Treatment with edaravone improves the structure and functional changes in the hippocampus after chronic cerebral hypoperfusion in rat

Meftahi, Gholam Hossein; Bayat, Mahnaz; Zarifkar, Amir Hossein; Akbari, Somaye; Haghighi, Afshin Borhani; Naseh, Maryam; Nejad, Amirhossein Yousefi; Haghani, Masoud

doi:10.1016/j.brainresbull.2021.06.006

Cited by 14 publications

(12 citation statements)

References 33 publications

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“…The structural adaptation of neurons is also an important form of synaptic plasticity. The loss of neurons, abnormal neuronal morphology like reduced dendritic spine density, and abnormal synaptic structure were all constantly associated with impaired LTP ( Bencsik et al, 2019 ; Reza-Zaldivar et al, 2020 ; Meftahi et al, 2021 ). We found aberrant dendritic length, complexity, and decreased dendritic spine density of pyramidal neurons in the CA1 area of APP/PS1 mice.…”

Section: Discussionmentioning

confidence: 99%

Deficits in N-Methyl-D-Aspartate Receptor Function and Synaptic Plasticity in Hippocampal CA1 in APP/PS1 Mouse Model of Alzheimer’s Disease

Zhou

et al. 2021

Front. Aging Neurosci.

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The N-methyl-D-aspartate receptor is a critical molecule for synaptic plasticity and cognitive function. Impaired synaptic plasticity is thought to contribute to the cognitive impairment associated with Alzheimer’s disease (AD). However, the neuropathophysiological alterations of N-methyl-D-aspartate receptor (NMDAR) function and synaptic plasticity in hippocampal CA1 in transgenic rodent models of AD are still unclear. In the present study, APP/PS1 mice were utilized as a transgenic model of AD, which exhibited progressive cognitive impairment including defective working memory, recognition memory, and spatial memory starting at 6 months of age and more severe by 8 months of age. We found an impaired long-term potentiation (LTP) and reduced NMDAR-mediated spontaneous excitatory postsynaptic currents (sEPSCs) in the hippocampal CA1 of APP/PS1 mice with 8 months of age. Golgi staining revealed that dendrites of pyramidal neurons had shorter length, fewer intersections, and lower spine density in APP/PS1 mice compared to control mice. Further, the reduced expression levels of NMDAR subunits, PSD95 and SNAP25 were observed in the hippocampus of APP/PS1 mice. These results suggest that NMDAR dysfunction, impaired synaptic plasticity, and disrupted neuronal morphology constitute an important part of the neuropathophysiological alterations associated with cognitive impairment in APP/PS1 mice.

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Section: Discussionmentioning

confidence: 99%

Deficits in N-Methyl-D-Aspartate Receptor Function and Synaptic Plasticity in Hippocampal CA1 in APP/PS1 Mouse Model of Alzheimer’s Disease

Zhou

et al. 2021

Front. Aging Neurosci.

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Section: Hippocampal Dysfunction In Neurodegenerative Diseasesmentioning

confidence: 99%

“…Synaptic dysfunction in VD has been reported in terms of decreased synaptic proteins [ 221 , 222 , 223 ], synaptic vesicles [ 224 ], and LTP [ 224 , 225 ] ( Figure 1 ). In rat models of VD with bilateral common carotid artery occlusion (BCCAO), impaired basal synaptic transmission [ 225 ] and damaged synaptic ultrastructure [ 222 ] were observed. Most plasticity changes were alleviated with antioxidative therapies [ 65 , 225 ], supporting the strong correlation between hippocampal synaptic dysfunction and oxidative stress in VD [ 226 ].…”

Section: Hippocampal Dysfunction In Neurodegenerative Diseasesmentioning

confidence: 99%

“…In rat models of VD with bilateral common carotid artery occlusion (BCCAO), impaired basal synaptic transmission [ 225 ] and damaged synaptic ultrastructure [ 222 ] were observed. Most plasticity changes were alleviated with antioxidative therapies [ 65 , 225 ], supporting the strong correlation between hippocampal synaptic dysfunction and oxidative stress in VD [ 226 ]. FTD and ALS are discussed for their common pathogenic mechanisms that have different outcomes [ 227 ].…”

Section: Hippocampal Dysfunction In Neurodegenerative Diseasesmentioning

confidence: 99%

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Structural Plasticity of the Hippocampus in Neurodegenerative Diseases

Weerasinghe-Mudiyanselage

Ang

Kang

et al. 2022

IJMS

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Neuroplasticity is the capacity of neural networks in the brain to alter through development and rearrangement. It can be classified as structural and functional plasticity. The hippocampus is more susceptible to neuroplasticity as compared to other brain regions. Structural modifications in the hippocampus underpin several neurodegenerative diseases that exhibit cognitive and emotional dysregulation. This article reviews the findings of several preclinical and clinical studies about the role of structural plasticity in the hippocampus in neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and multiple sclerosis. In this study, literature was surveyed using Google Scholar, PubMed, Web of Science, and Scopus, to review the mechanisms that underlie the alterations in the structural plasticity of the hippocampus in neurodegenerative diseases. This review summarizes the role of structural plasticity in the hippocampus for the etiopathogenesis of neurodegenerative diseases and identifies the current focus and gaps in knowledge about hippocampal dysfunctions. Ultimately, this information will be useful to propel future mechanistic and therapeutic research in neurodegenerative diseases.

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“…Neurons play a central role in the NVU. Neural dysfunction or death, especially in the hippocampus and prefrontal lobe, which are engaged in the learning and memory processes, is considered as a major cause of VCI ( Deramecourt et al, 2012 ; Bartsch and Wulff, 2015 ; Meftahi et al, 2021 ). It has been shown that RIC is capable of reducing neural death and improve cognitive function in VCI animal models ( Khan et al, 2015 , 2018 ; Ren et al, 2018a ).…”

Section: Role Of Ric In Mitigating Vcimentioning

confidence: 99%

Therapeutic Potential of Remote Ischemic Conditioning in Vascular Cognitive Impairment

Wang

et al. 2021

Front. Cell. Neurosci.

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Vascular cognitive impairment (VCI) is a heterogeneous disease caused by a variety of cerebrovascular diseases. Patients with VCI often present with slower cognitive processing speed and poor executive function, which affects their independence in daily life, thus increasing social burden. Remote ischemic conditioning (RIC) is a non-invasive and efficient intervention that triggers endogenous protective mechanisms to generate neuroprotection. Over the past decades, evidence from basic and clinical research has shown that RIC is promising for the treatment of VCI. To further our understanding of RIC and improve the management of VCI, we summarize the evidence on the therapeutic potential of RIC in relation to the risk factors and pathobiologies of VCI, including reducing the risk of recurrent stroke, decreasing high blood pressure, improving cerebral blood flow, restoring white matter integrity, protecting the neurovascular unit, attenuating oxidative stress, and inhibiting the inflammatory response.

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Treatment with edaravone improves the structure and functional changes in the hippocampus after chronic cerebral hypoperfusion in rat

Cited by 14 publications

References 33 publications

Deficits in N-Methyl-D-Aspartate Receptor Function and Synaptic Plasticity in Hippocampal CA1 in APP/PS1 Mouse Model of Alzheimer’s Disease

Deficits in N-Methyl-D-Aspartate Receptor Function and Synaptic Plasticity in Hippocampal CA1 in APP/PS1 Mouse Model of Alzheimer’s Disease

Structural Plasticity of the Hippocampus in Neurodegenerative Diseases

Therapeutic Potential of Remote Ischemic Conditioning in Vascular Cognitive Impairment

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