Acrolein, an endogenous aldehyde induces synaptic dysfunction in vitro and in vivo: Involvement of RhoA/ROCK2 pathway

Zhu, Zhaowen; Lu, Junfeng; Wang, Shuyi; Peng, Weijia; Yang, Yang; Chen, Chen; Zhou, Xin; Yang, Xifei; Xin, Wenjun; Chen, Xinyi; Pi, JiaKai; Yin, Wei; Yao, Lin

doi:10.1111/acel.13587

Cited by 14 publications

(4 citation statements)

References 65 publications

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“…On the other hand, acrolein is a highly reactive aldehyde and a known byproduct of lipid peroxidation, a process associated with oxidative stress ( Chen et al, 2017 ; Zhu et al, 2022 ). In AD, elevated levels of acrolein have been detected in the brains of affected individuals ( Sanotra et al, 2023 ).…”

Section: Discussionmentioning

confidence: 99%

A comprehensive bibliometric analysis of global research on the role of acrolein in Alzheimer’s disease pathogenesis: involvement of amyloid-beta

Jallow,

Nguyen,

Sanotra

et al. 2024

Front. Aging Neurosci.

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BackgroundAlzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive and behavioral decline. Acrolein, an environmental pollutant and endogenous compound, is implicated in AD development. This research employs bibliometric analysis to assess current trends and key areas concerning acrolein-AD interaction.MethodsThe Web of Science was used to extensively review literature on acrolein and AD. Relevant data were systematically gathered and analyzed using VOSviewer, CiteSpace, and an online bibliometric tool.ResultsWe identified 120 English publications in this specialized field across 19 journals. The Journal of Alzheimer’s Disease was the most prominent. The primary contributors, both in terms of scientific output and influence, were the USA, the University of Kentucky, and Ramassamy C, representing countries/regions, institutions, and authors, respectively. In this field, the primary focus was on thoroughly studying acrolein, its roles, and its mechanisms in AD utilizing both in vivo and in vitro approaches. A significant portion of the research was based on proteomics, revealing complex molecular processes. The main focuses in the field were “oxidative stress,” “lipid peroxidation,” “amyloid-beta,” and “cognitive impairment.” Anticipated future research trajectories focus on the involvement of the internalization pathway, covering key areas such as synaptic dysfunction, metabolism, mechanisms, associations, neuroinflammation, inhibitors, tau phosphorylation, acrolein toxicity, brain infarction, antioxidants, chemistry, drug delivery, and dementia. Our analysis also supported our previous hypothesis that acrolein can interact with amyloid-beta to form a protein adduct leading to AD-like pathology and altering natural immune responses.ConclusionThis study provides a broad and all-encompassing view of the topic, offering valuable insights and guidance to fellow researchers. These emerging directions underscore the continuous exploration of the complexities associated with AD. The analyses and findings aim to enhance our understanding of the intricate relationship between acrolein and AD for future research.

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Section: Discussionmentioning

confidence: 99%

A comprehensive bibliometric analysis of global research on the role of acrolein in Alzheimer’s disease pathogenesis: involvement of amyloid-beta

Jallow,

Nguyen,

Sanotra

et al. 2024

Front. Aging Neurosci.

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“…However, most studies have focused on neuronal death and have not evaluated the cytoskeleton, even though the cytoskeleton is an important biological factor, and tauopathy causes cytoskeletal changes that lead to neuronal dysfunction even before neuronal death occurs. For example, 5 μM acrolein does not cause neuronal death but triggers synaptic dysfunction [156] . Therefore, more research is needed on neuronal cytoskeletons in AD models.…”

Section: Nanomedicines For Targeting Tauopathymentioning

confidence: 99%

“…For example, 5 μM acrolein does not cause neuronal death but triggers synaptic dysfunction. [156] Therefore, more research is needed on neuronal cytoskeletons in AD models.…”

Section: Nanomedicines For Targeting Tauopathymentioning

confidence: 99%

Nanomedicines for Alzheimer's disease: Therapies based on pathological mechanisms

Cheng

Xie

Zhao

et al. 2023

Brain-X

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Alzheimer's disease (AD) is the most common neurodegenerative disorder worldwide. Because of the complex pathogenesis of AD and the unique location of AD lesions, effective clinical treatment strategies for this disease remain elusive. However, the development of nanotechnology has allowed a new era of AD treatment to emerge. AD nanomedicines are products of interdisciplinary research that enable high precision and targeted delivery. Additionally, they can specifically regulate various pathogenic factors. This review focuses on nanomedicines based on the pathological mechanisms of AD that can target AD lesions. We also discuss the precise regulatory effects of nanomedicines (including the nanomaterials themselves) on pathogenic proteins, neuroinflammatory molecules, and other pathogenic factors. We summarize the clinical trials that have examined new AD drugs, highlighting the development of new nanomedicines and the progress in their clinical translation. Nanotechnology‐based AD treatment is a nascent field, and a complete cure is distant at present; therefore, we also elaborate on the shortcomings of current AD nanomedicines. Finally, we discuss the prospects to guide the future development of AD nanomedicines.

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“… Amyloid-β1-42 15 days 14 days [ 142 , 143 ] 6. Acrolein 12 weeks 4 weeks [ 144 , 145 ] 7. Heavy metals 25 days 21 days [ 146 , 147 ] 8.…”

Section: Main Textmentioning

confidence: 99%

Insight into the emerging and common experimental in-vivo models of Alzheimer’s disease

Dhapola,

Kumari,

Sharma

et al. 2023

Lab Anim Res

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Alzheimer’s disease (AD) is a multifactorial, rapidly progressing neurodegenerative disorder. As the exact cause of the disease is still unclear, the drug development is very challenging. This review encompasses the commonly used AD models involving various chemicals, heavy metals and endogenous substances induced models and the transgenic models. It also provides insight into the reliable emerging models of AD that may overcome the shortcomings associated with available models. Chemicals like streptozotocin, scopolamine, colchicine and okadaic acid render the animal susceptible to neuroinflammation and oxidative stress induced neurodegeneration along with amyloid-β deposition and tau hyperphosphorylation. Similarly, endogenous substances like acrolein and amyloid-β 1–42 are efficient in inducing the major pathologies of AD. Heavy metals like aluminum and fluoride and mixture of these have been reported to induce neurotoxicity therefore are used as animal models for AD. Transgenic models developed as a result of knock-in or knock-out of certain genes associated with AD including PDAPP, APP23, Tg2576, APP/PS1, 3 × Tg and 5 × FAD have also been incorporated in this study. Further, emerging and advanced pathomimetic models of AD are provided particular interest here which will add on to the current knowledge of animal models and may aid in the drug development process and deepen our understanding related to AD pathogenesis. These newly discovered models include oAβ25-35 model, transgenic model expressing 82-kDa ChAT, oDGal mouse and APP knock-in rat. This study may aid in the selection of suitable model for development of novel potent therapeutics and for exploring detailed pathogenic mechanism of AD. Graphical abstract

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Acrolein, an endogenous aldehyde induces synaptic dysfunction in vitro and in vivo: Involvement of RhoA/ROCK2 pathway

Cited by 14 publications

References 65 publications

A comprehensive bibliometric analysis of global research on the role of acrolein in Alzheimer’s disease pathogenesis: involvement of amyloid-beta

A comprehensive bibliometric analysis of global research on the role of acrolein in Alzheimer’s disease pathogenesis: involvement of amyloid-beta

Nanomedicines for Alzheimer's disease: Therapies based on pathological mechanisms

Insight into the emerging and common experimental in-vivo models of Alzheimer’s disease

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