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Article ; Online: The neuronal nucleus: a new battlefield in fight against neurodegeneration.

Eftekharpour, Eftekhar

Aging

2023 Volume 15, Issue 4, Page(s) 898–904

Abstract: Aging is an inevitable fact of life which brings along a series of age-associated diseases. Although medical innovations and patient care improvement have increased our life expectancy, the rate of age-associated diseases have also increased. Nervous ... ...

Abstract	Aging is an inevitable fact of life which brings along a series of age-associated diseases. Although medical innovations and patient care improvement have increased our life expectancy, the rate of age-associated diseases have also increased. Nervous system is specifically prone to these diseases that cause neuronal loss in different anatomical regions. Alzheimer's disease is the best-known example of age-associated illnesses and is diagnosed by accumulation of intracellular Neurofibrillary tangles and extracellular Amyloid Plaques resulting in dementia. However, therapeutic attempts aiming at the removal of these plaques and tangles to reverse the cognitive decline have generally failed in human patients and may compromise the patient's health. We have learnt that interruption of neuronal housekeeping systems such as autophagy contributes to formation of these aggregates, and therefore understanding the underlying mechanisms that lead to failure of these endogenous protective systems may provide valuable information and novel therapies. The house keeping systems are delicately regulated through gene expression and chromatin modifications in the nucleus, however, the contribution of this largest cellular organelle in pathophysiology of the disease has been overlooked. During the last few years, a wealth of information on neuronal nucleus has emerged that provides a strong rationale for examining its contribution to the pathophysiology of the disease. In this research perspective, I have attempted to summarize the latest research on neuronal nucleus, with a special focus on nuclear lamina damage and its downstream events to rationalize the need for focusing on the neuronal nucleus as a therapeutic target.
MeSH term(s)	Humans ; Alzheimer Disease/metabolism ; Neurofibrillary Tangles/metabolism ; Aging ; Nuclear Lamina/metabolism ; Neurons/metabolism ; Amyloid beta-Peptides/metabolism
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2023-02-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.204519
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Insights into the Multifaceted Roles of Thioredoxin-1 System: Exploring Knockout Murine Models.

Shcholok, Tetiana / Eftekharpour, Eftekhar

Biology

2024 Volume 13, Issue 3

Abstract: Redox balance is increasingly identified as a major player in cellular signaling. A fundamentally simple reaction of oxidation and reduction of cysteine residues in cellular proteins is the central concept in this complex regulatory mode of protein ... ...

Abstract	Redox balance is increasingly identified as a major player in cellular signaling. A fundamentally simple reaction of oxidation and reduction of cysteine residues in cellular proteins is the central concept in this complex regulatory mode of protein function. Oxidation of key cysteine residues occurs at the physiological levels of reactive oxygen species (ROS), but they are reduced by a supply of thiol antioxidant molecules including glutathione, glutaredoxin, and thioredoxin. While these molecules show complex compensatory roles in experimental conditions, transgenic animal models provide a comprehensive picture to pinpoint the role of each antioxidant. In this review, we have specifically focused on the available literature on thioredoxin-1 system transgenic models that include thioredoxin and thioredoxin reductase proteins. As the identification of thioredoxin protein targets is technically challenging, the true contribution of this system in maintaining cellular balance remains unidentified, including the role of this system in the brain.
Language	English
Publishing date	2024-03-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology13030180
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Article: Tau; One Protein, So Many Diseases.

Tabeshmehr, Parisa / Eftekharpour, Eftekhar

Biology

2023 Volume 12, Issue 2

Abstract: Tau, a member of the microtubule-associated proteins, is a known component of the neuronal cytoskeleton; however, in the brain tissue, it is involved in other vital functions beyond maintaining the cellular architecture. The pathologic tau forms ... ...

Abstract	Tau, a member of the microtubule-associated proteins, is a known component of the neuronal cytoskeleton; however, in the brain tissue, it is involved in other vital functions beyond maintaining the cellular architecture. The pathologic tau forms aggregates inside the neurons and ultimately forms the neurofibrillary tangles. Intracellular and extracellular accumulation of different tau isoforms, including dimers, oligomers, paired helical filaments and tangles, lead to a highly heterogenous group of diseases named "Tauopathies". About twenty-six different types of tauopathy diseases have been identified that have different clinical phenotypes or pathophysiological characteristics. Although all these diseases are identified by tau aggregation, they are distinguishable based on the specific tau isoforms, the affected cell types and the brain regions. The neuropathological and phenotypical heterogeneity of these diseases impose significant challenges for discovering new diagnostic and therapeutic strategies. Here, we review the recent literature on tau protein and the pathophysiological mechanisms of tauopathies. This article mainly focuses on physiologic and pathologic tau and aims to summarize the upstream and downstream events and discuss the current diagnostic approaches and therapeutic strategies.
Language	English
Publishing date	2023-02-03
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology12020244
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Article: Reevaluating the cause of laminopathy in Alzheimer's disease.

