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Novel indanone derivatives as probes for senile plaques in Alzheimer's disease

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Novel indanone derivatives as probes for senile plaques in A...

Imaging and Spectral Characteristics of Amyloid Plaque Autofluorescence in Brain Slices from the APP/PS1 Mouse Model of Alzheimer’s Disease

中国神经科学学会第十届全国学术会议

作者： Dou-Dou NAN Chang-Sheng GAN Chen-Wei WANG Jin-Ping QIAO Jiang-Ning ZHOU CAS Key Laboratory of Brain Function and Disease School of Life SciencesUniversity of Science and Technology of China Engineering Research Center of Bio-process of Ministry of Education Hefei University of Technology

Objectives senile plaques(SPs) is one of the main pathological feature of Alzheimer’s disease that composed of p-amyloid(Aβ) protein *** detection of SPs is an effective method for the early diagnosis of Alzheimer’s *** our published work,we developed a series of indanone derivatives with high affinity to senile plaques in vitro and ex *** on that,several novel indanone derivatives were synthesized with optimization in functional *** We designed and synthesized two indanone *** K value was measured by the competitive radioligand binding assay with Aβ aggregates,and the radioligand was[I]IMPY[3].Fluorescent staining of Br-NID and I-NID to human AD brain tissue slices was detected by fluorescence microscope.[I]I-NTD was synthesized,and purified by *** Coefficient Measurement was obtained from[I]*** of[I]I-NTD was measured by ICR mice in different period.[I]I-NID was mixed with tissue homogenates and detected by HPLC to study the stability in *** AD brain tissue slice was labeled by[I]I-NTD and exposed to X-ray film to obtain the autoradiography in *** Br-NID and I-NID exhibited the K value of 6.65 and 11.83 nM with Aβ aggregates competed with[I]*** AD brain tissue fluorescent staining,both Br-NID and I-NID were specific binding to *** log P value of[I]I-NTD is *** biodistribution in ICR mice,[I]I-NID displayed the concentration of 5.28%ID at 2 min and 0.84%ID at 60min post-injection in *** human AD and control brain homogenates,the percentage of unchanged[I]I-NTD is 98%at 60min and 95%at120min.[I]I-NID labeled SPs of human AD brain tissue slice in vitro *** The K value shows high affinity of Br-NID and I-NID to Aβ aggregates,and the increase of log P value leads to the improvement of initial brain uptake.[I]I-NID is stable in human AD and control brain homogenates from 2 min to 120 *** staining and autoradiography d

关键词： Alzheimer’s disease senile plaques indanone derivatives PET

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Neuroscience Bulletin 2019年第6期35卷 1126-1137页

作者： Yunling Gao Qing Liu Lingling Xu Ning Zheng Xiaoming He Fuqiang Xu Research Section Xiangyang Central HospitalAffiliated Hospital of Hubei University of Arts and ScienceXiangyang 441021China Center for Brain Science State Key Laboratory of Magnetic Resonance and Atomic Molecular PhysicsNational Center for Magnetic Resonance in WuhanKey Laboratory of Magnetic Resonance in Biological SystemsWuhan Institute of Physics and MathematicsChinese Academy of SciencesWuhan 430071China National Center for Magnetic Resonance in Wuhan State Key Laboratory of Magnetic Resonance and Atomic and Molecular PhysicsWuhan Institute of Physics and MathematicsChinese Academy of SciencesWuhan 430071China Neurology Department Xiangyang Central HospitalAffiliated Hospital of Hubei University of Arts and ScienceXiangyang 441021China Wuhan National Laboratory for Optoelectronics Wuhan 430074China

Amyloid deposits are one of the hallmark pathological lesions of Alzheimer's disease(AD). They can be visualized by thioflavin-S, silver impregnation,Congo red staining, and immunohistochemical ***, that amyloid deposits generate blue autofluorescence(auto-F) has been ignored. Here, we report that visible light-induced auto-F of senile plaques(SPs) was detected and validated with conventional methods. Brain slices from APP/PS1(amyloid precursor protein/presenilin1) transgenic mice were mounted on slides, rinsed,coverslipped and observed for details of the imaging and spectral characteristics of the auto-F of SPs. Then the slices were treated with the above classic methods for comparative validation. We found that the SP auto-F was greatest under blue-violet excitation with a specific emission spectrum, and was much easier, more sensitive, and reliable than the classic methods. Because it does not damage slices, observation of auto-F can be combined with all post-staining techniques in slices and for brain-wide imaging in AD.

