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Article ; Online: HDAC9-mediated calmodulin deacetylation induces memory impairment in Alzheimer's disease.

Zhang, Hai-Long / Hu, Shufen / Yang, Pin / Long, Han-Chun / Ma, Quan-Hong / Yin, Dong-Min / Xu, Guang-Yin

2024 Volume 30, Issue 2, Page(s) e14573

Abstract: Aims: Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive dysfunction and memory impairment. AD pathology involves protein acetylation. Previous studies have mainly focused on histone acetylation in AD, however, ...

Abstract	Aims: Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive dysfunction and memory impairment. AD pathology involves protein acetylation. Previous studies have mainly focused on histone acetylation in AD, however, the roles of nonhistone acetylation in AD are less explored. Methods: The protein acetylation and expression levels were detected by western blotting and co-immunoprecipitation. The stoichiometry of acetylation was measured by home-made and site-specific antibodies against acetylated-CaM (Ac-CaM) at K22, K95, and K116. Hippocampus-dependent learning and memory were evaluated by using the Morris water maze, novel object recognition, and contextual fear conditioning tests. Results: We showed that calmodulin (CaM) acetylation is reduced in plasma of AD patients and mice. CaM acetylation and its target Ca Conclusions: HDAC9-mediated CaM deacetylation induces memory impairment in AD, HDAC9, or CaM acetylation may become potential therapeutic targets for AD.
MeSH term(s)	Mice ; Humans ; Animals ; Alzheimer Disease/metabolism ; Calmodulin ; Neurodegenerative Diseases ; Mice, Transgenic ; Memory Disorders/etiology ; Hippocampus/metabolism ; Disease Models, Animal ; Histone Deacetylases/metabolism ; Repressor Proteins/metabolism
Chemical Substances	Calmodulin ; HDAC9 protein, human (EC 3.5.1.98) ; Histone Deacetylases (EC 3.5.1.98) ; Repressor Proteins
Language	English
Publishing date	2024-02-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2423461-8
ISSN	1755-5949 ; 1755-5930
ISSN (online)	1755-5949
ISSN	1755-5930
DOI	10.1111/cns.14573
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Analysis of the influences of social isolation on cognition and the therapeutic potential of deep brain stimulation in a mouse model.

Hu, Yun-Yun / Ding, Xuan-Si / Yang, Gang / Liang, Xue-Song / Feng, Lei / Sun, Yan-Yun / Chen, Rui / Ma, Quan-Hong

Frontiers in psychiatry

2023 Volume 14, Page(s) 1186073

Abstract: Background: Social interaction is a fundamental human need. Social isolation (SI) can have negative effects on both emotional and cognitive function. However, it is currently unclear how age and the duration of SI affect emotion and recognition function. ...

Abstract	Background: Social interaction is a fundamental human need. Social isolation (SI) can have negative effects on both emotional and cognitive function. However, it is currently unclear how age and the duration of SI affect emotion and recognition function. In addition, there is no specific treatment for the effects of SI. Methods: The adolescence or adult mice were individually housed in cages for 1, 6 or 12 months and for 2 months to estabolish SI mouse model. We investigated the effects of SI on behavior in mice at different ages and under distinct durations of SI, and we explored the possible underlying mechanisms. Then we performed deep brain stimulation (DBS) to evaluate its influences on SI induced behavioral abnormalities. Results: We found that social recognition was affected in the short term, while social preference was damaged by extremely long periods of SI. In addition to affecting social memory, SI also affects emotion, short-term spatial ability and learning willingness in mice. Myelin was decreased significantly in the medial prefrontal cortex (mPFC) and dorsal hippocampus of socially isolated mice. Cellular activity in response to social stimulation in both areas was impaired by social isolation. By stimulating the mPFC using DBS, we found that DBS alleviated cellular activation disorders in the mPFC after long-term SI and improved social preference in mice. Conclusion: Our results suggest that the therapeutic potential of stimulating the mPFC with DBS in individuals with social preference deficits caused by long-term social isolation, as well as the effects of DBS on the cellular activity and density of OPCs.
Language	English
Publishing date	2023-06-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564218-2
ISSN	1664-0640
ISSN	1664-0640
DOI	10.3389/fpsyt.2023.1186073
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Correction: Reduction of NgR in perforant path decreases amyloid-β peptide production and ameliorates synaptic and cognitive deficits in APP/PS1 mice.

