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Detecting and Tracking β-Amyloid Oligomeric Forms and Dynamics In Vitro by a High-Sensitivity Fluorescent-Based Assay
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2024-11-29 DOI: 10.1021/acschemneuro.4c0031210.1021/acschemneuro.4c00312
Yanyan Zhao, Oleksandr Brener, Ewa Andrzejewska, Jiapeng Wei, CloudOuterMan Reiß, Ole Tietz, Tuomas P. J. Knowles and Franklin I. Aigbirhio*, 
{"title":"Detecting and Tracking β-Amyloid Oligomeric Forms and Dynamics In Vitro by a High-Sensitivity Fluorescent-Based Assay","authors":"Yanyan Zhao,&nbsp;Oleksandr Brener,&nbsp;Ewa Andrzejewska,&nbsp;Jiapeng Wei,&nbsp;CloudOuterMan Reiß,&nbsp;Ole Tietz,&nbsp;Tuomas P. J. Knowles and Franklin I. Aigbirhio*,&nbsp;","doi":"10.1021/acschemneuro.4c0031210.1021/acschemneuro.4c00312","DOIUrl":"https://doi.org/10.1021/acschemneuro.4c00312https://doi.org/10.1021/acschemneuro.4c00312","url":null,"abstract":"<p >Aggregation of β-amyloid protein is a hallmark pathology of the neurodegenerative disorder Alzheimer’s disease and proceeds from monomers to insoluble misfolded fibril forms via soluble and highly toxic oligomeric intermediates. Given the dual feature of being the most toxic form of the Aβ aggregate proteome and an early marker of pathogenesis, there is a need for sensitive methods that can be used to detect Aβ oligomers and investigate the dynamics of aggregation. Herein, we describe a method based on the application of an oligomer-sensitive fluorescent chemical probe pTP-TFE combined with the use of a QIAD (Quantitative determination of Interference with Aβ Aggregate Size Distribution) assay to correctly identify Aβ oligomers in high sensitivity. pTP-TFE was evaluated and compared to thioflavin T and pFTAA, the two most widely used amyloid fibril dyes, and shown to be the only probe capable of detecting significant differences across all oligomeric species of β-amyloid. Furthermore, by observing changes in pTP-TFE fluorescence emission over time, we could track the dynamics of oligomer populations and thereby obtain kinetic information on the Aβ42 dynamic aggregation model. Therefore, we have established a highly sensitive, readily available, and simple method for studying β-amyloid protein aggregation dynamics.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"15 24","pages":"4383–4389 4383–4389"},"PeriodicalIF":4.1,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/acschemneuro.4c00312","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142843786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Kratom Alkaloids for the Treatment of Alcohol Use Disorder
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2024-11-29 DOI: 10.1021/acschemneuro.4c0067510.1021/acschemneuro.4c00675
Joydip Das*, 
{"title":"Kratom Alkaloids for the Treatment of Alcohol Use Disorder","authors":"Joydip Das*,&nbsp;","doi":"10.1021/acschemneuro.4c0067510.1021/acschemneuro.4c00675","DOIUrl":"https://doi.org/10.1021/acschemneuro.4c00675https://doi.org/10.1021/acschemneuro.4c00675","url":null,"abstract":"<p >Alcohol use disorder (AUD) accounts for nearly 4.7% of all deaths and imposes a huge economic burden on society. Despite the magnitude of the problem, only a few Food and Drug Administration (FDA)/European Medicines Agency (EMA)-approved drugs are currently available for AUD treatment. Despite being efficacious, these drugs are not without problems, adverse effects being a major issue. That combined with medication adherence and compliance problems, the discovery of new drugs is imperative. Kratom (<i>Mitragyna speciosa</i>) alkaloids and some of their semisynthetic derivatives reduce alcohol intake and alcohol-induced withdrawal symptoms in animal models. These compounds act as G-protein-biased ligands at the μ-, δ-, and κ-opioid receptors, and their effect in reducing alcohol intake is mediated through the δ-opioid receptor. This article provides a critical overview of recent preclinical studies involving kratom alkaloids for AUD treatment, with a particular focus on the pharmacology and medicinal chemistry of these alkaloids. FDA/EMA approved drugs, repurposed drugs, and plant-based compounds for the treatment of AUD are briefly mentioned. Finally, important caveats and future research directions on this topic are discussed.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"15 24","pages":"4352–4359 4352–4359"},"PeriodicalIF":4.1,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142843787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Patent Review of Novel Biologics Targeting Opioid Use Disorder (2018–2024)
