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Article: Postmortem Neocortical

Pivtoraiko, Violetta N / Racic, Tamara / Abrahamson, Eric E / Villemagne, Victor L / Handen, Benjamin L / Lott, Ira T / Head, Elizabeth / Ikonomovic, Milos D

Frontiers in aging neuroscience

2021 Volume 13, Page(s) 728739

Abstract: Individuals with Down syndrome (DS) have a genetic predisposition for amyloid-β (Aβ) overproduction and earlier onset of Aβ deposits compared to patients with sporadic late-onset Alzheimer's disease (AD). Positron emission tomography (PET) with ... ...

Abstract	Individuals with Down syndrome (DS) have a genetic predisposition for amyloid-β (Aβ) overproduction and earlier onset of Aβ deposits compared to patients with sporadic late-onset Alzheimer's disease (AD). Positron emission tomography (PET) with Pittsburgh Compound-B (PiB) detects fibrillar Aβ pathology in living people with DS and AD, but its relationship with heterogeneous Aβ forms aggregated within amyloid deposits is not well understood. We performed quantitative
Language	English
Publishing date	2021-08-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2021.728739
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Thesis ; Online: Regulation of neuronal death by the autophagy lysosomal pathway

Pivtoraiko, Violetta N.

Implications for Parkinson disease

2011

Abstract: Parkinson Disease (PD) is the second most common age-related neurodegenerative disorder and is characterized pathologically by the loss of dopaminergic (DA) neurons in the stubstantia nigra pars compacta (SNpc). Mitochondrial dysfunction, increased ... ...

Abstract	Parkinson Disease (PD) is the second most common age-related neurodegenerative disorder and is characterized pathologically by the loss of dopaminergic (DA) neurons in the stubstantia nigra pars compacta (SNpc). Mitochondrial dysfunction, increased oxidative stress, and accumulation of aggregated α-synuclein (α-syn), an intracellular protein involved in synaptic function, are all pathological hallmarks of PD have been implicated in PD pathogenesis. However, it is debated whether α-syn aggregates themselves are responsible for neurodegeneration in PD, cellular pathways involved in degradation of α-syn aggregates are believed to promote neuron survival. The autophagy lysosomal pathway (ALP), a physiological mechanism for recycling of intracellular components, has been shown to clear α-syn, its aggregates, and regulate neuron survival in PD. The first part of this dissertation reviews the developments regarding the contribution of the ALP to neuron survival and death regulation. It discusses the effects of oxidative stress on ALP function and vice versa. The role of the lysosome, a cellular organelle responsible for digestion of intracellular constituents delivered via ALP, in regulation of neuron survival is highlighted. Increased oxidative stress and α-syn aggregate accumulation has been reported in PD models of mitochondrial dysfunction such as that induced by the insecticide rotenone. Another part of this dissertation focused on rotenone's effects on ALP function. Rotenone-induced inhibition of lysosomal function has been observed. Our findings suggested that lysosomal dysfunction may be responsible for α-syn accumulation and neuron death observed in PD, implying that mechanisms improving lysosomal function may be cytoprotective. This hypothesis was tested in the second chapter of this dissertation using a chloroquine (CQ) model of lysosome dysfunction. CQ, a known antimalarial agent, induced α-syn accumulation and neuron death by inhibiting ALP function. Bafilomycin A1, a plecomacrolide antibiotic, attenuated CQ-induced neuron death, an effect accompanied by restoration of lysosomal function. These studies expand our knowledge of the potential role of the ALP in PD pathogenesis and suggest that further studies are needed to both decipher the neuroprotective role of the ALP in preventing neuron death in response to PD-associated stimuli, such as rotenone, and to identify novel ALP-related molecular targets for PD therapy.
Keywords	Neurosciences\|Cellular biology\|Pathology
Subject code	572
Language	ENG
Publishing date	2011-01-01 00:00:01.0
Publisher	The University of Alabama at Birmingham
Publishing country	us
Document type	Thesis ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Oxidative stress and autophagy in the regulation of lysosome-dependent neuron death.