Jiang, Rong / Wu, Xue-Fei / Wang, Bin / Guan, Rong-Xiao / Lv, Lang-Man / Li, Ai-Ping / Lei, Lei / Ma, Ye / Li, Na / Li, Qi-Fa / Ma, Quan-Hong / Zhao, Jie / Li, Shao

Alzheimer's research & therapy

2024 Volume 16, Issue 1, Page(s) 47

Language	English
Publishing date	2024-02-27
Publishing country	England
Document type	Published Erratum
ZDB-ID	2506521-X
ISSN	1758-9193 ; 1758-9193
ISSN (online)	1758-9193
ISSN	1758-9193
DOI	10.1186/s13195-024-01389-9
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Article ; Online: Transplantation of human neural stem cell prevents symptomatic motor behavior disability in a rat model of Parkinson's disease.

Wang, Fen / Cheng, Xiao-Yu / Zhang, Yu-Ting / Bai, Qing-Ran / Zhang, Xiao-Qi / Sun, Xi-Cai / Ma, Quan-Hong / Zhao, Xiong-Fei / Liu, Chun-Feng

Open life sciences

2024 Volume 19, Issue 1, Page(s) 20220834

Abstract: Parkinson's disease (PD) is a ubiquitous brain cell degeneration disease and presents a significant therapeutic challenge. By injecting 6-hydroxydopamine (6-OHDA) into the left medial forebrain bundle, rats were made to exhibit PD-like symptoms and ... ...

Abstract	Parkinson's disease (PD) is a ubiquitous brain cell degeneration disease and presents a significant therapeutic challenge. By injecting 6-hydroxydopamine (6-OHDA) into the left medial forebrain bundle, rats were made to exhibit PD-like symptoms and treated by intranasal administration of a low-dose (2 × 10
Language	English
Publishing date	2024-02-24
Publishing country	Poland
Document type	Journal Article
ZDB-ID	2817958-4
ISSN	2391-5412 ; 2391-5412
ISSN (online)	2391-5412
ISSN	2391-5412
DOI	10.1515/biol-2022-0834
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Article: Transcranial low-intensity ultrasound stimulation for treating central nervous system disorders: A promising therapeutic application.

Hu, Yun-Yun / Yang, Gang / Liang, Xue-Song / Ding, Xuan-Si / Xu, De-En / Li, Zhe / Ma, Quan-Hong / Chen, Rui / Sun, Yan-Yun

Frontiers in neurology

2023 Volume 14, Page(s) 1117188

Abstract: Transcranial ultrasound stimulation is a neurostimulation technique that has gradually attracted the attention of researchers, especially as a potential therapy for neurological disorders, because of its high spatial resolution, its good penetration ... ...

Abstract	Transcranial ultrasound stimulation is a neurostimulation technique that has gradually attracted the attention of researchers, especially as a potential therapy for neurological disorders, because of its high spatial resolution, its good penetration depth, and its non-invasiveness. Ultrasound can be categorized as high-intensity and low-intensity based on the intensity of its acoustic wave. High-intensity ultrasound can be used for thermal ablation by taking advantage of its high-energy characteristics. Low-intensity ultrasound, which produces low energy, can be used as a means to regulate the nervous system. The present review describes the current status of research on low-intensity transcranial ultrasound stimulation (LITUS) in the treatment of neurological disorders, such as epilepsy, essential tremor, depression, Parkinson's disease (PD), and Alzheimer's disease (AD). This review summarizes preclinical and clinical studies using LITUS to treat the aforementioned neurological disorders and discusses their underlying mechanisms.
Language	English
Publishing date	2023-03-08
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564214-5
ISSN	1664-2295
ISSN	1664-2295
DOI	10.3389/fneur.2023.1117188
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Article ; Online: Effects of sleep fragmentation on white matter pathology in a rat model of cerebral small vessel disease.

Fu, Xiang / Wan, Xiao-Jie / Liu, Jun-Yi / Sun, Qian / Shen, Yun / Li, Jie / Mao, Cheng-Jie / Ma, Quan-Hong / Wang, Fen / Liu, Chun-Feng

Sleep

2023 Volume 47, Issue 4

Abstract: Study objectives: Mounting evidence indicated the correlation between sleep and cerebral small vessel disease (CSVD). However, little is known about the exact causality between poor sleep and white matter injury, a typical signature of CSVD, as well as ... ...

