Molecular and Cellular Neuroscience最新文献

{"title":"Alpha-synuclein pathology is associated with astrocyte senescence in a midbrain organoid model of familial Parkinson's disease","authors":"Mudiwa N. Muwanigwa ,&nbsp;Jennifer Modamio-Chamarro ,&nbsp;Paul M.A. Antony ,&nbsp;Gemma Gomez-Giro ,&nbsp;Rejko Krüger ,&nbsp;Silvia Bolognin ,&nbsp;Jens C. Schwamborn","doi":"10.1016/j.mcn.2024.103919","DOIUrl":"10.1016/j.mcn.2024.103919","url":null,"abstract":"<div><p>Parkinson's disease (PD) is a complex, progressive neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta in the midbrain. Despite extensive research efforts, the molecular and cellular changes that precede neurodegeneration in PD are poorly understood. To address this, here we describe the use of patient specific human midbrain organoids harboring the <em>SNCA</em> triplication to investigate mechanisms underlying dopaminergic degeneration. Our midbrain organoid model recapitulates key pathological hallmarks of PD, including the aggregation of α-synuclein and the progressive loss of dopaminergic neurons. We found that these pathological hallmarks are associated with an increase in senescence associated cellular phenotypes in astrocytes including nuclear lamina defects, the presence of senescence associated heterochromatin foci, and the upregulation of cell cycle arrest genes. These results suggest a role of pathological α-synuclein in inducing astrosenescence which may, in turn, increase the vulnerability of dopaminergic neurons to degeneration.</p></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"128 ","pages":"Article 103919"},"PeriodicalIF":3.5,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1044743124000046/pdfft?md5=db59b16e7b32392637c0190037ff0106&pid=1-s2.0-S1044743124000046-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139670096","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}

{"title":"A neural mass model for disturbance of alpha rhythm in the minimal hepatic encephalopathy","authors":"Jiangling Song ,&nbsp;M. Brandon Westover ,&nbsp;Rui Zhang","doi":"10.1016/j.mcn.2024.103918","DOIUrl":"10.1016/j.mcn.2024.103918","url":null,"abstract":"<div><p>One of the early markers of minimal hepatic encephalopathy (MHE) is the disruption of alpha rhythm observed in electroencephalogram (EEG) signals. However, the underlying mechanisms responsible for this occurrence remain poorly understood. To address this gap, we develop a novel biophysical model MHE-AWD-NCM, encompassing the communication dynamics between a cortical neuron population (CNP) and an astrocyte population (AP), aimed at investigating the relationship between alpha wave disturbance (AWD) and mechanistical principles, specifically concerning astrocyte-neuronal communication in the context of MHE. In addition, we introduce the concepts of peak power density and peak frequency within the alpha band as quantitative measures of AWD. Our model faithfully reproduces the characteristic EEG phenomenology during MHE and shows how impairments of communication between CNP and AP could promote AWD. The results suggest that the disruptions in feedback neurotransmission from AP to CNP, along with the inhibition of GABA uptake by AP from the extracellular space, contribute to the observed AWD. Moreover, we found that the variation of external excitatory stimuli on CNP may play a key role in AWD in MHE. Finally, the sensitivity analysis is also performed to assess the relative significance of above factors in influencing AWD. Our findings align with the physiological observations and provide a more comprehensive understanding of the complex interplay of astrocyte-neuronal communication that underlies the AWD observed in MHE, which potentially may help to explore the targeted therapeutic interventions for the early stage of hepatic encephalopathy.</p></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"128 ","pages":"Article 103918"},"PeriodicalIF":3.5,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139662421","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}