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2024-11-28 DOI: 10.1021/acschemneuro.4c0069110.1021/acschemneuro.4c00691
Samuel Obeng*, Lance R. McMahon and Edward Ofori*, 
{"title":"Patent Review of Novel Biologics Targeting Opioid Use Disorder (2018–2024)","authors":"Samuel Obeng*,&nbsp;Lance R. McMahon and Edward Ofori*,&nbsp;","doi":"10.1021/acschemneuro.4c0069110.1021/acschemneuro.4c00691","DOIUrl":"https://doi.org/10.1021/acschemneuro.4c00691https://doi.org/10.1021/acschemneuro.4c00691","url":null,"abstract":"<p >Drug overdose deaths in 2023 in the United States exceeded 107,000, with 80,000 of these deaths attributed to opioids alone. The emergence of synthetic opioids such as fentanyl and its analogues have worsened the opioid overdose epidemic. A novel approach to treat opioid overdose and opioid use disorder (OUD) has been the introduction of biologics, which include monoclonal antibodies that bind to circulating opioids, preventing them from reaching the central nervous system, or peptides that have antinociceptive effects but lack the abuse liability of synthetic opioids. A challenge in the treatment of opioid overdose has been renarcotization, where an overdose patient revived with naloxone can re-enter an overdose state from residual opioid in the body. Biologics such as vaccines and monoclonal antibodies are excellent strategies that have been demonstrated to prevent renarcotization. In this review, we retrieved and discussed patents filed in the past six (6) years that focus on novel biologics reported as treatments for opioid overdose and OUD. We also provide a perspective on the use of biologics as therapeutics for OUD and opioid overdose.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"15 24","pages":"4360–4368 4360–4368"},"PeriodicalIF":4.1,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142851105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
From Nutritional Patterns to Behavior: High-Fat Diet Influences on Inhibitory Control, Brain Gene Expression, and Metabolomics in Rats
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2024-11-28 DOI: 10.1021/acschemneuro.4c0029710.1021/acschemneuro.4c00297
Diego Ruiz-Sobremazas, Ana Cristina Abreu, Ángeles Prados-Pardo, Elena Martín-González, Ana Isabel Tristán, Ignacio Fernández, Margarita Moreno and Santiago Mora*, 
{"title":"From Nutritional Patterns to Behavior: High-Fat Diet Influences on Inhibitory Control, Brain Gene Expression, and Metabolomics in Rats","authors":"Diego Ruiz-Sobremazas,&nbsp;Ana Cristina Abreu,&nbsp;Ángeles Prados-Pardo,&nbsp;Elena Martín-González,&nbsp;Ana Isabel Tristán,&nbsp;Ignacio Fernández,&nbsp;Margarita Moreno and Santiago Mora*,&nbsp;","doi":"10.1021/acschemneuro.4c0029710.1021/acschemneuro.4c00297","DOIUrl":"https://doi.org/10.1021/acschemneuro.4c00297https://doi.org/10.1021/acschemneuro.4c00297","url":null,"abstract":"<p >Impulsive and compulsive behaviors are associated with inhibitory control deficits. Diet plays a pivotal role in normal development, impacting both physiology and behavior. However, the specific effects of a high-fat diet (HFD) on inhibitory control have not received adequate attention. This study aimed to explore how exposure to a HFD from postnatal day (PND) 33 to PND77 affects impulsive and compulsive behaviors. The experiment involved 40 Wistar rats subjected to HFD or chow diets. Several tasks were employed to assess behavior, including variable delay to signal (VDS), five choice serial reaction time task (5-CSRTT), delay discounting task (DDT), and rodent gambling task (rGT). Genetic analyses were performed on the frontal cortex, and metabolomics and fatty acid profiles were examined by using stool samples collected on PND298. Our results showed that the HFD group exhibited increased motor impulsive behaviors while not affecting cognitive impulsivity. Surprisingly, reduced impulsive decision-making was shown in the HFD group. Furthermore, abnormal brain plasticity and dopamine gene regulation were shown in the frontal cortex, while metabolomics revealed abnormal fatty acid levels.