transporter, Zip7, in a childhood neurodegenerative disorder
Deregulation of subcellular biometal homeostasis through loss of the metal transporter, Zip7, in a childhood neurodegenerative disorder
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Deregulation of subcellular biometal homeostasis through loss of the metal transporter, Zip7, in a childhood neurodegenerative disorder

Acta neuropathologica communications, 2014-02, Vol.2 (1), p.25-25, Article 25 [Peer Reviewed Journal]

COPYRIGHT 2014 BioMed Central Ltd. ;COPYRIGHT 2014 BioMed Central Ltd. ;Copyright © 2014 Grubman et al.; licensee BioMed Central Ltd. 2014 Grubman et al.; licensee BioMed Central Ltd. ;ISSN: 2051-5960 ;EISSN: 2051-5960 ;DOI: 10.1186/2051-5960-2-25 ;PMID: 24581221

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