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Detection of Femtomolar Amyloid-β Peptides for Early-Stage Identification of Alzheimer’s Amyloid-β Aggregation with Functionalized Gold Nanoparticles

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ACS Applied Materials and Interfaces 2024年第3期16卷 3819-3828页

作者： Chang, Yu-Jen Chien, Yi-Hsin Chang, Chieh-Chun Wang, Pei-Ning Chen, Yun-Ru Chang, Yun-Chorng Genomics Research Center Academia Sinica Taipei115 Taiwan Taiwan International Graduate Program in Interdisciplinary Neuroscience National Taiwan University and Academia Sinica Taipei115 Taiwan Research Center for Applied Sciences Academia Sinica Taipei115 Taiwan Department of Physics National Taiwan University Taipei106 Taiwan Nano Science and Technology Program Taiwan International Graduate Program Academia Sinica and National Taiwan University Taipei115 Taiwan Brain Research Center National Yang Ming Chiao Tung University Taipei112 Taiwan Division of General Neurology Department of Neurological Institute Taipei Veterans General Hospital Taipei112 Taiwan

Progressive amyloid-β (Aβ) fibrillar aggregates have long been considered as the pathogenesis of Alzheimer’s disease (AD). Biocompatible and stable cysteine-Aβ peptide-conjugated gold nanoparticles (Cys-Aβ@AuNP) are demonstrated as suitable materials for detecting subfemtomolar Aβ peptides in human plasma. Incubation with Aβ peptides causes the Cys-Aβ@AuNP to aggregate and changes its absorption spectra. The spectral change is especially apparent and noticeable when detecting subfemtomolar Aβ peptides, and the aggregates contain only two or three AuNPs. Cys-Aβ@AuNP can also be used to identify early-stage Aβ oligomerization, which is not possible using the conventional method, in which the fluorescence of thioflavin-T is measured. The ability to detect Aβ oligomerization can facilitate therapeutics for AD. In addition, the binding of Aβ peptides by Cys-Aβ@AuNP in combination with centrifugation redirects the conventional Aβ aggregation pathway and can effectively inhibit the formation of toxic Aβ oligomers or fibrils. Therefore, the proposed Cys-Aβ@AuNP can also be used to develop effective therapeutic agents to inhibit Aβ aggregation. The results obtained in this study are expected to open revolutionary ways to both detect and inhibit Aβ aggregation at an early stage. © 2024 American Chemical Society

关键词： Oligomers

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In the presence of danger: the extracellular matrix defensive response to central nervous system injury

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Neural Regeneration Research 2014年第4期9卷 377-384页

作者： Lyn B.Jakeman Kent E.Williams Bryan Brautigam Department of Physiology and Cell Biology Ohio State University Wexner Medical CenterColumbusOHUSA Neuroscience Graduate Studies Program Ohio State University Wexner Medical CenterColumbusOHUSA Biomedical Research Graduate Program Ohio State University Wexner Medical CenterColumbusOHUSA OSU Center for Brain and Spinal Cord Repair Ohio State University Wexner Medical CenterColumbusOHUSA

Glial cells in the central nervous system （CNS） contribute to formation of the extracellular matrix, which provides adhesive sites, signaling molecules, and a diffusion barrier to enhance efficient on and axon potential propagation. In the normal adult CNS, the extracellular matrix （ECM） is relatively stable except in selected regions characterized by dynamic remodeling. However, after trauma such as a spinal cord injury or cortical contusion, the lesion epicenter becomes a focus of acute neuroinflammation. The activation of the surrounding glial cells leads to a dramatic change in the composition of the ECM at the edges of the lesion, creating a perilesion environment dominated by growth inhibitory molecules and restoration of the peripheral/ central nervous system border. An advantage of this response is to limit the invasion of damaging cells and diffusion of toxic molecules into the spared tissue regions, but this occurs at the cost of inhibiting migration of endogenous repair cells and preventing axonal regrowth. The following review was prepared by reading and discussing over 200 research articles in the field published in PubMed and selecting those with significant impact and/or controversial points. This article highlights structural and functional features of the normal adult CNS ECM and then focuses on the reactions of glial cells and changes in the perilesion border that occur following spinal cord or contusive brain injury. Current research strategies directed at modifying the inhibitory perilesion microenvironment without eliminating the protective functions of glial cell activation are discussed.