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"15 24","pages":"4369–4382 4369–4382"},"PeriodicalIF":4.1,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/acschemneuro.4c00297","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142843949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Imidazo[2,1-b][1,3]thiazine Derivatives as Potential Modulators of Alpha-Synuclein Amyloid Aggregation
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2024-11-27 DOI: 10.1021/acschemneuro.4c0045110.1021/acschemneuro.4c00451
Indrė Misiu̅naitė, Kamilė Mikalauskaitė, Martyna Paulauskaitė, Ru̅ta Sniečkutė, Vytautas Smirnovas, Algirdas Brukštus, Mantas Žiaunys and Ieva Žutautė*, 
{"title":"Imidazo[2,1-b][1,3]thiazine Derivatives as Potential Modulators of Alpha-Synuclein Amyloid Aggregation","authors":"Indrė Misiu̅naitė,&nbsp;Kamilė Mikalauskaitė,&nbsp;Martyna Paulauskaitė,&nbsp;Ru̅ta Sniečkutė,&nbsp;Vytautas Smirnovas,&nbsp;Algirdas Brukštus,&nbsp;Mantas Žiaunys and Ieva Žutautė*,&nbsp;","doi":"10.1021/acschemneuro.4c0045110.1021/acschemneuro.4c00451","DOIUrl":"https://doi.org/10.1021/acschemneuro.4c00451https://doi.org/10.1021/acschemneuro.4c00451","url":null,"abstract":"<p >Insoluble amyloid fibrils accumulate in the intercellular spaces of organs and tissues, leading to various amyloidosis-related disorders in the human body. Specifically, Parkinson’s disease is associated with the aggregation of alpha-synuclein. However, current treatments for Parkinson’s primarily focus on managing motor symptoms and slowing disease progression. Efforts to prevent and halt the progression of these diseases involve the search for small molecular compounds. In this work, we synthesized imidazo[2,1-<i>b</i>][1,3]thiazines in an atom-economic way by cyclization of 2-alkynylthioimidazoles using 10% AuCl as the catalyst. We identified several compounds with specific functional groups capable of both inhibiting the aggregation of alpha-synuclein and redirecting the fibril formation pathway. The investigation into how these substances function revealed that imidazo[2,1-<i>b</i>][1,3]thiazine derivatives can influence alpha-synuclein aggregation in several ways. They not only inhibit the primary nucleation process and maintain a balance toward nonaggregated protein states but also stabilize smaller oligomeric species of alpha-synuclein and cause the formation of fibrils with unique structures and forms. These imidazo[2,1-<i>b</i>][1,3]thiazines could potentially be used in developing highly efficient, small molecular weight protein aggregation inhibitors.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"15 24","pages":"4418–4430 4418–4430"},"PeriodicalIF":4.1,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/acschemneuro.4c00451","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142843536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Lipopolysaccharide Effects on Neurotransmission: Understanding Implications for Depression
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2024-11-27 DOI: 10.1021/acschemneuro.4c0059110.1021/acschemneuro.4c00591
L. Batey, B. Baumberger, H. Khoshbouei and P. Hashemi*, 