{"title":"Amyloid-β deposits in human astrocytes contain truncated and highly resistant proteoforms","authors":"C. Beretta ,&nbsp;E. Svensson ,&nbsp;A. Dakhel ,&nbsp;M. Zyśk ,&nbsp;J. Hanrieder ,&nbsp;D. Sehlin ,&nbsp;W. Michno ,&nbsp;A. Erlandsson","doi":"10.1016/j.mcn.2024.103916","DOIUrl":"10.1016/j.mcn.2024.103916","url":null,"abstract":"<div><p>Alzheimer's disease (AD) is a neurodegenerative disorder that develops over decades. Glial cells, including astrocytes are tightly connected to the AD pathogenesis, but their impact on disease progression is still unclear. Our previous data show that astrocytes take up large amounts of aggregated amyloid-beta (Aβ) but are unable to successfully degrade the material, which is instead stored intracellularly. The aim of the present study was to analyze the astrocytic Aβ deposits composition in detail in order to understand their role in AD propagation. For this purpose, human induced pluripotent cell (hiPSC)-derived astrocytes were exposed to sonicated Aβ₄₂ fibrils and magnetic beads. Live cell imaging and immunocytochemistry confirmed that the ingested Aβ aggregates and beads were transported to the same lysosomal compartments in the perinuclear region, which allowed us to successfully isolate the Aβ deposits from the astrocytes. Using a battery of experimental techniques, including mass spectrometry, western blot, ELISA and electron microscopy we demonstrate that human astrocytes truncate and pack the Aβ aggregates in a way that makes them highly resistant. Moreover, the astrocytes release specifically truncated forms of Aβ via different routes and thereby expose neighboring cells to pathogenic proteins. Taken together, our study establishes a role for astrocytes in mediating Aβ pathology, which could be of relevance for identifying novel treatment targets for AD.</p></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"128 ","pages":"Article 103916"},"PeriodicalIF":3.5,"publicationDate":"2024-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1044743124000010/pdfft?md5=70c6cf3b3b1c003b5b3ec4ea57e7a57c&pid=1-s2.0-S1044743124000010-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139496149","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}

{"title":"TREM2 in Alzheimer's disease: Structure, function, therapeutic prospects, and activation challenges","authors":"Emilia Zgorzynska","doi":"10.1016/j.mcn.2024.103917","DOIUrl":"10.1016/j.mcn.2024.103917","url":null,"abstract":"<div><p><span><span>Triggering receptor expressed on myeloid cells 2<span> (TREM2) is a membrane glycoprotein<span> that plays a crucial role in the regulation of microglial survival, activation, phagocytosis, as well as in the maintenance of brain </span></span></span>homeostasis<span> and the inflammatory response to injury or neurodegeneration. This review provides a comprehensive overview of TREM2 structure and functions, highlighting the role of its variants in the development and progression of </span></span>Alzheimer's disease<span> (AD), a devastating neurodegenerative disease<span> that affects millions of people worldwide. Additionally, the article discusses the potential of TREM2 as a therapeutic target in AD, analyzing the current state of research and future prospects. Given the significant challenges associated with the activation of TREM2, particularly due to its diverse isoforms and the delicate balance required to modulate the immune response without triggering hyperactivation, this review aims to enhance our understanding of TREM2 in AD and inspire further research into this promising yet challenging therapeutic target.</span></span></p></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"128 ","pages":"Article 103917"},"PeriodicalIF":3.5,"publicationDate":"2024-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139496108","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}

