Netrin-1 protects the SH-SY5Y cells against amyloid beta neurotoxicity through NF-κB/Nrf2 dependent mechanism

Zamani, Elham; Parviz, Mohsen; Roghani, Mehrdad; Hosseini, Marjan; Mohseni‐Moghaddam, Parvaneh; Nikbakhtzadeh, Marjan

doi:10.1007/s11033-020-05996-1

Cited by 10 publications

(7 citation statements)

References 25 publications

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“…In the transgenic AD mouse model, it was observed that the accumulation of Aβ caused NF-κB upregulation with, the destruction of BBB integrity, and a decline in mouse learning ability ( Scheffer et al, 2021 ). Another study showed that NF-κB signaling mediates the inhibition on P-gp expression induced by Aβ 1 – 42 , thereby affecting the function of BBB ( Zamani et al, 2020 ). Another study showed that NF-κB signaling mediates the reduction of P-gp expression induced by Aβ 1 – 42 , thereby affecting the function of BBB ( Park et al, 2014 ).…”

Section: Blood–brain Barrier Impairment Caused By Amyloid-β Depositionmentioning

confidence: 99%

Relationship Between Amyloid-β Deposition and Blood–Brain Barrier Dysfunction in Alzheimer’s Disease

Wang

Chen²,

Han

et al. 2021

Front. Cell. Neurosci.

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Amyloid-β (Aβ) is the predominant pathologic protein in Alzheimer’s disease (AD). The production and deposition of Aβ are important factors affecting AD progression and prognosis. The deposition of neurotoxic Aβ contributes to damage of the blood–brain barrier. However, the BBB is also crucial in maintaining the normal metabolism of Aβ, and dysfunction of the BBB aggravates Aβ deposition. This review characterizes Aβ deposition and BBB damage in AD, summarizes their interactions, and details their respective mechanisms.

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Section: Blood–brain Barrier Impairment Caused By Amyloid-β Depositionmentioning

confidence: 99%

Relationship Between Amyloid-β Deposition and Blood–Brain Barrier Dysfunction in Alzheimer’s Disease

Wang

Chen²,

Han

et al. 2021

Front. Cell. Neurosci.

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“…From this perspective, NF-κB is considered a major target, and Aβ peptide, a major causative molecule in AD, is implicated in the regulation of inflammatory responses through NF-κB activation ( Liu et al, 2014 ). In addition, several related studies have reported that inhibition of NF-κB signaling reduces Aβ-induced neurotoxicity in neuron and glial cells ( Yan et al, 2020 ; Zamani et al, 2020 ). It is also notable that Aβ peptide induces aberrant cilia formation by interfering with Shh signaling ( Vorobyeva and Saunders, 2018 ).…”

Section: Conclusion and Perspectivementioning

confidence: 99%

Primary Cilia in Glial Cells: An Oasis in the Journey to Overcoming Neurodegenerative Diseases

Jeong

Lee

2021

Front. Neurosci.

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Many neurodegenerative diseases have been associated with defects in primary cilia, which are cellular organelles involved in diverse cellular processes and homeostasis. Several types of glial cells in both the central and peripheral nervous systems not only support the development and function of neurons but also play significant roles in the mechanisms of neurological disease. Nevertheless, most studies have focused on investigating the role of primary cilia in neurons. Accordingly, the interest of recent studies has expanded to elucidate the role of primary cilia in glial cells. Correspondingly, several reports have added to the growing evidence that most glial cells have primary cilia and that impairment of cilia leads to neurodegenerative diseases. In this review, we aimed to understand the regulatory mechanisms of cilia formation and the disease-related functions of cilia, which are common or specific to each glial cell. Moreover, we have paid close attention to the signal transduction and pathological mechanisms mediated by glia cilia in representative neurodegenerative diseases. Finally, we expect that this field of research will clarify the mechanisms involved in the formation and function of glial cilia to provide novel insights and ideas for the treatment of neurodegenerative diseases in the future.

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“…Previous data also indicates that down-regulation of netrin-1 attribute to hyper-methylation of its gene can result in memory loss ( Kalani et al, 2019 ). In addition, netrin-1 protected Aβ1-42-exposed SH-SY5Y cells through NF-κB/Nrf2 dependent mechanism ( Zamani et al, 2020 ). Netrin-1 receptor UNC5C has also been proven an AD risk gene previously ( Wetzel-Smith et al, 2014 ; Chen et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

“…Results from previous studies have shown that netrin-1, via its interaction with amyloid precursor protein (APP, from which Aβ, the main component of the amyloid plaques associated with AD is derived) ( Lourenço et al, 2009 ; Rama et al, 2012 ; Borel et al, 2017 ), suppresses Aβ peptide production as demonstrated both in vivo and in vitro . As a result of netrin-1 treatment, there are improvements in cognitive dysfunction in animal models of AD and a prevention of Aβ-induced cell death in AD cell models and Aβ-induced oxidative stress and neuroinflammation ( Lourenço et al, 2009 ; Spilman et al, 2016 ; Zamani et al, 2019 , 2020 ). Within our laboratory, decreases in netrin-1 were correlated with a Th17/Tregs (T helper 17/regulatory T cells) balance disorder in a rat model of Aβ-induced AD ( Sun et al, 2019 ).…”

Section: Objectivementioning

confidence: 99%

Decreased Netrin-1 in Mild Cognitive Impairment and Alzheimer’s Disease Patients

Sun

Fan

et al. 2022

Front. Aging Neurosci.

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Background and ObjectiveInflammatory mediators are closely associated with the pathogenesis of Alzheimer’s disease (AD) and mild cognitive impairment (MCI). Netrin-1 is an axon guidance protein and despite its capacity to function as a neuroimmune guidance signal, its role in AD or MCI is poorly understood. In addition, the association among netrin-1, cognitive impairment and serum inflammatory cytokines such as interleukin-17 (IL-17) and tumor necrosis (TNF-α) remains unclear. The aim of this study was to determine serum levels of IL-17, TNF-α and netrin-1in a cohort of AD and MCI patients, and to study the relationship between these cytokines and cognitive status, as well as to assess the possible relationships between netrin-1 levels and inflammatory molecules.MethodsSerum concentrations of netrin-1, TNF-α and IL-17 were determined in 20 AD patients, 22 MCI patients and 22 healthy controls using an enzyme-linked immunosorbent assay (ELISA). In addition, neuropsychological evaluations and psychometric assessments were performed in all subjects.ResultsSerum netrin-1 levels were decreased in AD and MCI patients and were positively correlated with Mini Mental State Examination (MMSE) scores. In contrast, serum TNF-α and IL-17 levels were elevated in AD and MCI cohorts and negatively correlated with MMSE scores. Serum netrin-1 levels were inversely related with TNF-α and IL-17 levels in AD, but not MCI, patients.ConclusionBased on the findings reported here, netrin-1 may serve as a marker for the early recognition of dementia and predict cognitive impairment.

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Netrin-1 protects the SH-SY5Y cells against amyloid beta neurotoxicity through NF-κB/Nrf2 dependent mechanism

Cited by 10 publications

References 25 publications

Relationship Between Amyloid-β Deposition and Blood–Brain Barrier Dysfunction in Alzheimer’s Disease

Relationship Between Amyloid-β Deposition and Blood–Brain Barrier Dysfunction in Alzheimer’s Disease

Primary Cilia in Glial Cells: An Oasis in the Journey to Overcoming Neurodegenerative Diseases

Decreased Netrin-1 in Mild Cognitive Impairment and Alzheimer’s Disease Patients

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