{"title":"Lipopolysaccharide Effects on Neurotransmission: Understanding Implications for Depression","authors":"L. Batey,&nbsp;B. Baumberger,&nbsp;H. Khoshbouei and P. Hashemi*,&nbsp;","doi":"10.1021/acschemneuro.4c0059110.1021/acschemneuro.4c00591","DOIUrl":"https://doi.org/10.1021/acschemneuro.4c00591https://doi.org/10.1021/acschemneuro.4c00591","url":null,"abstract":"<p >Immune activation in the body is well studied; however, much less is known about how peripheral inflammation changes brain chemistry. Because depression and inflammation are close comorbidities, investigating how inflammation affects the brain’s chemicals will help us to better understand depression. The levels of the monoamines dopamine, serotonin and norepinephrine are thought to be affected by both inflammation and depression. In this Perspective, we review studies that find chemical changes in the brain after administration of the endotoxin LPS, which is a robust method to induce rapid inflammation. From these studies, we interpreted LPS to reduce dopamine and serotonin and increase norepinephrine levels in various regions in the brain. These changes are not a sign of “dysfunction” but serve an important evolutionary purpose that encourages the body to recover from an immune insult by altering mood.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"15 24","pages":"4339–4347 4339–4347"},"PeriodicalIF":4.1,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/acschemneuro.4c00591","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142843548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Investigating the Mechanism of Neurotoxic Effects of PFAS in Differentiated Neuronal Cells through Transcriptomics and Lipidomics Analysis
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2024-11-27 DOI: 10.1021/acschemneuro.4c0065210.1021/acschemneuro.4c00652
Logan Running, Judith R. Cristobal, Charikleia Karageorgiou, Michelle Camdzic, John Michael N. Aguilar, Omer Gokcumen, Diana S. Aga* and G. Ekin Atilla-Gokcumen*, 
{"title":"Investigating the Mechanism of Neurotoxic Effects of PFAS in Differentiated Neuronal Cells through Transcriptomics and Lipidomics Analysis","authors":"Logan Running,&nbsp;Judith R. Cristobal,&nbsp;Charikleia Karageorgiou,&nbsp;Michelle Camdzic,&nbsp;John Michael N. Aguilar,&nbsp;Omer Gokcumen,&nbsp;Diana S. Aga* and G. Ekin Atilla-Gokcumen*,&nbsp;","doi":"10.1021/acschemneuro.4c0065210.1021/acschemneuro.4c00652","DOIUrl":"https://doi.org/10.1021/acschemneuro.4c00652https://doi.org/10.1021/acschemneuro.4c00652","url":null,"abstract":"<p >Per- and polyfluorinated alkyl substances (PFAS) are pervasive environmental contaminants that bioaccumulate in tissues and pose risks to human health. Increasing evidence links PFAS to neurodegenerative and behavioral disorders, yet the underlying mechanisms of their effects on neuronal function remain largely unexplored. In this study, we utilized SH-SY5Y neuroblastoma cells, differentiated into neuronal-like cells, to investigate the impact of six PFAS compounds─perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), perfluorodecanoic acid (PFDA), perfluorodecanesulfonic acid (PFDS), 8:2 fluorotelomer sulfonate (8:2 FTS), and 8:2 fluorotelomer alcohol (8:2 FTOH)─on neuronal health. Following a 30 μM exposure for 24 h, PFAS accumulation ranged from 40–6500 ng/mg of protein. Transcriptomic analysis revealed 721 differentially expressed genes (DEGs) across treatments (<i>p</i><sub>adj</sub> &lt; 0.05), with 11 DEGs shared among all PFAS exposures, indicating potential biomarkers for neuronal PFAS toxicity. PFOA-treated cells showed downregulation of genes involved in synaptic growth and neural function, while PFOS, PFDS, 8:2 FTS, and 8:2 FTOH exposures resulted in the upregulation of genes related to hypoxia response and amino acid metabolism. Lipidomic profiling further demonstrated significant increases in fatty acid levels with PFDA, PFDS, and 8:2 FTS and depletion of triacylglycerols with 8:2 FTOH treatments. These findings suggest that the neurotoxic effects of PFAS are structurally dependent, offering insights into the molecular processes that may drive PFAS-induced neuronal dysfunction.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"15 24","pages":"4568–4579 4568–4579"},"PeriodicalIF":4.1,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142843549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Psychedelics and Entactogens: Call for Papers. 迷幻剂和迷幻药:征集论文。
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2024-11-25 DOI: 10.1021/acschemneuro.4c00773
Craig W Lindsley, Jacob M Hooker, Kelly Chibale, Christa E Müller, Squire J Booker