{"title":"Role and mechanism of EphB3 in epileptic seizures and epileptogenesis through Kalirin","authors":"Hao Huang ,&nbsp;Ling Chen ,&nbsp;Jinxian Yuan ,&nbsp;Haiqing Zhang ,&nbsp;Juan Yang ,&nbsp;Zucai Xu ,&nbsp;Yangmei Chen","doi":"10.1016/j.mcn.2023.103915","DOIUrl":"10.1016/j.mcn.2023.103915","url":null,"abstract":"<div><h3>Background</h3><p>The EphB receptor tyrosine kinase family participates in intricate signaling pathways that orchestrate neural networks, guide neuronal axon development, and modulate synaptic plasticity through interactions with surface-bound ephrinB ligands. Additionally, Kalirin, a Rho guanine nucleotide exchange factor, is notably expressed in the postsynaptic membrane of excitatory neurons and plays a role in synaptic morphogenesis. This study postulates that Kalirin may act as a downstream effector of EphB3 in epilepsy. This investigation focuses on understanding the link between EphB3 and epilepsy.</p></div><div><h3>Materials and methods</h3><p>Chronic seizure models using LiCl-pilocarpine (LiCl/Pilo) and pentylenetetrazol were developed in rats. Neuronal excitability was gauged through whole-cell patch clamp recordings on rat hippocampal slices. Real-time PCR determined Kalirin's mRNA expression, and Western blotting was employed to quantify EphB3 and Kalirin protein levels. Moreover, dendritic spine density in epileptic rats was evaluated using Golgi staining.</p></div><div><h3>Results</h3><p>Modulation of EphB3 functionality influenced acute seizure severity, latency duration, and frequency of spontaneous recurrent seizures. Golgi staining disclosed an EphB3-driven alteration in dendritic spine density within the hippocampus of epileptic rats, underscoring its pivotal role in the reconfiguration of hippocampal neural circuits. Furthermore, our data propose Kalirin as a prospective downstream mediator of the EphB3 receptor.</p></div><div><h3>Conclusions</h3><p>Our findings elucidate that EphB3 impacts the action potential dynamics in isolated rat hippocampal slices and alters dendritic spine density in the inner molecular layer of epileptic rat hippocampi, likely through Kalirin-mediated pathways. This hints at EphB3's significant role in shaping excitatory circuit loops and recurrent seizure activity via Kalirin.</p></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"128 ","pages":"Article 103915"},"PeriodicalIF":3.5,"publicationDate":"2023-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1044743123001094/pdfft?md5=0901e831af72e5c05a617a22678336c1&pid=1-s2.0-S1044743123001094-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138943969","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}

{"title":"The exocyst subunit Sec15 is critical for proper synaptic development and function at the Drosophila NMJ","authors":"Chris J. Kang ,&nbsp;Luis E. Guzmán-Clavel ,&nbsp;Katherine Lei ,&nbsp;Martin Koo ,&nbsp;Steven To ,&nbsp;John P. Roche","doi":"10.1016/j.mcn.2023.103914","DOIUrl":"10.1016/j.mcn.2023.103914","url":null,"abstract":"<div><p>The exocyst protein complex is important for targeted vesicle fusion in a variety of cell types, however, its function in neurons is still not entirely known. We found that presynaptic knockdown (KD) of the exocyst component <em>sec15</em> by transgenic RNAi expression caused a number of unexpected morphological and physiological defects in the synapse. These include the development of active zones (AZ) devoid of essential presynaptic proteins, an increase in the branching of the presynaptic arbor, the appearance of satellite boutons, and a decrease in the amplitude of stimulated postsynaptic currents as well as a decrease in the frequency of spontaneous synaptic vesicle release. We also found the release of extracellular vesicles from the presynaptic neuron was greatly diminished in the Sec15 KDs. These effects were mimicked by presynaptic knockdown of Rab11, a protein known to interact with the exocyst. <em>sec15 RNAi</em> expression caused an increase in phosphorylated Mothers against decapentaplegic (pMad) in the presynaptic terminal, an indication of enhanced bone morphogenic protein (BMP) signaling. Some morphological phenotypes caused by Sec15 knockdown were reduced by attenuation of BMP signaling through knockdown of <em>wishful thinking (Wit</em>), while other phenotypes were unaffected. Individual knockdown of multiple proteins of the exocyst complex also displayed a morphological phenotype similar to Sec15 KD. We conclude that Sec15, functioning as part of the exocyst complex, is critically important for proper formation and function of neuronal synapses. We propose a model in which Sec15 is involved in the trafficking of vesicles from the recycling endosome to the cell membrane as well as possibly trafficking extracellular vesicles for presynaptic release and these processes are necessary for the correct structure and function of the synapse.</p></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"128 ","pages":"Article 103914"},"PeriodicalIF":3.5,"publicationDate":"2023-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1044743123001082/pdfft?md5=44dcb81f68b5b0609f5ada63093ea1ac&pid=1-s2.0-S1044743123001082-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138584388","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}