Pivtoraiko, Violetta N / Stone, Sara L / Roth, Kevin A / Shacka, John J

Antioxidants & redox signaling

2008 Volume 11, Issue 3, Page(s) 481–496

Abstract: Lysosomes critically regulate the pH-dependent catabolism of extracellular and intracellular macromolecules delivered from the endocytic/heterophagy and autophagy pathways, respectively. The importance of lysosomes to cell survival is underscored not ... ...

Abstract	Lysosomes critically regulate the pH-dependent catabolism of extracellular and intracellular macromolecules delivered from the endocytic/heterophagy and autophagy pathways, respectively. The importance of lysosomes to cell survival is underscored not only by their unique ability effectively to degrade metalloproteins and oxidatively damaged macromolecules, but also by the distinct potential for induction of both caspase-dependent and -independent cell death with a compromise in the integrity of lysosome function. Oxidative stress and free radical damage play a principal role in cell death induced by lysosome dysfunction and may be linked to several upstream and downstream stimuli, including alterations in the autophagy degradation pathway, inhibition of lysosome enzyme function, and lysosome membrane damage. Neurons are sensitive to lysosome dysfunction, and the contribution of oxidative stress and free radical damage to lysosome dysfunction may contribute to the etiology of neurodegenerative disease. This review provides a broad overview of lysosome function and explores the contribution of oxidative stress and autophagy to lysosome dysfunction-induced neuron death. Putative signaling pathways that either induce lysosome dysfunction or result from lysosome dysfunction or both, and the role of oxidative stress, free radical damage, and lysosome dysfunction in pediatric lysosomal storage disorders (neuronal ceroid lipofuscinoses or NCL/Batten disease) and in Alzheimer's disease are emphasized.
MeSH term(s)	Alzheimer Disease/metabolism ; Autophagy ; Cell Death/physiology ; Humans ; Lysosomes/physiology ; Neurons/cytology ; Oxidative Stress ; Reactive Oxygen Species/metabolism
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2008-08-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ARS.2008.2263
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Article ; Online: Cortical pyroglutamate amyloid-β levels and cognitive decline in Alzheimer's disease.

Pivtoraiko, Violetta N / Abrahamson, Eric E / Leurgans, Sue E / DeKosky, Steven T / Mufson, Elliott J / Ikonomovic, Milos D

Neurobiology of aging

2014 Volume 36, Issue 1, Page(s) 12–19

Abstract: Posterior cingulate cortex (PCC) accumulates amyloid-β (Aβ) early in Alzheimer's disease (AD). The relative concentrations of full-length Aβ and truncated, pyroglutamate-modified Aβ (NpE3) forms, and their correlations to cognitive dysfunction in AD, are ...

Abstract	Posterior cingulate cortex (PCC) accumulates amyloid-β (Aβ) early in Alzheimer's disease (AD). The relative concentrations of full-length Aβ and truncated, pyroglutamate-modified Aβ (NpE3) forms, and their correlations to cognitive dysfunction in AD, are unknown. We quantified AβNpE3-42, AβNpE3-40, Aβ1-42, and Aβ1-40 concentrations in soluble (nonfibrillar) and insoluble (fibrillar) pools in PCC from subjects with an antemortem clinical diagnosis of no cognitive impairment, mild cognitive impairment, or mild-moderate AD. In clinical AD, increased PCC concentrations of Aβ were observed for all Aβ forms in the insoluble pool but only for Aβ1-42 in the soluble pool. Lower Mini-Mental State Exam and episodic memory scores correlated most strongly with higher concentrations of soluble and insoluble Aβ1-42. Greater neuropathology severity by Consortium to Establish a Registry for Alzheimer's Disease and National Institute on Aging-Reagan pathologic criteria was associated with higher concentrations of all measured Aβ forms, except soluble AβNpE3-40. Low concentrations of soluble pyroglutamate Aβ across clinical groups likely reflect its rapid sequestration into plaques, thus, the conversion to fibrillar Aβ may be a therapeutic target.
MeSH term(s)	Aged ; Aged, 80 and over ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/psychology ; Alzheimer Disease/therapy ; Amyloid beta-Peptides/metabolism ; Cognition ; Disease Progression ; Female ; Gyrus Cinguli/metabolism ; Humans ; Male ; Molecular Targeted Therapy ; Peptide Fragments/metabolism ; Pyrrolidonecarboxylic Acid/metabolism ; Solubility
Chemical Substances	Amyloid beta-Peptides ; Peptide Fragments ; amyloid beta-protein (1-42) ; Pyrrolidonecarboxylic Acid (SZB83O1W42)
Language	English
Publishing date	2014-06-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	604505-4
ISSN	1558-1497 ; 0197-4580
ISSN (online)	1558-1497
ISSN	0197-4580
DOI	10.1016/j.neurobiolaging.2014.06.021
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Article ; Online: Rotenone inhibits autophagic flux prior to inducing cell death.