关键词： nerve regeneration glial scar proteoglycan axon growth spinal cord injury contusion inhibitory inflammation astrocyte macrophage neural regeneration

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Linking cellular mechanisms to behavior: Entorhinal persistent spiking and membrane potential oscillations may underlie path integration, grid cell firing, and episodic memory

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Neural Plasticity 2008年第1期2008卷 658323页

作者： Hasselmo, Michael E. Brandon, Mark P. Center for Memory and Brain Department of Psychology and Program in Neuroscience Boston University Boston MA 02215 2 Cummington Sreet United States

The entorhinal cortex plays an important role in spatial memory and episodic memory functions. These functions may result from cellular mechanisms for integration of the afferent input to entorhinal cortex. This article reviews physiological data on persistent spiking and membrane potential oscillations in entorhinal cortex then presents models showing how both these cellular mechanisms could contribute to properties observed during unit recording, including grid cell firing, and how they could underlie behavioural functions including path integration. The interaction of oscillations and persistent firing could contribute to encoding and retrieval of trajectories through space and time as a mechanism relevant to episodic memory.

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Magnetic resonance spectroscopy and the menstrual cycle: A multi-centre assessment of menstrual cycle effects on GABA & GSH

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Journal of neuroscience Methods 2025年 418卷 110430页

作者： Song, Yulu Prisciandaro, James J. Apšvalka, Dace Bernard, Mae Berrington, Adam Castelo-Branco, Miguel Britton, Mark K. Correia, Marta M. Cuypers, Koen Domagalik, Aleksandra Dydak, Ulrike Duncan, Niall W. Dwyer, Gerard E. Gong, Tao Greenhouse, Ian Hat, Katarzyna Hehl, Melina Honda, Shiori Horton, Chris Hui, Steve C.N. Jackson, Stephen R. Jones, Daniella L. Klan, Maren S. Lyoo, In Kyoon Mada, Marius O. McNamara, Bronte V. Mullins, Paul G. Muska, Emlyn Nakajima, Shinichiro Nishio, Hayami Pereira, Andreia C. Porges, Eric C. Rowsell, Michelle Ruopp, Rubi Shortell, Destin D. Smith, Caitlin M. Swinnen, Stephan Šušnjar, Antonia Tseng, Lin-Yuan Violante, Ines R. Yoon, Sujung Edden, Richard A.E. Dyke, Katherine Russell H. Morgan Department of Radiology and Radiological Science The Johns Hopkins University School of Medicine Baltimore MD United States F. M. Kirby Research Center for Functional Brain Imaging Kennedy Krieger Institute Baltimore MD United States Addiction Sciences Division Department of Psychiatry and Behavioral Sciences Medical University of South Carolina Charleston United States MRC Cognition and Brain Sciences Unit University of Cambridge United Kingdom School of Psychology and Sports Sciences Bangor University Bangor United Kingdom Sir Peter Mansfield Imaging Centre School of Physics and Astronomy University of Nottingham Nottingham United Kingdom Institute for Nuclear Sciences Applied to Health (ICNAS) Coimbra Institute for Biomedical Imaging and Translational Research (CIBIT) University of Coimbra Portugal Center for Cognitive Aging and Memory and McKnight Brain Institute University of Florida Gainesville FL United States Neuroplasticity and Movement Control Research Group Rehabilitation Research Institute (REVAL) Hasselt University Diepenbeek Belgium Movement Control & Neuroplasticity Research Group Department of Movement Sciences Group Biomedical Sciences KU Leuven Heverlee Belgium Leuven Brain Institute (LBI) KU Leuven Leuven Belgium Centre for Brain Research Jagiellonian University Krakow Poland School of Health Sciences Purdue University West Lafayette IN United States Department of Radiology and Imaging Sciences Indiana University School of Medicine Indianapolis IN United States Graduate Institute of Mind Brain and Consciousness Taipei Medical University Taipei Taiwan Brain and Consciousness Research Centre TMU Shuang-Ho Hospital New Taipei City Taiwan Department of Biological and Medical Psychology University of Bergen Bergen Norway NORMENT Centre of Excellence Haukeland University Hospital Bergen Norway Departments of Radiology Shandong Provincial Hospital Affiliated to Shandong First Medical University Shandong Jinan China D