{"title":"Suppression of BMP signaling restores mitral cell development impaired by FGF signaling deficits in mouse olfactory bulb","authors":"Ayako Ito,&nbsp;Claire Miller,&nbsp;Fumiaki Imamura","doi":"10.1016/j.mcn.2023.103913","DOIUrl":"10.1016/j.mcn.2023.103913","url":null,"abstract":"<div><p><span>Fibroblast growth factors (FGFs) and </span>bone morphogenic proteins<span><span><span> (BMPs) play various important roles in the development of the central nervous system<span><span>. However, the roles of FGF and BMP signaling in the development of the olfactory bulb<span> (OB) are largely unknown. In this study, we first showed the expression of FGF receptors (FGFRs) and BMP receptors (BMPRs) in OB </span></span>RGCs, radial glial cells (RGCs) in the developing OB, which generate the OB projection neurons, mitral and </span></span>tufted cells<span>. When the FGF signaling was inhibited by a dominant-negative form of FGFR1 (dnFGFR1), OB RGCs accelerated their state transition to mitral cell precursors without affecting their transcription cascade and fate. However, the mitral cell precursors could not radially migrate to form the mitral cell layer (MCL). In addition, FGF signaling inhibition reduced the expression of a BMP antagonist, </span></span>Noggin<span>, in the developing OB. When BMP signaling was suppressed by the ectopic expression of Noggin or a dominant-negative form of BMPR1a (dnBMPR1a) in the developing OB, the defect in MCL formation caused by the dnFGFR1 was rescued. However, the dnBMPR1a did not rescue the accelerated state transition of OB RGCs. These results demonstrate that FGF signaling is important for OB RGCs to maintain their self-renewal state and MCL formation. Moreover, the suppression of BMP signaling is required for mitral cells to form the MCL. This study sheds new light on the roles of FGFs and BMPs in OB development.</span></span></p></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"128 ","pages":"Article 103913"},"PeriodicalIF":3.5,"publicationDate":"2023-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138498862","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}

{"title":"Neuron navigators: A novel frontier with physiological and pathological implications","authors":"Parth Sandeep ,&nbsp;Poonam Sharma ,&nbsp;Kanishk Luhach ,&nbsp;Neerupma Dhiman ,&nbsp;Harsha Kharkwal ,&nbsp;Bhupesh Sharma","doi":"10.1016/j.mcn.2023.103905","DOIUrl":"10.1016/j.mcn.2023.103905","url":null,"abstract":"<div><p><span>Neuron navigators are microtubule plus-end tracking proteins containing basic and serine rich regions which are encoded by neuron navigator genes (</span><em>NAVs</em><span><span>). Neuron navigator proteins are essential for neurite outgrowth<span><span><span>, neuronal migration, and overall </span>neurodevelopment<span> along with some other functions as well. The navigator proteins are substantially expressed in the developing brain and have been reported to be differentially expressed in various tissues at different ages. Over the years, the research has found neuron navigators to be implicated in a spectrum of pathological conditions such as developmental anomalies, neurodegenerative disorders, </span></span>neuropathic pain, anxiety, cancers, and certain inflammatory conditions. The existing knowledge about neuron navigators remains sparse owing to their differential functions, undiscovered modulators, and unknown molecular mechanisms. Investigating the possible role of neuron navigators in various </span></span>physiological processes and pathological conditions pose as a novel field that requires extensive research and might provide novel mechanistic insights and understanding of these aspects.</span></p></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"127 ","pages":"Article 103905"},"PeriodicalIF":3.5,"publicationDate":"2023-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135764530","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}

