Correction: Corrigendum: Regulation of synaptic plasticity and cognition by SUMO in normal physiology and Alzheimer’s disease

Lee, Linda; Dale, Elena; Staniszewski, Agnes; Zhang, Hong; Saeed, Faisal; Sakurai, Mikako; Fà, Mauro; Orozco, Ian J.; Michelassi, Francesco; Akpan, Nsikan; Lehrer, Helaina; Arancio, Ottavio

doi:10.1038/srep11782

Cited by 8 publications

(6 citation statements)

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“…Synaptic loss is another pathologic hallmark of the AD brain that is highly correlated with the pathogenesis of the disease ( Gylys et al, 2004 ; Dong et al, 2015 ; Lee et al, 2015 ; Mcdole et al, 2015 ). Since BDNF regulates neurite outgrowth and synaptic plasticity, the reduction of the BDNF level is also involved in this pathophysiology.…”

Section: Discussionmentioning

confidence: 99%

Ultrasound Combined With Microbubbles Loading BDNF Retrovirus to Open Blood–Brain Barrier for Treatment of Alzheimer’s Disease

et al. 2021

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Background: Brain-derived nerve growth factor (BDNF) is a promising effective target for the treatment of Alzheimer’s disease (AD). BDNF, which has a high molecular weight, has difficulty in crossing the blood–brain barrier (BBB). The study aimed to prepare microbubbles loading brain-derived nerve growth factor (BDNF) retrovirus (MpLXSN-BDNF), to verify the characteristics of the microbubbles, and to study the therapeutic effect of the microbubbles combined with ultrasound on the opening of the blood–brain barrier in an AD rat model.Methods: 32 adult male SD rats were randomly divided into four groups: control group, ultrasound + pLXSN-EGFP microbubble group (U + MpLXSN-BDNF), ultrasound + pLXSN-BDNF microbubble group, and ultrasound + microbubble + pLXSN-BDNF virus group (U + MpLXSN-BDNF), with eight rats in each group. At the same time, the left hippocampus of rats was irradiated with low-frequency focused ultrasound guided by MRI to open the blood–brain barrier (BBB). The effects of BDNF overexpression on AD rats were evaluated behaviorally before and 1 month after the treatment. The number of acetylcholinesterase (ChAT)-positive cells and the content of acetylcholine (ACh) in brain tissues were determined by immunohistochemistry and high-performance liquid chromatography (HPLC), respectively. IF staining of synaptic spines and Western blot of synaptophysin presented herein detected synaptic density recovery.Results: Signal intensity enhancement at the BBB disruption sites could be observed on the MR images. The behavioral evaluation showed that the times of crossing the original platform in the U + MpLXSN-BDNF group increased significantly after treatment. Immunohistochemistry and HPLC revealed that the number of ChAT-positive neurons and the contents of ACh in the brain were significantly decreased in the treated groups compared with the controls. IF staining of synaptic spines and Western blot data of synaptophysin showed that the U + MpLXSN-BDNF group can recover the synaptic loss better by BDNF supplementation than the other treatment groups.Conclusion: Ultrasound combined with viral microbubbles carrying BDNF can increase the transfection efficiency of brain neurons, promote the high expression of exogenous gene BDNF, and play a therapeutic role in the AD model rats.

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Section: Discussionmentioning

confidence: 99%

Ultrasound Combined With Microbubbles Loading BDNF Retrovirus to Open Blood–Brain Barrier for Treatment of Alzheimer’s Disease

et al. 2021

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“…Although neuronal activation induced the upregulation of SUMOylation, this effect was destroyed by Aβ. However, by transducing the SUMO E2 binding enzyme Ubc9 to enhance SUMOylation, the LTP (long‐term potentiation) defect caused by the loss of Aβ and altered hippocampus‐dependent learning and memory were restored 25 . In the synaptosome of Tg2576 mice, increased SUMOylation reduced glutamate release evoked by KCl, whereas reduced SUMOylation restored impaired glutamate release 26 .…”

Section: Alzheimer’s Diseasementioning

confidence: 99%

The function of SUMOylation and its crucial roles in the development of neurological diseases

et al. 2021

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Neurological diseases are relatively complex diseases of a large system; however, the detailed mechanism of their pathogenesis has not been completely elucidated, and effective treatment methods are still lacking for some of the diseases. The SUMO (small ubiquitin‐like modifier) modification is a dynamic and reversible process that is catalyzed by SUMO‐specific E1, E2, and E3 ligases and reversed by a family of SENPs (SUMO/Sentrin‐specific proteases). SUMOylation covalently conjugates numerous cellular proteins, and affects their cellular localization and biological activity in numerous cellular processes. A wide range of neuronal proteins have been identified as SUMO substrates, and the disruption of SUMOylation results in defects in synaptic plasticity, neuronal excitability, and neuronal stress responses. SUMOylation disorders cause many neurodegenerative diseases, such as Parkinson’s disease, Alzheimer’s disease, and Huntington’s disease. By modulating the ion channel subunit, SUMOylation imbalance is responsible for the development of various channelopathies. The regulation of protein SUMOylation in neurons may provide a new strategy for the development of targeted therapeutic drugs for neurodegenerative diseases and channelopathies.

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“…However, whether Miz1 located in astrocytes in the central nervous system is associated with the anti-inflammatory process in AD remains unclear. Notably, the disruption of normal posttranslational modification-based signaling at the synapse is a pathological mechanism that likely contributes to cognitive dysfunction in diseases such as AD ( 43 ). A previous study reported that Miz1 may participate in small ubiquitin-like modifier (SUMO) conjugation and SUMO ligase activity ( 44 ).…”

Section: Discussionmentioning

confidence: 99%

Increased expression of Myc‑interacting zinc finger protein 1 in APP/PS1 mice

et al. 2017

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Myc-interacting zinc-finger protein 1 (Miz1) is a member of the poxvirus and zinc-finger domain/zinc finger transcription factor family. Its transcription activation and repression functions in the nucleus are well elucidated; however its cytoplasmic inflammation function is poorly understood and may be associated with the pathogenesis of Alzheimer's disease (AD). The aim of the present study was to investigate the association between AD and Miz1 expression. In the present study, the expression and distribution of Miz1 in wild-type (WT) and amyloid precursor protein/presenelin-1 (AD) mice was studied using reverse transcription-quantitative polymerase chain reaction, western blot analysis, and immunohistochemical and immunofluorescence staining. The results indicated that Miz1 was significantly upregulated in the cortex of AD mice (P<0.05). Double immunofluorescence labeling revealed that Miz1 protein was predominantly expressed in neurons and astrocytes, as evidenced by co-localization with the dendritic markers microtubule associated protein 2 and glial fibrillary acidic protein, respectively. The results of the present study suggest that the expression of Miz1 in the brain tissue of AD mice may serve an important role in AD pathogenesis.

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Correction: Corrigendum: Regulation of synaptic plasticity and cognition by SUMO in normal physiology and Alzheimer’s disease

Cited by 8 publications

References 0 publications

Ultrasound Combined With Microbubbles Loading BDNF Retrovirus to Open Blood–Brain Barrier for Treatment of Alzheimer’s Disease

Ultrasound Combined With Microbubbles Loading BDNF Retrovirus to Open Blood–Brain Barrier for Treatment of Alzheimer’s Disease

The function of SUMOylation and its crucial roles in the development of neurological diseases

Increased expression of Myc‑interacting zinc finger protein 1 in APP/PS1 mice

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