Regulation of Keap1-Nrf2 axis in temporal lobe epilepsy—hippocampal sclerosis patients may limit the seizure outcomes

Madhamanchi, Kishore; Madhamanchi, Pradeep; Narne, Parimala; Jayalakshmi, Sita; Panigrahi, Manas; Patil, Anuja; Babu, Phanithi Prakash

doi:10.1007/s10072-023-06936-0

Cited by 7 publications

(7 citation statements)

References 56 publications

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“…NQO1 expression in the human epileptic brain may also be linked to the outcomes of epilepsy surgery. An investigation of the brain specimens from 26 patients who underwent surgery for medically refractory epilepsy revealed a significant reduction of NQO1 expression among patients who experienced aura after surgery (ILAE class 2), in comparison to seizure-free patients (ILAE class 1) [ 222 ]. Activation of this pathway has been suggested as a potential interventional approach to alleviating epilepsy and associated comorbidities [ 223 ].…”

Section: The Involvement Of Nqo1 In Neurological Disordersmentioning

confidence: 99%

Impact of NQO1 dysregulation in CNS disorders

Yuhan,

Khaleghi Ghadiri,

Gorji

2024

J Transl Med

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NAD(P)H Quinone Dehydrogenase 1 (NQO1) plays a pivotal role in the regulation of neuronal function and synaptic plasticity, cellular adaptation to oxidative stress, neuroinflammatory and degenerative processes, and tumorigenesis in the central nervous system (CNS). Impairment of the NQO1 activity in the CNS can result in abnormal neurotransmitter release and clearance, increased oxidative stress, and aggravated cellular injury/death. Furthermore, it can cause disturbances in neural circuit function and synaptic neurotransmission. The abnormalities of NQO1 enzyme activity have been linked to the pathophysiological mechanisms of multiple neurological disorders, including Parkinson's disease, Alzheimer's disease, epilepsy, multiple sclerosis, cerebrovascular disease, traumatic brain injury, and brain malignancy. NQO1 contributes to various dimensions of tumorigenesis and treatment response in various brain tumors. The precise mechanisms through which abnormalities in NQO1 function contribute to these neurological disorders continue to be a subject of ongoing research. Building upon the existing knowledge, the present study reviews current investigations describing the role of NQO1 dysregulations in various neurological disorders. This study emphasizes the potential of NQO1 as a biomarker in diagnostic and prognostic approaches, as well as its suitability as a target for drug development strategies in neurological disorders.

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Section: The Involvement Of Nqo1 In Neurological Disordersmentioning

confidence: 99%

Impact of NQO1 dysregulation in CNS disorders

Yuhan,

Khaleghi Ghadiri,

Gorji

2024

J Transl Med

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“… 10 , 11 These findings strongly suggest that the Keap1/Nrf2 pathway may play an important role in the progression of EP. A recent study by Kishore M et al suggested that the development of EP might be inhibited by modulating the Keap1/Nrf2 axis, 12 but they did not experimentally validate this. In addition, a study by Hu QP et al found that Genistein protects EP-induced brain injury by regulating the JAK2/STAT3 and Keap1/Nrf2 signaling pathways in the developing rats, 13 which further confirmed the important role of Keap1/Nrf2 in EP.…”

Section: Introductionmentioning

confidence: 96%

Keap1/Nrf2 signaling pathway participating in the progression of epilepsy via regulation of oxidative stress and ferroptosis in neurons

Wang,

Cui,

Gao

et al. 2024

Clinics

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“…Therefore, histology remains the Gold Standard method to unveil cellular changes that directly reflect underlying physio-pathological mechanisms (Cardoso et al, 2014;den Bakker, 2017;Durand-Martel et al, 2010). Ideally, brain tissue biopsies and surgical resections could be used for histological analysis (such as seen in (Kishore et al, 2023) for example) and correlated with in vivo MRI, but these samples are rarely available for research given the invasiveness and risks associated with brain biopsies. Hence, postmortem (i.e., ex vivo) research is the preferred methodological approach, as it provides a larger amount of cerebral tissue available for histology and study of the molecular and cellular brain alterations.…”

Section: Introductionmentioning

confidence: 99%

Comparison of histological procedures and antigenicity of human post-mortem brains fixed with solutions used in gross anatomy laboratories

Frigon,

Gérin-Lajoie,

Dadar

et al. 2024

Preprint

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Background: Brain banks provide small tissue samples to researchers, while gross anatomy laboratories could provide larger samples, including complete brains to neuroscientists. However, they are preserved with solutions appropriate for gross-dissection, different from the classic neutral-buffered formalin (NBF) used in brain banks. Our previous work in mice showed that two gross-anatomy laboratory solutions, a saturated-salt-solution (SSS) and an alcohol-formaldehyde-solution (AFS), preserve antigenicity of the main cellular markers. Our goal is now to compare the quality of histology and antigenicity preservation of human brains fixed with NBF by immersion (practice of brain banks) vs. those fixed with a SSS and an AFS by whole body perfusion, practice of gross-anatomy laboratories. Methods: We used a convenience sample of 42 brains (31 males, 11 females; 25-90 years old) fixed with NBF (N=12), SSS (N=13), and AFS (N=17). One cm3 tissue blocks were cut, cryoprotected, frozen and sliced into 40 um sections. The four cell populations were labeled using immunohistochemistry (neuronal-nuclei (NeuN), glial-fibrillary-acidic-protein (GFAP), ionized-calcium-binding-adaptor-molecule1 (Iba1) and myelin-proteolipid-protein (PLP)). We qualitatively assessed antigenicity and cell distribution, and compared the ease of manipulation of the sections, the microscopic tissue quality, and the quality of common histochemical stains (e.g., Cresyl violet, Luxol fast blue, etc.) across solutions. Results: Sections of SSS-fixed brains were more difficult to manipulate and showed poorer tissue quality than those from brains fixed with the other solutions. The four antigens were preserved, and cell labeling was more often homogenous in AFS-fixed specimens. NeuN and GFAP were not always present in the NBF and SSS samples. Some antigens were heterogeneously distributed in some specimens, independently of the fixative, but an antigen retrieval protocol successfully recovered them. Finally, the histochemical stains were of sufficient quality regardless of the fixative, although neurons were more often paler in SSS-fixed specimens. Conclusion: Antigenicity was preserved in human brains fixed with solutions used in human gross-anatomy (albeit the poorer quality of SSS-fixed specimens). For some specific variables, histology quality was superior in AFS-fixed brains. Furthermore, we show the feasibility of frequently used histochemical stains. These results are promising for neuroscientists interested in using brain specimens from anatomy laboratories.

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Regulation of Keap1-Nrf2 axis in temporal lobe epilepsy—hippocampal sclerosis patients may limit the seizure outcomes

Cited by 7 publications

References 56 publications

Impact of NQO1 dysregulation in CNS disorders

Impact of NQO1 dysregulation in CNS disorders

Keap1/Nrf2 signaling pathway participating in the progression of epilepsy via regulation of oxidative stress and ferroptosis in neurons

Comparison of histological procedures and antigenicity of human post-mortem brains fixed with solutions used in gross anatomy laboratories

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