{"title":"The elastin-derived peptide (VGVAPG) activates autophagy in neuroblastoma (SH-SY5Y) cells via peroxisome proliferator-activated receptor gamma (PPARγ)","authors":"Konrad A. Szychowski,&nbsp;Bartosz Skóra","doi":"10.1016/j.mcn.2023.103902","DOIUrl":"10.1016/j.mcn.2023.103902","url":null,"abstract":"<div><p>Autophagy is a self-degradative process important for balancing the sources of energy and involved in the development of Alzheimer's disease (AD). To date, a number of papers have shown that elastin-derived peptides (EDPs) affect the expression and activation of peroxisome proliferator-activated receptor gamma (PPARγ), which is crucial for the development of AD and autophagy initiation. Therefore, the aim of the present study was to determine whether EDPs with a Val–Gly–Val–Ala–Pro–Gly (VGVAPG) amino acid sequence activate the autophagic process in undifferentiated SH-SY5Y human neuroblastoma cells. Our study is the first to show that EDPs with the VGVAPG sequence initiate the autophagy process in the undifferentiated SH-SY5Y cell line exhibiting a number of features of normal neuroblasts. In particular, we observed in our study that VGAVPG peptide increased ULK1, AKT, PPARγ, and LC3B protein expression. Moreover, our experiments with the agonist (rosiglitazone) and antagonist (GW9662) of PPARγ confirm that the studied EDP acts through the PPARγ pathway affecting mTOR and finally autophagy. Some studies have shown that autophagy disturbances are involved in the development of AD. Therefore, we believe that our study will provide new evidence of the possible involvement of EDPs (especially VGVAPG) in the development of AD.</p></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"127 ","pages":"Article 103902"},"PeriodicalIF":3.5,"publicationDate":"2023-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1044743123000969/pdfft?md5=fa4c7ef43c6fc1a0439ce02b36a326ca&pid=1-s2.0-S1044743123000969-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71425065","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}

{"title":"Alpha-secretase dependent nuclear localization of the amyloid-β precursor protein-binding protein Fe65 promotes DNA repair","authors":"Rebecca S. Revol,&nbsp;Niina A. Koistinen,&nbsp;Preeti K. Menon,&nbsp;Almudena Chicote-Gonzàlez,&nbsp;Kerstin Iverfeldt ,&nbsp;Anna-Lena Ström","doi":"10.1016/j.mcn.2023.103903","DOIUrl":"10.1016/j.mcn.2023.103903","url":null,"abstract":"<div><p>Fe65 is a brain enriched adaptor protein involved in various cellular processes, including actin cytoskeleton regulation, DNA repair and transcription. A well-studied interacting partner of Fe65 is the transmembrane amyloid-β precursor protein (APP), which can undergo regulated intramembrane proteolysis (RIP). Following β- and γ-secretase-mediated RIP, the released APP intracellular domain (AICD) together with Fe65 can translocate to the nucleus and regulate transcription. In this study, we investigated if Fe65 nuclear localization can also be regulated by different α-secretases, also known to participate in RIP of APP and other transmembrane proteins. We found that in both Phorbol 12-myristate 13-acetate and all-trans retinoic acid differentiated neuroblastoma cells a strong negative impact on Fe65 nuclear localization, equal to the effect observed upon γ-secretase inhibition, could be detected following inhibition of all three (ADAM9, ADAM10 and ADAM17) α-secretases. Moreover, using the comet assay and analysis of Fe65 dependent DNA repair associated posttranslational modifications of histones, we could show that inhibition of α-secretase-mediated Fe65 nuclear translocation resulted in impaired capacity of the cells to repair DNA damage. Taken together this suggests that α-secretase processing of APP and/or other Fe65 interacting transmembrane proteins play an important role in regulating Fe65 nuclear translocation and DNA repair.</p></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"127 ","pages":"Article 103903"},"PeriodicalIF":3.5,"publicationDate":"2023-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1044743123000970/pdfft?md5=86f63fd27ceb1975c8da32015ef75c5f&pid=1-s2.0-S1044743123000970-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71424954","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}