Islam, Md Imamul / Eftekharpour, Eftekhar

Neural regeneration research

2023 Volume 18, Issue 10, Page(s) 2200–2201

Language	English
Publishing date	2023-04-14
Publishing country	India
Document type	Journal Article
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.367841
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Article ; Online: Tau; One Protein, So Many Diseases

Tabeshmehr, Parisa / Eftekharpour, Eftekhar

Biology (Basel). 2023 Feb. 03, v. 12, no. 2

2023

Abstract	Tau, a member of the microtubule-associated proteins, is a known component of the neuronal cytoskeleton; however, in the brain tissue, it is involved in other vital functions beyond maintaining the cellular architecture. The pathologic tau forms aggregates inside the neurons and ultimately forms the neurofibrillary tangles. Intracellular and extracellular accumulation of different tau isoforms, including dimers, oligomers, paired helical filaments and tangles, lead to a highly heterogenous group of diseases named “Tauopathies”. About twenty-six different types of tauopathy diseases have been identified that have different clinical phenotypes or pathophysiological characteristics. Although all these diseases are identified by tau aggregation, they are distinguishable based on the specific tau isoforms, the affected cell types and the brain regions. The neuropathological and phenotypical heterogeneity of these diseases impose significant challenges for discovering new diagnostic and therapeutic strategies. Here, we review the recent literature on tau protein and the pathophysiological mechanisms of tauopathies. This article mainly focuses on physiologic and pathologic tau and aims to summarize the upstream and downstream events and discuss the current diagnostic approaches and therapeutic strategies.
Keywords	brain ; cytoskeleton ; neurons ; therapeutics
Language	English
Dates of publication	2023-0203
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article ; Online
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology12020244
Database	NAL-Catalogue (AGRICOLA)

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Article: Cre-recombinase systems for induction of neuron-specific knockout models: a guide for biomedical researchers.

Shcholok, Tetiana / Eftekharpour, Eftekhar

Neural regeneration research

2022 Volume 18, Issue 2, Page(s) 273–279

Abstract: Gene deletion has been a valuable tool for unraveling the mysteries of molecular biology. Early approaches included gene trapping and gene targetting to disrupt or delete a gene randomly or at a specific location, respectively. Using these technologies ... ...

Abstract	Gene deletion has been a valuable tool for unraveling the mysteries of molecular biology. Early approaches included gene trapping and gene targetting to disrupt or delete a gene randomly or at a specific location, respectively. Using these technologies in mouse embryos led to the generation of mouse knockout models and many scientific discoveries. The efficacy and specificity of these approaches have significantly increased with the advent of new technology such as clustered regularly interspaced short palindromic repeats for targetted gene deletion. However, several limitations including unwanted off-target gene deletion have hindered their widespread use in the field. Cre-recombinase technology has provided additional capacity for cell-specific gene deletion. In this review, we provide a summary of currently available literature on the application of this system for targetted deletion of neuronal genes. This article has been constructed to provide some background information for the new trainees on the mechanism and to provide necessary information for the design, and application of the Cre-recombinase system through reviewing the most frequent promoters that are currently available for genetic manipulation of neurons. We additionally will provide a summary of the latest technological developments that can be used for targeting neurons. This may also serve as a general guide for the selection of appropriate models for biomedical research.
Language	English
Publishing date	2022-08-24
Publishing country	India
Document type	Journal Article ; Review
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.346541
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Oxidative Stress and Mitochondrial Dysfunction Associated with Peripheral Neuropathy in Type 1 Diabetes.

Eftekharpour, Eftekhar / Fernyhough, Paul

Antioxidants & redox signaling

2021 Volume 37, Issue 7-9, Page(s) 578–596

Abstract: Significance: ...

Abstract	Significance:
MeSH term(s)	Diabetes Mellitus, Type 1/metabolism ; Glucose/metabolism ; Humans ; Hydrogen Peroxide/metabolism ; Mitochondria/metabolism ; Oxidative Stress ; Peripheral Nervous System Diseases/etiology ; Peripheral Nervous System Diseases/metabolism ; Reactive Oxygen Species/metabolism ; Superoxides/metabolism
Chemical Substances	Reactive Oxygen Species ; Superoxides (11062-77-4) ; Hydrogen Peroxide (BBX060AN9V) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-12-07
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.2021.0152
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Zs.A 5488: Show issues

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Article: Environmental Stimulus on Stem Cell Behaviour.