Background: Gamma-aminobutyric acid (GABA) and glutathione (GSH) play a significant role in the functioning of a healthy brain and can both be quantified using magnetic resonance spectroscopy (MRS). Several small-scale studies have suggested MRS measured GABA may fluctuate with the menstrual cycle, but the effects on GSH are unknown. Utilising recent developments in MRS acquisition, this multi-lab study explores this issue across 4 distinctive brain regions. New methods: Data were analysed from 12 independent sites from which a total of 30 women were scanned during three phases of their menstrual cycle corresponding to early follicular, ovulation and mid luteal phases. HERMES and HERCULES sequences were used to measure GABA and GSH in voxels located in the left motor cortex, left posterior insular, medial parietal and medial frontal. Linear mixed models were used to assess the variability contributed by site, participant and menstrual cycle phase. Results: Similar variance was attributed to site and menstrual cycle phase for both GABA and GSH data. No systematic changes in GABA or GSH were revealed for any voxel as a consequence of menstrual cycle phase. Comparison with existing methods: Despite our larger sample size and inclusion of more brain regions we fail to replicate previous findings of GABA change as a consequence of menstrual cycle phase. We also show for the first time that MRS measures of GSH so not significantly alter with cycle. Conclusions: Our findings suggest that the menstrual cycle has minimal impact on MRS measures of GABA and GSH. The presence of a menstrual cycle should not be used as justification for exclusion of women in MRS studies. © 2025 The Authors

关键词： Gamma-aminobutyric acid (GABA) Glutathione (GSH) Hadamard Encoding and Reconstruction of MEGA-Edited Magnetic resonance, spectroscopy (MRS) Menstrual cycle Oestrogen Spectroscopy (HERMES)

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A structural haplotype in the 17q21.31 MAPT region is associated with increased risk for chronic traumatic encephalopathy endophenotypes

Cell Reports Medicine

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Cell Reports Medicine 2025年第5期6卷 102084-102084页

作者： Han, Xudong Zhang, Yichi Petrosky, Jillian N. Bald, Sarah Sherva, Richard M. Labadorf, Adam Cherry, Jonathan D. Chung, Jaeyoon Farrell, Kurt Abdolmohammadi, Bobak Durape, Shruti Martin, Brett M. Palmisano, Joseph N. Farrell, John J. Alvarez, Victor E. Huber, Bertrand R. Dwyer, Brigid Daneshvar, Daniel H. Jun, Gyungah R. Lunetta, Kathryn L. Goldstein, Lee E. Katz, Douglas I. Cantu, Robert C. Shenton, Martha E. Cummings, Jeffrey L. Reiman, Eric M. Stern, Robert A. Alosco, Michael L. Tripodis, Yorghos Farrer, Lindsay A. Stein, Thor D. Crary, John F. McKee, Ann C. Mez, Jesse Bioinformatics Graduate Program Boston University Boston MA United States Section of Biomedical Genetics Department of Medicine Boston University Chobanian & Avedisian School of Medicine Boston MA United States Department of Neurology Boston University Chobanian & Avedisian School of Medicine Boston MA United States Boston University Alzheimer's Disease Research Center Boston University Chobanian & Avedisian School of Medicine Boston MA United States Boston VA Healthcare System Boston MA United States Boston University Chronic Traumatic Encephalopathy Center Boston University Boston MA United States Department of Pathology and Laboratory Medicine Boston University Chobanian & Avedisian School of Medicine Boston MA United States Departments of Pathology Neuroscience and Artificial Intelligence & Human Health Neuropathology Brain Bank & Research CoRE Friedman Brain Institute Ronald M. Loeb Center for Alzheimer's Disease Icahn School of Medicine at Mount Sinai New York NY United States Biostatistics and Epidemiology Data Analytics Center Boston University School of Public Health Boston MA United States Bedford VA Healthcare System Bedford MA United States Braintree Rehabilitation Hospital Braintree MA United States Department of Physical Medicine and Rehabilitation Harvard Medical School Boston MA United States Department of Rehabilitation and Human Performance Brain Injury Research Center Icahn School of Medicine at Mount Sinai New York NY United States Department of Neurology Icahn School of Medicine at Mount Sinai New York NY United States Department of Biostatistics Boston University School of Public Health Boston MA United States Department of Ophthalmology Boston University Chobanian & Avedisian School of Medicine Boston MA United States Departments of Biomedical Electrical & Computer Engineering Boston University College of Engineering Boston MA United States Departments of Radiology and Psychiatry Boston University Chobanian & Avedisia

Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy associated with repetitive head impact (RHI) exposure. Genetic variation in the 17q21.31 region, containing microtubule-associated protein tau (MAPT), has been implicated in tauopathies but has not been investigated in CTE. The region includes a megabase-long inversion (H1/H2) and copy-number variations, including α, β, and γ segments, which can be characterized as nine segregating structural haplotypes. We leveraged array SNP data and a reference panel across the 17q21.31 region to impute structural haplotypes and test their association with CTE endophenotypes in 447 European ancestry brain donors with RHI exposure. The H1β1γ1 haplotype was significantly associated with dementia and semi-quantitative tau burden in multiple cortical and medial temporal regions commonly affected in CTE. H1β1γ1 differential expression analyses in dorsolateral frontal cortex implicated cis-acting genes and inflammatory pathways. Taken together, the H1β1γ1 haplotype may help explain CTE heterogeneity among those with similar RHI exposure. © 2025 The Authors

关键词： 17q21.31 chronic traumatic encephalopathy dementia differential gene expression immune system MAPT repetitive head impacts structural haplotypes tauopathy traumatic brain injury

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Adult Hippocampal Neurogenesis in Aging and Alzheimer's Disease

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Stem Cell Reports 2021年第4期16卷 681-693页

作者： Babcock, Kelsey R. Page, John S. Fallon, Justin R. Webb, Ashley E. Graduate Program in Neuroscience Brown University Providence 02912 RI United States Warren Alpert Medical School of Brown University Providence 02912 RI United States Department of Neuroscience Brown University Providence 02912 RI United States Carney Institute for Brain Science Brown University Providence 02912 RI United States Center for Translational Neuroscience Brown University Providence 02912 RI United States Department of Molecular Biology Cell Biology and Biochemistry Brown University Providence 02912 RI United States Center on the Biology of Aging Brown University Providence 02912 RI United States

Cognitive deficits associated with Alzheimer's disease (AD) severely impact daily life for the millions of affected individuals. Progressive memory impairment in AD patients is associated with degeneration of the hippocampus. The dentate gyrus of the hippocampus, a region critical for learning and memory functions, is a site of adult neurogenesis in mammals. Recent evidence in humans indicates that hippocampal neurogenesis likely persists throughout life, but declines with age and is strikingly impaired in AD. Our understanding of how neurogenesis supports learning and memory in healthy adults is only beginning to emerge. The extent to which decreased neurogenesis contributes to cognitive decline in aging and AD remains poorly understood. However, studies in rodent models of AD and other neurodegenerative diseases raise the possibility that targeting neurogenesis may ameliorate cognitive dysfunction in AD. Here, we review recent progress in understanding how adult neurogenesis is impacted in the context of aging and AD. © 2021 The Authors

关键词： adult neurogenesis aging Alzheimer's disease cognitive decline neural stem cell

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Predicting the future with a scale-invariant temporal memory for the past

arXiv

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arXiv 2021年

作者： Goh, Wei Zhong Ursekar, Varun Howard, Marc W. Graduate Program in Neuroscience Center for Systems Neuroscience Boston University 610 Commonwealth Avenue United States Department of Physics Center for Systems Neuroscience Boston University 610 Commonwealth Avenue United States Department of Psychological and Brain Sciences Center for Systems Neuroscience Boston University 610 Commonwealth Avenue United States

In recent years it has become clear that the brain maintains a temporal memory of recent events stretching far into the past. This paper presents a neurally-inspired algorithm to use a scale-invariant temporal representation of the past to predict a scale-invariant future. The result is a scale-invariant estimate of future events as a function of the time at which they are expected to occur. The algorithm is time-local, with credit assigned to the present event by observing how it affects the prediction of the future. To illustrate the potential utility of this approach, we test the model on simultaneous renewal processes with different time scales. The algorithm scales well on these problems despite the fact that the number of states needed to describe them as a Markov process grows exponentially. Copyright © 2021, The Authors. All rights reserved.

关键词： Forecasting

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Equilibrative nucleoside transporter 3 supports microglial functions and protects against the progression of Huntington's disease in the mouse model

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brain, Behavior, and Immunity 2024年 120卷 413-429页

作者： Lu, Ying-Sui Hung, Wei-Chien Hsieh, Yu-Ting Tsai, Pei-Yuan Tsai, Tsai-Hsien Fan, Hsiu-Han Chang, Ya-Gin Cheng, Hui-Kuei Huang, Shen-Yan Lin, Hsin-Chuan Lee, Yan-Hua Shen, Tzu-Hsiang Hung, Bing-Yu Tsai, Jin-Wu Dzhagalov, Ivan Cheng, Irene Han-Juo Lin, Chun-Jung Chern, Yijuang Hsu, Chia-Lin Institute of Microbiology and Immunology National Yang Ming Chiao Tung University Taipei Taiwan Taiwan International Graduate Program in Molecular Medicine National Yang Ming Chiao Tung University and Academia Sinica Taipei Taiwan Institute of Brain Science National Yang Ming Chiao Tung University Taipei Taiwan Institute of Biomedical Sciences Academia Sinica Taipei Taiwan Taiwan International Graduate Program in Interdisciplinary Neuroscience National Yang Ming Chiao Tung University and Academia Sinica Taipei Taiwan Biomedical Industry Ph.D. Program National Yang Ming Chiao Tung University Taipei Taiwan Brain Research Center National Yang Ming Chiao Tung University Taipei Taiwan School of Pharmacy College of Medicine National Taiwan University Taipei Taiwan