关键词： Alzheimer's disease Amyloid deposits senile plaques Autofluorescence Spectral imaging Glial activation

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Degenerative alterations in noradrenergic neurons of the locus coeruleus in Alzheimer's disease

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Neural Regeneration Research 2013年第24期8卷 2249-2255页

作者： Lihua Liu Saiping Luo Leping Zeng Weihong Wang Liming Yuan Xiaohong Jian Department of Histology & Embryology School of Basic Medical Sciences Central South University Department of Nursing Medical College of Hunan Normal University Third Department of Surgery Agricultural Division Four Hospital Xinjiang Production and Construction Corps Department of Anatomy & Neurobiology School of Basic Medical Sciences Central South University Department of Anatomy Medical College of Hunan Normal University

Mice carrying mutant amyloid precursor protein and presenilin-1 genes （APP/PS1 double trans- genic mice） have frequently been used in studies of Alzheimer＇s disease; however, such studies have focused mainly on hippocampal and cortical changes. The severity of Alzheimer＇s disease is known to correlate with the amount of amyloid-13 protein deposition and the number of dead neurons in the locus coeruleus. In the present study, we assigned APP/PS1 double transgenic mice to two groups according to age： young mice （5-6 months old） and aged mice （16-17 months old）. Age-matched wild-type mice were used as controls. Immunohistochemistry for tyrosine hydroxylase （a marker of catecholaminergic neurons in the locus coeruleus） revealed that APP/PS1 mice had 23% fewer cells in the locus coeruleus compared with aged wild-type mice. APP/PS1 mice also had increased numbers of cell bodies of neurons positive for tyrosine hydroxylase, but fewer tyrosine hydroxylase-positive fibers, which were also short, thick and broken. Quantitative analysis using unbiased stereology showed a significant age-related increase in the mean volume of tyrosine hy- droxylase-positive neurons in aged APP/PS1 mice compared with young APP/PS1 mice. Moreover, the mean volume of tyrosine hydroxylase-positive neurons was positively correlated with the total volume of the locus coeruleus. These findings indicate that noradrenergic neurons and fibers in the locus coeruleus are predisposed to degenerative alterations in APP/PS1 double transgenic mice.

关键词： neural regeneration presenilin-1 Alzheimer's disease tyrosine hydroxylase locus coeruleus noradrenergic neuron ^-amyloid senile plaques grants-supported paper neuroregeneration

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The origin and development of plaques and phosphorylated tau are associated with axonopathy in Alzheimer’s disease

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Neuroscience Bulletin 2011年第5期27卷 287-299页

作者：肖爱武何敬王茜罗艺孙燕周艳平官阳 Paul J.Lucassen 戴甲培中南民族大学武汉神经科学和神经工程研究所武汉430074 阿姆斯特丹大学生命科学研究所神经科学研究中心华中科技大学同济医学院病理学系超微病理研究室武汉430030

Objective The production of neurotoxic β-amyloid and the formation of hyperphosphorylated tau are thought to be critical steps contributing to the neuropathological mechanisms in Alzheimer’s disease （AD）. However, there remains an argument as to their importance in the onset of *** studies have shown that axonopathy is considered as an early stage of AD. However, the exact relationship between axonopathy and the origin and development of classic neuropathological changes such as senile plaques （SPs） and neurofibrillary tangles （NFTs） is unclear. The present study aimed to investigate this relationship. Methods Postmortem tracing, combined with the immunohistochemical or immunofluo-rescence staining, was used to detect axonopathy and the formation of SPs and NFTs. Results ＂Axonal leakage＂–a novel type of axonopathy, was usually accompanied with the extensive swollen axons and varicosities, and was associated with the origin and development of Aβ plaques and hyperphosphorylated tau in the brains of AD patients. Conclusion Axonopathy, particularly axonal leakage, might be a key event in the initiation of the neuropathological processes in AD.

关键词： Alzheimer’s disease axonopathy senile plaques neurofibrillary tangles postmortem tracing

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Dcf1 Deletion Improves the Cognitive Ability in AD Mice

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神经药理学报 2019年第Z1期 105-106页

作者： LI Wei-hao WANG Jiao FENG Rui-li WEN Tie-qiao Laboratory of Molecular Neural Biology School of Life SciencesShanghai University