{"title":"Psychedelics and Entactogens: Call for Papers.","authors":"Craig W Lindsley, Jacob M Hooker, Kelly Chibale, Christa E Müller, Squire J Booker","doi":"10.1021/acschemneuro.4c00773","DOIUrl":"https://doi.org/10.1021/acschemneuro.4c00773","url":null,"abstract":"","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142708507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A VEGF Fragment Encompassing Residues 10–30 Inhibits Aβ1–42 Amyloid Aggregation and Exhibits Neuroprotective Properties Matching the Full-Length Protein
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2024-11-25 DOI: 10.1021/acschemneuro.4c0066910.1021/acschemneuro.4c00669
Stefania Zimbone, M. Laura Giuffrida, Michele F.M. Sciacca, Rita Carrotta, Fabio Librizzi, Danilo Milardi* and Giulia Grasso*, 
{"title":"A VEGF Fragment Encompassing Residues 10–30 Inhibits Aβ1–42 Amyloid Aggregation and Exhibits Neuroprotective Properties Matching the Full-Length Protein","authors":"Stefania Zimbone,&nbsp;M. Laura Giuffrida,&nbsp;Michele F.M. Sciacca,&nbsp;Rita Carrotta,&nbsp;Fabio Librizzi,&nbsp;Danilo Milardi* and Giulia Grasso*,&nbsp;","doi":"10.1021/acschemneuro.4c0066910.1021/acschemneuro.4c00669","DOIUrl":"https://doi.org/10.1021/acschemneuro.4c00669https://doi.org/10.1021/acschemneuro.4c00669","url":null,"abstract":"<p >The intricate relationship between brain vascular diseases and neurodegeneration has garnered increased attention in the scientific community. With an aging population, the incidence of these two conditions is likely to increase, making it imperative to understand the underlying common molecular mechanisms and unveiling novel avenues for therapy. Prompted by the observation that Aβ peptide aggregation has been implicated in the development of cerebral amyloid angiopathy (CAA) and that elevated concentrations of vascular endothelial growth factor (VEGF) in the cerebrospinal fluid (CSF) have been correlated with less cognitive decline in Alzheimer’s disease (AD), we demonstrate that a small peptide (Pep9) encompassing the 10–30 sequence of VEGF exhibits significant ability to inhibit the aggregation of the Aβ1–42 peptide, as well as the formation of toxic oligomers. AFM studies confirmed this inhibitory capacity, which is also paralleled by a significant reduction of the random coil to a beta-sheet conformational transition. Further studies have shown that Pep9 protects differentiated neuroblastoma SH-SY5Y cells from Aβ toxicity, being even more effective than full-length protein in preventing amyloid-induced neuronal death. The use of a control peptide wherein two histidines are substituted with glycines (H11G and H12G) suggests a close relationship between the peptide amino acid sequence and its antiaggregating/neuroprotective activity. Overall, this study provides insight into the role of VEGF in AD and suggests that specific VEGF fragments could be beneficial in the treatment of this condition.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"15 24","pages":"4580–4590 4580–4590"},"PeriodicalIF":4.1,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142843957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Psychedelics and Entactogens: Call for Papers 迷幻剂和迷幻药:论文征集
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2024-11-25 DOI: 10.1021/acschemneuro.4c0077310.1021/acschemneuro.4c00773
Craig W. Lindsley*, Jacob M. Hooker, Kelly Chibale, Christa E. Müller and Squire J. Booker, 
{"title":"Psychedelics and Entactogens: Call for Papers","authors":"Craig W. Lindsley*,&nbsp;Jacob M. Hooker,&nbsp;Kelly Chibale,&nbsp;Christa E. Müller and Squire J. Booker,&nbsp;","doi":"10.1021/acschemneuro.4c0077310.1021/acschemneuro.4c00773","DOIUrl":"https://doi.org/10.1021/acschemneuro.4c00773https://doi.org/10.1021/acschemneuro.4c00773","url":null,"abstract":"","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"15 24","pages":"4337–4338 4337–4338"},"PeriodicalIF":4.1,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142843399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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