Huntington's disease (HD) is a hereditary neurodegenerative disorder characterized by involuntary movements, cognitive deficits, and psychiatric symptoms. Currently, there is no cure, and only limited treatments are available to manage the symptoms and to slow down the disease's progression. The molecular and cellular mechanisms of HD's pathogenesis are complex, involving immune cell activation, altered protein turnover, and disturbance in brain energy homeostasis. Microglia have been known to play a dual role in HD, contributing to neurodegeneration through inflammation but also enacting neuroprotective effects by clearing mHTT aggregates. However, little is known about the contribution of microglial metabolism to HD progression. This study explores the impact of a microglial metabolite transporter, equilibrative nucleoside transporter 3 (ENT3), in HD. Known as a lysosomal membrane transporter protein, ENT3 is highly enriched in microglia, with its expression correlated with HD severity. Using the R6/2 ENT3^−/− mouse model, we found that the deletion of ENT3 increases microglia numbers yet worsens HD progression, leading to mHTT accumulation, cell death, and disturbed energy metabolism. These results suggest that the delicate balance between microglial metabolism and function is crucial for maintaining brain homeostasis and that ENT3 has a protective role in ameliorating neurodegenerative processes. © 2024 The Authors

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Prothrombin Kringle-2 induced Microglial Activation Produces Cell Death of Nigral Dopaminergic Neurons in Vivo

Prothrombin Kringle-2 induced Microglial Activation Produces...

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The 7th China-India-Japan-Korea Joint Workshop on Neurobiology and Neuroinformatics 2005

作者： Sang R Kim So Y Won Soung S Kim Tae H Kim Byung K Jin Brain Disease Research Center Neurosdence Graduate Program Ajou University School of Medicine Suwon 442-721 Korea Brain Disease Research Center Neurosdence Graduate Program Ajou University School of Medicine Suwon 442-721 Korea Department of Biochemistry College of Science Yonsei University Seoul 151-742 Korea Department of Biochemistry College of Science Yonsei University Seoul 151-742 Korea Brain Disease Research Center Neuroscience Graduate Program Ajou University School of Medicine Suwon 442-721 Korea

The present study examined whether kringle-2 (Kr-2), a domain of prothrombin distinct from thrombin, could induce microglial activation in vivo and whether activated microglia were implicated in Kr-2-induced degeneration of nigral dopaminergic neurons. Seven days after Intranigral injection of Kr-2, tyrosine hydroxylase (TH) immunohistochemistry showed a significant loss of nigral dopaminergic neurons. In parallel, Kr-2-activated microglia in the substantia nigra (SN) were visualized by immunohistochemical staining. Reverse transcription PCR (RT-PCR) at various time

关键词： Prothrombin Kringle-2 induced Microglial Activation Produces Cell Death of Nigral Dopaminergic Neurons in Vivo

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Opportunities and Challenges from Using Animal Videos in Reinforcement Learning for Navigation

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IFAC-PapersOnLine 2023年第2期56卷 9056-9061页

作者： Vittorio Giammarino James Queeney Lucas C. Carstensen Michael E. Hasselmo Ioannis Ch Paschalidis Division of Systems Engineering Boston University Boston MA 02215 USA Center for Systems Neuroscience Department of Psychological and Brain Sciences and Graduate Program for Neuroscience Boston University Boston MA 02215 USA College of Engineering and Hariri Institute for Computing & Computational Science & Engineering Boston University Boston MA 02215 USA

We investigate the use of animal videos (observations) to improve Reinforcement Learning (RL) efficiency and performance in navigation tasks with sparse rewards. Motivated by theoretical considerations, we make use of weighted policy optimization for off-policy RL and describe the main challenges when learning from animal videos. We propose solutions and test our ideas on a 2D navigation task. We show how the use of animal videos improves performance over RL algorithms that do not leverage such observations.

关键词： Learning for Control Reinforcement Learning Deep Learning RL with demonstrations Imitation Learning Bio-inspired Control

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