Abstract	Study objectives: Mounting evidence indicated the correlation between sleep and cerebral small vessel disease (CSVD). However, little is known about the exact causality between poor sleep and white matter injury, a typical signature of CSVD, as well as the underlying mechanisms. Methods: Spontaneously hypertensive rats (SHR) and control Wistar Kyoto rats were subjected to sleep fragmentation (SF) for 16 weeks. The effects of chronic sleep disruption on the deep white matter and cognitive performance were observed. Results: SHR were validated as a rat model for CSVD. Fragmented sleep induced strain-dependent white matter abnormalities, characterized by reduced myelin integrity, impaired oligodendrocytes precursor cells (OPC) maturation and pro-inflammatory microglial polarization. Partially reversible phenotypes of OPC and microglia were observed in parallel following sleep recovery. Conclusions: Long-term SF-induced pathological effects on the deep white matter in a rat model of CSVD. The pro-inflammatory microglial activation and the block of OPC maturation may be involved in the mechanisms linking sleep to white matter injury.
MeSH term(s)	Rats ; Animals ; White Matter ; Sleep Deprivation ; Rats, Inbred SHR ; Sleep ; Rats, Inbred WKY ; Cerebral Small Vessel Diseases/complications ; Cerebral Small Vessel Diseases/pathology
Language	English
Publishing date	2023-08-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	424441-2
ISSN	1550-9109 ; 0161-8105
ISSN (online)	1550-9109
ISSN	0161-8105
DOI	10.1093/sleep/zsad225
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Zs.A 1475: Show issues

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Article ; Online: Alzheimer's disease: amyloid-based pathogenesis and potential therapies.

Zhou, Yixiu / Sun, Yuhui / Ma, Quan-Hong / Liu, Yaobo

Cell stress

2018 Volume 2, Issue 7, Page(s) 150–161

Abstract: Alzheimer's disease is one of the most severe neurodegenerative diseases among elderly people. Different pathogenic factors for Alzheimer's disease have been posited and studied in recent decades, but no effective treatment has been found, necessitating ... ...

Abstract	Alzheimer's disease is one of the most severe neurodegenerative diseases among elderly people. Different pathogenic factors for Alzheimer's disease have been posited and studied in recent decades, but no effective treatment has been found, necessitating further studies. In this Viewpoint article, we assess studies on the mechanisms underlying the accumulation of amyloid (Aβ) peptide and the formation of Aβ oligomers because their accumulation in amyloid plaques in brain tissue has become a well-studied hallmark of Alzheimer's disease. We focus on the production of Aβ and its impact on the function of synapses and neural circuits, and also discuss the clinical prospects for amyloid-targeted therapies.
Language	English
Publishing date	2018-06-29
Publishing country	Austria
Document type	Journal Article
ISSN	2523-0204
ISSN (online)	2523-0204
DOI	10.15698/cst2018.07.143
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Article ; Online: Advances in intranasal application of stem cells in the treatment of central nervous system diseases.

Zhang, Yu-Ting / He, Kai-Jie / Zhang, Jin-Bao / Ma, Quan-Hong / Wang, Fen / Liu, Chun-Feng

Stem cell research & therapy

2021 Volume 12, Issue 1, Page(s) 210

Abstract: Stem cells are characterized by their self-renewal and multipotency and have great potential in the therapy of various disorders. However, the blood-brain barrier (BBB) limits the application of stem cells in the therapy of neurological disorders, ... ...

Abstract	Stem cells are characterized by their self-renewal and multipotency and have great potential in the therapy of various disorders. However, the blood-brain barrier (BBB) limits the application of stem cells in the therapy of neurological disorders, especially in a noninvasive way. It has been shown that small molecular substances, macromolecular proteins, and even stem cells can bypass the BBB and reach the brain parenchyma following intranasal administration. Here, we review the possible brain-entry routes of transnasal treatment, the cell types, and diseases involved in intranasal stem cell therapy, and discuss its advantages and disadvantages in the treatment of central nervous system diseases, to provide a reference for the application of intranasal stem cell therapy.
MeSH term(s)	Administration, Intranasal ; Blood-Brain Barrier ; Brain ; Central Nervous System Diseases/drug therapy ; Drug Delivery Systems ; Humans ; Stem Cells
Language	English
Publishing date	2021-03-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2548671-8
ISSN	1757-6512 ; 1757-6512
ISSN (online)	1757-6512
ISSN	1757-6512
DOI	10.1186/s13287-021-02274-0
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Article ; Online: Repairing neural injuries using human umbilical cord blood.