Objective:Alzheimer's disease(AD) is a progressive neurodegenerative disease that affects more than 40 million people worldwide. One of the characteristics of AD is the accumulation of the β-amyloid(Aβ) derived from proteolytic fragment of APP. senile plaques caused by the aggregation of Aβ can lead to synaptic damage and neuronal loss,eventually leads to a decline in cognitive ability and a lack of learning and memory. However,the cause leading to Aβ aggregation is not well understood. It has been found that dendritic cytokine 1(Dcf1) is highly expressed in the olfactory cortical neurons in AD patients. Whole-genome DNA methylation profiles in the frontal cortex showed a 7.3% reduction in Dcf1 promoter methylation in AD patients. We therefore hypothesized that dcf1 plays an important role in Aβ aggregation during AD development. Methods:In this study,APP-PS1 mice were used as an AD model in which dcf1 gene was knockouted by crossing with dcf1 KO mice. We examined the molecular mechanism of dcf1 by detecting changes in APP,BACE1(β-secretase 1) and Aβ expression,and then stained with Thioflavin S and immunofluorescence to detect the formation of senile plaques,and finally detected learning and memory in AD-dcf1 KO mice. Results:We found a high expression of Dcf1 in hippocampus and prefrontal lobe in APP-PS1 mice,while knockout of dcf1 from APP-PS1 mice significantly improves cognitive ability. Analysis of APP,BACE1 and Aβ levels in APP-PS1-Dcf1-/-mice suggested that knockout of Dcf1 up-regulated APP and down-regulated Aβ but did not affect BACE1. Staining with Thioflavin S showed that knockout of Dcf1 reduced the deposition of Aβ in the hippocampus. Moreover,deletion of Dcf1 rescued the protein level of AMPA Receptor(GluA2) in the hippocampus of APP-PS1 mice. Immunofluorescence revealed co-localization of dcf1 and senile plaques in APP-PS1 mice and AD patients. Furthermore,UV Spectroscopy assay showed that dcf1 contributed to Aβ aggregation in vitro. Finally,stereota

关键词： Alzheimer’s disease dcf1 β-amyloid senile plaques APP-PS1

Intracerebroventricular Injection of Tumor Necrosis Factor-alpha Monoclonal Antibody(Infliximab) Reduce Cerebral Amyloid plaques in Aged APP/PS1 Double Transgenic Mouse

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Intracerebroventricular Injection of Tumor Necrosis Factor-a...

Pathological and biochemical alterations of astrocytes in ovariectomized rats injected with D-galactose: A potential contribution to Alzheimer's disease processes

2009全国抗衰老与老年痴呆学术会议

作者： Jian-quan Shi Jun Xu Ying-dong Zhang Jun Chen Qiao-quan Zhang 南京医科大学南京脑科医院神经科

Objective To investigate whether tumor necrosis factor-alpha monoclonal antibody(Infliximab) can directly reduce amyloid plaques by intracerebroventricular(ICV) injection in ***,we try to explore the time-course effec... 详细信息

关键词： tumor necrosis factor-alpha Alzheimer’s Disease Infliximab senile plaques APP/PS1 double transgenic mouse

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南京医科大学学报(自然科学版) 2008年第5期 574-574页

作者： Hua, X. D. Lei, M. Ding, H. Han, Q. Y. Hu, G. Xiao, M. Nanjing Med Univ, Dept Anat Histol & Pharmacol, Jiangsu Prov Key Lab Neurodegenerat, Nanjing 210029, Peoples R China

Astrocytes are implicated in the pathological changes of Alzheimer's disease. Our previous studies have demonstratedthat estrogen deprivation and oxidative stress act synergistically to accelerate0 the progress of Alzheimer's disease. Long-term D-galac-tose injection combined with ovariectomy may serve as a rodent model for Alzheimer's disease. To address the potential contributionof astroglia to the Alzheimer's disease pathogenesis, we investigated pathological and biochemical alterations of astrocytes under thisanimal model. Ovadectomized rats injected with D-galactose for 2 weeks showed extensive localization of glial fibrillary acidic proteinimmunoreactive astrocytes and slightly elevated glutathione levels in the hippocampus without significant impairments in the watermaze test and deficits of the cholinergic analyses, compared to the saline-injected rats. Ovariectomized rats injected with D-galactosefor 6 weeks, however, exhibited degeneration of astrocytes and decreased glutathione levels in the hippocampus, accompanied withsevere dysfunction of behavioral test and deficiency of cholinergic terminals. Electron microscopy further confirmed the pathologicalchanges of astrocytes, especially in the aggregated area of synapse and brain microvessels. Consistent with degeneration of perivascu-lar astrocytic endfeet, analysis of the horseradish peroxidase demonstrated an impairment of the blood-brain barrier *** findings indicate that biochemical and pathological alterations of astrocytes may partially contribute to exacerbating neuronaldeficits in the course of Alzheimer's disease. Restoring neuroprotective potential of astrocytes may be a useful therapeutic target forAlzheimer's disease and other neurodegenerative diseases.

关键词： Alzheimer’s disease astrocytes estrogen deprivation oxidative stress rats blood-brain-barrier senile plaques estrogen mice neuroprotection expression cortex acetylcholinesterase neurodegeneration innervation