Eftekharpour, Eftekhar / Buttigieg, Josef

Stem cells international

2018 Volume 2018, Page(s) 4910185

Language	English
Publishing date	2018-02-18
Publishing country	United States
Document type	Editorial
ZDB-ID	2573856-2
ISSN	1687-9678 ; 1687-966X
ISSN (online)	1687-9678
ISSN	1687-966X
DOI	10.1155/2018/4910185
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Article ; Online: Oxidative damage of lysosomes in regulated cell death systems: Pathophysiology and pharmacologic interventions.

Nagakannan, Pandian / Tabeshmehr, Parisa / Eftekharpour, Eftekhar

Free radical biology & medicine

2020 Volume 157, Page(s) 94–127

Abstract: Lysosomes are small specialized organelles containing a variety of different hydrolase enzymes that are responsible for degradation of all macromolecules, entering the cells through the endosomal system or originated from the internal sources. This ... ...

Abstract	Lysosomes are small specialized organelles containing a variety of different hydrolase enzymes that are responsible for degradation of all macromolecules, entering the cells through the endosomal system or originated from the internal sources. This allows for transport and recycling of nutrients and internalization of surface proteins for antigen presentation as well as maintaining cellular homeostasis. Lysosomes are also important storage compartments for metal ions and nutrients. The integrity of lysosomal membrane is central to maintaining their normal function, but like other cellular membranes, lysosomal membrane is subject to damage mediated by reactive oxygen species. This results in spillage of lysosomal enzymes into the cytoplasm, leading to proteolytic damage to cellular systems and organelles. Several forms of lysosomal dependent cell death have been identified in diseases. Examination of these events are important for finding treatment strategies relevant to cancer or neurodegenerative diseases as well as autoimmune deficiencies. In this review, we have examined the current literature on involvement of lysosomes in induction of programed cell death and have provided an extensive list of therapeutic approaches that can modulate cell death. Exploitation of these mechanisms can lead to novel therapies for cancer and neurodegenerative diseases.
MeSH term(s)	Apoptosis ; Cell Death ; Endosomes ; Lysosomes/metabolism ; Oxidative Stress
Language	English
Publishing date	2020-04-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2020.04.001
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Zs.A 2109: Show issues

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Article ; Online: Redox Protein Thioredoxin Mediates Neurite Outgrowth in Primary Cultured Mouse Cerebral Cortical Neurons.

Alejandra Llanes-Cuesta, M / Hoi, Vanessa / Ha, Ryan / Tan, Hua / Imamul Islam, Md / Eftekharpour, Eftekhar / Wang, Jun-Feng

Neuroscience

2023 Volume 537, Page(s) 165–173

Abstract: Thioredoxin system plays an important role in maintaining the cellular redox balance. Recent evidence suggests that thioredoxin (Trx) system may promote cell survival and neuroprotection. In this study, we explored the role of thioredoxin system in ... ...

Abstract	Thioredoxin system plays an important role in maintaining the cellular redox balance. Recent evidence suggests that thioredoxin (Trx) system may promote cell survival and neuroprotection. In this study, we explored the role of thioredoxin system in neuronal differentiation using a primary mouse cortical neuronal cell culture. First, Trx and Trx reductase (TrxR) protein levels were analyzed in cultured neurons from 1 to 32 days in vitro (DIV). The result showed that Trx and TrxR protein levels time-dependently increased in the neuron cell culture from 1 to 18 DIV. To establish the role of Trx in neuronal differentiation, Trx gene expression was knockdown in cultured neurons using Trx sgRNA CRISPR/Cas9 technology. Treatment with CRISPR/Cas9/Trx sgRNA decreased Trx protein levels and caused a reduction in dendritic outgrowth and branching of cultured neurons. Then, primary cortical neurons were treated with the Trx inhibitor PX12 to block Trx reducing activity. Treatment with PX12 also reduced dendritic outgrowth and branching. Furthermore, PX12 treatment reduced the ratio of phosphorylated cyclic AMP response element-binding protein (CREB)/total CREB protein levels. To investigate whether CREB phosphorylation is redox regulated, SH-SY5Y cells were treated with H
MeSH term(s)	Mice ; Humans ; Animals ; RNA, Guide, CRISPR-Cas Systems ; Cyclic AMP Response Element-Binding Protein/metabolism ; Hydrogen Peroxide/metabolism ; Neuroblastoma/metabolism ; Thioredoxins/metabolism ; Neurons/metabolism ; Oxidation-Reduction ; Neuronal Outgrowth
Chemical Substances	RNA, Guide, CRISPR-Cas Systems ; Cyclic AMP Response Element-Binding Protein ; Hydrogen Peroxide (BBX060AN9V) ; Thioredoxins (52500-60-4)
Language	English
Publishing date	2023-12-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	196739-3
ISSN	1873-7544 ; 0306-4522
ISSN (online)	1873-7544
ISSN	0306-4522
DOI	10.1016/j.neuroscience.2023.12.002
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 1215: Show issues

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ab Jg. 2022: Lesesaal (EG)

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