Sun, Tao / Ma, Quan-Hong

Molecular neurobiology

2012 Volume 47, Issue 3, Page(s) 938–945

Abstract: Stem cells are promising sources for repairing damaged neurons and glial cells in neural injuries and for replacing dead cells in neurodegenerative diseases. An essential step for stem cell-based therapy is to generate large quantities of stem cells and ... ...

Abstract	Stem cells are promising sources for repairing damaged neurons and glial cells in neural injuries and for replacing dead cells in neurodegenerative diseases. An essential step for stem cell-based therapy is to generate large quantities of stem cells and develop reliable culture conditions to direct efficient differentiation of specific neuronal and glial subtypes. The human umbilical cord and umbilical cord blood (UCB) are rich sources of multiple stem cells, including hematopoietic stem cells, mesenchymal stem cells, unrestricted somatic stem cells, and embryonic-like stem cells. Human UC/UCB-derived cells are able to give rise to multiple cell types of neural lineages. Studies have shown that UCB and UCB-derived cells can survive in injured sites in animal models of ischemic brain damage and spinal cord injuries, and promote survival and prevent cell death of local neurons and glia. Human UCB is easy to harvest and purify. Moreover, unlike embryonic stem cells, the use of human UCB is not limited by ethical quandaries. Therefore, human UCB is an attractive source of stem cells for repairing neural injuries.
MeSH term(s)	Animals ; Fetal Blood/cytology ; Humans ; Nerve Regeneration ; Neurons/pathology ; Stem Cell Transplantation ; Stem Cells/cytology
Language	English
Publishing date	2012-12-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-012-8388-0
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Zs.A 2411: Show issues

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Article ; Online: TRIM32 Deficiency Impairs the Generation of Pyramidal Neurons in Developing Cerebral Cortex.

Sun, Yan-Yun / Chen, Wen-Jin / Huang, Ze-Ping / Yang, Gang / Wu, Ming-Lei / Xu, De-En / Yang, Wu-Lin / Luo, Yong-Chun / Xiao, Zhi-Cheng / Xu, Ru-Xiang / Ma, Quan-Hong

Cells

2022 Volume 11, Issue 3

Abstract: Excitatory-inhibitory imbalance (E/I) is a fundamental mechanism underlying autism spectrum disorders (ASD). TRIM32 is a risk gene genetically associated with ASD. The absence of TRIM32 causes impaired generation of inhibitory GABAergic interneurons, ... ...

Abstract	Excitatory-inhibitory imbalance (E/I) is a fundamental mechanism underlying autism spectrum disorders (ASD). TRIM32 is a risk gene genetically associated with ASD. The absence of TRIM32 causes impaired generation of inhibitory GABAergic interneurons, neural network hyperexcitability, and autism-like behavior in mice, emphasizing the role of TRIM32 in maintaining E/I balance, but despite the description of TRIM32 in regulating proliferation and differentiation of cultured mouse neural progenitor cells (NPCs), the role of TRIM32 in cerebral cortical development, particularly in the production of excitatory pyramidal neurons, remains unknown. The present study observed that TRIM32 deficiency resulted in decreased numbers of distinct layer-specific cortical neurons and decreased radial glial cell (RGC) and intermediate progenitor cell (IPC) pool size. We further demonstrated that TRIM32 deficiency impairs self-renewal of RGCs and IPCs as indicated by decreased proliferation and mitosis. A TRIM32 deficiency also affects or influences the formation of cortical neurons. As a result, TRIM32-deficient mice showed smaller brain size. At the molecular level, RNAseq analysis indicated reduced Notch signalling in TRIM32-deficient mice. Therefore, the present study indicates a role for TRIM32 in pyramidal neuron generation. Impaired generation of excitatory pyramidal neurons may explain the hyperexcitability observed in TRIM32-deficient mice.
MeSH term(s)	Animals ; Cerebral Cortex/cytology ; Mice ; Neural Stem Cells/cytology ; Neurogenesis/genetics ; Neurons/cytology ; Pyramidal Cells/cytology ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	TRIM32 protein, mouse (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2022-01-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11030449
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