Mader, Burton J / Pivtoraiko, Violetta N / Flippo, Hilary M / Klocke, Barbara J / Roth, Kevin A / Mangieri, Leandra R / Shacka, John J

ACS chemical neuroscience

2012 Volume 3, Issue 12, Page(s) 1063–1072

Abstract: Rotenone, which selectively inhibits mitochondrial complex I, induces oxidative stress, α-synuclein accumulation, and dopaminergic neuron death, principal pathological features of Parkinson's disease. The autophagy-lysosome pathway degrades damaged ... ...

Abstract	Rotenone, which selectively inhibits mitochondrial complex I, induces oxidative stress, α-synuclein accumulation, and dopaminergic neuron death, principal pathological features of Parkinson's disease. The autophagy-lysosome pathway degrades damaged proteins and organelles for the intracellular maintenance of nutrient and energy balance. While it is known that rotenone causes autophagic vacuole accumulation, the mechanism by which this effect occurs has not been thoroughly investigated. Treatment of differentiated SH-SY5Y cells with rotenone (10 μM) induced the accumulation of autophagic vacuoles at 6 h and 24 h as indicated by Western blot analysis for microtubule associated protein-light chain 3-II (MAP-LC3-II). Assessment of autophagic flux at these time points indicated that autophagic vacuole accumulation resulted from a decrease in their effective lysosomal degradation, which was substantiated by increased levels of autophagy substrates p62 and α-synuclein. Inhibition of lysosomal degradation may be explained by the observed decrease in cellular ATP levels, which in turn may have caused the observed concomitant increase in acidic vesicle pH. The early (6 h) effects of rotenone on cellular energetics and autophagy-lysosome pathway function preceded the induction of cell death and apoptosis. These findings indicate that the classical mitochondrial toxin rotenone has a pronounced effect on macroautophagy completion that may contribute to its neurotoxic potential.
MeSH term(s)	Autophagy/drug effects ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; Cell Death/drug effects ; Cell Line, Tumor ; Humans ; Lysosomal-Associated Membrane Protein 1/metabolism ; Lysosomes/drug effects ; Lysosomes/metabolism ; Lysosomes/pathology ; Neurons/drug effects ; Neurons/metabolism ; Neurons/pathology ; Rotenone/pharmacology ; Uncoupling Agents/pharmacology ; Vacuoles/drug effects ; Vacuoles/metabolism ; Vacuoles/pathology
Chemical Substances	Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Lysosomal-Associated Membrane Protein 1 ; TFEB protein, human ; Uncoupling Agents ; Rotenone (03L9OT429T)
Language	English
Publishing date	2012-09-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1948-7193
ISSN (online)	1948-7193
DOI	10.1021/cn300145z
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Article ; Online: Reactive oxygen species production by forward and reverse electron fluxes in the mitochondrial respiratory chain.

Selivanov, Vitaly A / Votyakova, Tatyana V / Pivtoraiko, Violetta N / Zeak, Jennifer / Sukhomlin, Tatiana / Trucco, Massimo / Roca, Josep / Cascante, Marta

PLoS computational biology

2011 Volume 7, Issue 3, Page(s) e1001115

Abstract: Reactive oxygen species (ROS) produced in the mitochondrial respiratory chain (RC) are primary signals that modulate cellular adaptation to environment, and are also destructive factors that damage cells under the conditions of hypoxia/reoxygenation ... ...

