The synapse as a treatment avenue for Alzheimer’s Disease

Peng, Lin; Bestard-Lorigados, Isabel; Song, Weihong

doi:10.1038/s41380-022-01565-z

Cited by 76 publications

(39 citation statements)

References 142 publications

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“…Previous research has indicated that abnormal accumulation of tau protein contributes to disturbance of neural plasticity in AD ( Shao et al, 2011 ). Synapses are the functional units of neuronal communication, and synaptic dysfunction is directly linked to cognitive disturbances ( Singh et al, 2019 ; Peng et al, 2022 ). Synaptic impairment is likely to be the major contributor to memory loss in AD ( Arendt, 2009 ; Barthet and Mulle, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Dl-3-n-Butylphthalide mitigates stress-induced cognitive deficits in mice through inhibition of NLRP3-Mediated neuroinflammation

Chen¹,

He²,

Liu³

et al. 2022

Neurobiology of Stress

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Section: Discussionmentioning

confidence: 99%

Dl-3-n-Butylphthalide mitigates stress-induced cognitive deficits in mice through inhibition of NLRP3-Mediated neuroinflammation

Chen¹,

He²,

Liu³

et al. 2022

Neurobiology of Stress

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“…These clues support the synapse, a key site where the functional connection between neurons occurs ( Faria-Pereira and Morais, 2022 ), whose information transmission was in chaos post infection. Alterations in synaptic signaling, in the release of neurotransmitters from presynaptic neurons, changes in binding to postsynaptic receptors, and synaptic degeneration are evident in the course of many neurodegenerative diseases ( Parmar et al., 2022 ; Peng et al., 2022 ; Wang et al., 2022a ). Indeed, we found that several differentially expressed proteins were involved in the pathways of KEGG associated with neurodegenerative diseases, autophagy, and other signaling.…”

Section: Discussionmentioning

confidence: 99%

Understanding global changes of the mouse brain proteome after vaginal infection with HSV-2 using a label-free shotgun approach

Cheng

Wang

et al. 2022

Front. Cell. Infect. Microbiol.

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Herpes simplex virus type 2 (HSV-2) is a common human pathogen that establishes lifelong latency in neurons of the nervous system. The number of severe central nervous system infections caused by the virus has increased recently. However, the pathogenesis of HSV-2 infection in the nervous system is not fully understood. Here, we demonstrated global proteomic changes in the brain tissue in BALB/c mice vaginally infected with HSV-2. Data are available via ProteomeXchange with identifier PXD034186. A total of 249 differentially expressed proteins were identified in infected brain tissue. The GO and KEGG enrichment analysis of these proteins indicated that they were mainly involved in the regulation of synapse formation and synaptic excitability. In addition, genes affecting autophagy, the development of other neurodegenerative diseases, and signaling pathways relevant to other neurologic diseases were identified. Additional experiments, comparing the brain tissue of asymptomatic and symptomatic mice showed a differential expression of proteins involved in synapse formation and synaptic transmission. Others were involved in autophagy, addiction, and signaling pathways of other neurologic diseases. These results suggest that changes in synaptic structure and function, as well as autophagy, may be related to the development of neurologic abnormalities that follow HSV-2 infection. We also identified a protein GluN2A encoded by Grin2a was continuously expressed at high levels after infection. We propose that GluN2A may be a key molecule in the pathogenesis of HSV-2-induced neurologic diseases.

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“…C1q and C3 levels are parallel to Aβ deposition in AD mice [ 19 ]. Rescuing cognitive impairment in AD induced by Aβ-mediated synaptic loss by reducing C1q and C3 levels is a potential therapeutic avenue [ 20 , 21 , 22 ]. Microglia destabilize its homeostasis to an inflammatory state and release a series of inflammatory factors, such as IL-1α, TNF, and IFN-1, leading to synaptic loss, neuronal defects, and alterations in learning and memory [ 23 , 24 ] ( Figure 1 e).…”

Section: Role Of Mirnas In Regulating Astrocytes and Microglia In Admentioning

confidence: 99%

Diverse and Composite Roles of miRNA in Non-Neuronal Cells and Neuronal Synapses in Alzheimer’s Disease

Chen

2022

Biomolecules

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Neurons interact with astrocytes, microglia, and vascular cells. These interactions become unbalanced in disease states, resulting in damage to neurons and synapses, and contributing to cognitive impairment. Importantly, synaptic loss and synaptic dysfunction have been considered for years as a main pathological factor of cognitive impairment in Alzheimer’s disease (AD). Recently, miRNAs have emerged as essential regulators of physiological and pathological processes in the brain. Focusing on the role of miRNAs in regulating synaptic functions, as well as different cell types in the brain, offers opportunities for the early prevention, diagnosis, and potential treatment of AD-related cognitive impairment. Here, we review the recent research conducted on miRNAs regulating astrocytes, microglia, cerebrovasculature, and synaptic functions in the context of AD-related cognitive impairment. We also review potential miRNA-related biomarkers and therapeutics, as well as emerging imaging technologies relevant for AD research.

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The synapse as a treatment avenue for Alzheimer’s Disease

Cited by 76 publications

References 142 publications

Dl-3-n-Butylphthalide mitigates stress-induced cognitive deficits in mice through inhibition of NLRP3-Mediated neuroinflammation

Dl-3-n-Butylphthalide mitigates stress-induced cognitive deficits in mice through inhibition of NLRP3-Mediated neuroinflammation

Understanding global changes of the mouse brain proteome after vaginal infection with HSV-2 using a label-free shotgun approach

Diverse and Composite Roles of miRNA in Non-Neuronal Cells and Neuronal Synapses in Alzheimer’s Disease

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