Abstract	Reactive oxygen species (ROS) produced in the mitochondrial respiratory chain (RC) are primary signals that modulate cellular adaptation to environment, and are also destructive factors that damage cells under the conditions of hypoxia/reoxygenation relevant for various systemic diseases or transplantation. The important role of ROS in cell survival requires detailed investigation of mechanism and determinants of ROS production. To perform such an investigation we extended our rule-based model of complex III in order to account for electron transport in the whole RC coupled to proton translocation, transmembrane electrochemical potential generation, TCA cycle reactions, and substrate transport to mitochondria. It fits respiratory electron fluxes measured in rat brain mitochondria fueled by succinate or pyruvate and malate, and the dynamics of NAD(+) reduction by reverse electron transport from succinate through complex I. The fitting of measured characteristics gave an insight into the mechanism of underlying processes governing the formation of free radicals that can transfer an unpaired electron to oxygen-producing superoxide and thus can initiate the generation of ROS. Our analysis revealed an association of ROS production with levels of specific radicals of individual electron transporters and their combinations in species of complexes I and III. It was found that the phenomenon of bistability, revealed previously as a property of complex III, remains valid for the whole RC. The conditions for switching to a state with a high content of free radicals in complex III were predicted based on theoretical analysis and were confirmed experimentally. These findings provide a new insight into the mechanisms of ROS production in RC.
MeSH term(s)	ATP Synthetase Complexes/chemistry ; Algorithms ; Animals ; Brain/metabolism ; Citric Acid Cycle ; Computational Biology/methods ; Computer Simulation ; Electron Transport ; Electrons ; Membrane Potential, Mitochondrial ; Mitochondria/metabolism ; Rats ; Rats, Wistar ; Reactive Oxygen Species ; Spectrometry, Fluorescence/methods
Chemical Substances	Reactive Oxygen Species ; ATP Synthetase Complexes (EC 2.7.4.-)
Language	English
Publishing date	2011-03-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2193340-6
ISSN	1553-7358 ; 1553-734X
ISSN (online)	1553-7358
ISSN	1553-734X
DOI	10.1371/journal.pcbi.1001115
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Article ; Online: Low-dose bafilomycin attenuates neuronal cell death associated with autophagy-lysosome pathway dysfunction.

Pivtoraiko, Violetta N / Harrington, Adam J / Mader, Burton J / Luker, Austin M / Caldwell, Guy A / Caldwell, Kim A / Roth, Kevin A / Shacka, John J

Journal of neurochemistry

2010 Volume 114, Issue 4, Page(s) 1193–1204

Abstract: We have shown previously that the plecomacrolide antibiotics bafilomycin A1 and B1 significantly attenuate cerebellar granule neuron death resulting from agents that disrupt lysosome function. To further characterize bafilomycin-mediated cytoprotection, ... ...

Abstract	We have shown previously that the plecomacrolide antibiotics bafilomycin A1 and B1 significantly attenuate cerebellar granule neuron death resulting from agents that disrupt lysosome function. To further characterize bafilomycin-mediated cytoprotection, we examined its ability to attenuate the death of naïve and differentiated neuronal SH-SY5Y human neuroblastoma cells from agents that induce lysosome dysfunction in vitro, and from in vivo dopaminergic neuron death in C. elegans. Low-dose bafilomycin significantly attenuated SH-SY5Y cell death resulting from treatment with chloroquine, hydroxychloroquine amodiaquine and staurosporine. Bafilomycin also attenuated the chloroquine-induced reduction in processing of cathepsin D, the principal lysosomal aspartic acid protease, to its mature 'active' form. Chloroquine induced autophagic vacuole accumulation and inhibited autophagic flux, effects that were attenuated upon treatment with bafilomycin and were associated with a significant decrease in chloroquine-induced accumulation of detergent-insoluble alpha-synuclein oligomers. In addition, bafilomycin significantly and dose-dependently attenuated dopaminergic neuron death in C. elegans resulting from in vivo over-expression of human wild-type alpha-synuclein. Together, our findings suggest that low-dose bafilomycin is cytoprotective in part through its maintenance of the autophagy-lysosome pathway, and underscores its therapeutic potential for treating Parkinson's disease and other neurodegenerative diseases that exhibit disruption of protein degradation pathways and accumulation of toxic protein species.
MeSH term(s)	Animals ; Autophagy/drug effects ; Autophagy/physiology ; Caenorhabditis elegans/drug effects ; Cell Line, Tumor ; Cytoprotection/drug effects ; Cytoprotection/physiology ; Disease Progression ; Humans ; Lysosomes/drug effects ; Lysosomes/physiology ; Macrolides/pharmacology ; Nerve Degeneration/drug therapy ; Nerve Degeneration/metabolism ; Nerve Degeneration/pathology ; Neurons/drug effects ; Neurons/metabolism ; Signal Transduction/drug effects
Chemical Substances	Macrolides ; bafilomycin A (116764-51-3)
Language	English
Publishing date	2010-06-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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/j.1471-4159.2010.06838.x
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Article: Low-dose bafilomycin attenuates neuronal cell death associated with autophagy-lysosome pathway dysfunction

Pivtoraiko, Violetta N / Harrington, Adam J / Mader, Burton J / Luker, Austin M / Caldwell, Guy A / Caldwell, Kim A / Roth, Kevin A / Shacka, John J

Journal of neurochemistry. 2010 Aug., v. 114, no. 4

2010

Abstract: J. Neurochem. (2010) 114, 1193-1204. We have shown previously that the plecomacrolide antibiotics bafilomycin A1 and B1 significantly attenuate cerebellar granule neuron death resulting from agents that disrupt lysosome function. To further characterize ... ...

Abstract	J. Neurochem. (2010) 114, 1193-1204. We have shown previously that the plecomacrolide antibiotics bafilomycin A1 and B1 significantly attenuate cerebellar granule neuron death resulting from agents that disrupt lysosome function. To further characterize bafilomycin-mediated cytoprotection, we examined its ability to attenuate the death of naïve and differentiated neuronal SH-SY5Y human neuroblastoma cells from agents that induce lysosome dysfunction in vitro, and from in vivo dopaminergic neuron death in C. elegans. Low-dose bafilomycin significantly attenuated SH-SY5Y cell death resulting from treatment with chloroquine, hydroxychloroquine amodiaquine and staurosporine. Bafilomycin also attenuated the chloroquine-induced reduction in processing of cathepsin D, the principal lysosomal aspartic acid protease, to its mature 'active' form. Chloroquine induced autophagic vacuole accumulation and inhibited autophagic flux, effects that were attenuated upon treatment with bafilomycin and were associated with a significant decrease in chloroquine-induced accumulation of detergent-insoluble α-synuclein oligomers. In addition, bafilomycin significantly and dose-dependently attenuated dopaminergic neuron death in C. elegans resulting from in vivo over-expression of human wild-type α-synuclein. Together, our findings suggest that low-dose bafilomycin is cytoprotective in part through its maintenance of the autophagy-lysosome pathway, and underscores its therapeutic potential for treating Parkinson's disease and other neurodegenerative diseases that exhibit disruption of protein degradation pathways and accumulation of toxic protein species.
Keywords	Parkinson disease ; cathepsin D
Language	English
Dates of publication	2010-08
Size	p. 1193-1204.
Publisher	Blackwell Publishing Ltd
Publishing place	Oxford, UK
Document type	Article
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/j.1471-4159.2010.06838.x
Database	NAL-Catalogue (AGRICOLA)

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Article: Postmortem Neocortical

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Thesis ; Online: Regulation of neuronal death by the autophagy lysosomal pathway

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Article ; Online: Oxidative stress and autophagy in the regulation of lysosome-dependent neuron death.

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Article ; Online: Cortical pyroglutamate amyloid-β levels and cognitive decline in Alzheimer's disease.

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Article ; Online: Rotenone inhibits autophagic flux prior to inducing cell death.

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Article ; Online: Reactive oxygen species production by forward and reverse electron fluxes in the mitochondrial respiratory chain.

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Article ; Online: Low-dose bafilomycin attenuates neuronal cell death associated with autophagy-lysosome pathway dysfunction.

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Article: Low-dose bafilomycin attenuates neuronal cell death associated with autophagy-lysosome pathway dysfunction

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