Neurobiology of Disease最新文献

{"title":"microRNA-17-5p modulates ventral hippocampal transcriptome and synaptic proteome: Implications for emotional regulation in adult male rats.","authors":"F.A. Olave ,&nbsp;W.A. Corrales ,&nbsp;T.A. Guarnieri ,&nbsp;J.P. Silva ,&nbsp;F.I. Aguayo ,&nbsp;M. Alarcón-Mardones ,&nbsp;L. Román-Albasini ,&nbsp;J.C. Catalán ,&nbsp;P.I. González-Mori ,&nbsp;N. Palacios-Avendaño ,&nbsp;V. Mora-González ,&nbsp;C. Álvarez-Navarro ,&nbsp;E. Aliaga ,&nbsp;J.A. Cidlowski ,&nbsp;P. Zamorano ,&nbsp;J.L. Fiedler","doi":"10.1016/j.nbd.2025.107198","DOIUrl":"10.1016/j.nbd.2025.107198","url":null,"abstract":"<div><div>The hippocampus plays a crucial role in memory and emotional regulation, with its dorsal pole supporting cognitive functions and the ventral hippocampus modulating anxiety and affective processing via limbic interactions. Chronic restraint stress induces anxious- and depressive-like behaviors in rodents, alongside transcriptomic changes in the ventral hippocampus. Emerging evidence highlights microRNAs as modulators of synaptic architecture and gene expression. Notably, <em>miR-17-5p</em>—part of the <em>miR-17-92</em> cluster— shows increased cortical expression in individuals with mood disorders, and its levels in neural extracellular vesicles correlate directly with depressive symptom severity in male patients, suggesting translational relevance. In rodent models, chronic stress exposure produces divergent hippocampal expression patterns of <em>miR-17-5p</em>. Whether <em>miR-17-5p</em> acts as a passive biomarker of mood disorder or actively contributes to stress adaptation remains unclear.</div><div>In the present study, chronic stress exposure increased <em>miR-17-5p</em> expression specifically in the ventral hippocampus of male rats, with no changes detected in females. To assess its functional relevance, we reproduced this alteration in the ventral hippocampus of naïve male to evaluate behavioral outcomes and characterize both global and synaptic transcriptomic and proteomic profiles. Behaviorally, <em>miR-17-5p</em> mimic administration increased the sucrose preference, revealing an antidepressant-like effect. On the other hand, the open field test did not reveal anxiety-related differences, whereas the novelty-suppressed feeding test indicated a decrease in anxious-like behavior following <em>miR-17-5p</em> administration. Molecular analyses in ventral hippocampus homogenates and synaptic-enriched fractions revealed modulation of ribosomal protein composition and translational regulation—likely through mTOR pathway activation—favoring GABAergic adaptation and synaptic remodeling. These findings suggest a region-specific role of <em>miR-17-5p</em> in the ventral hippocampus that may contribute to its anxiolytic and antidepressant-like effects.</div><div>These results provide novel insights into <em>miR-17-5p</em>-mediated mood regulation, highlighting its potential as a therapeutic target for anxiety and depressive disorders.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"218 ","pages":"Article 107198"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145588352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Free-water imaging reveals cholinergic pathway damage in multiple system atrophy","authors":"Yao Wang ,&nbsp;Han Zhang ,&nbsp;Shan Ren ,&nbsp;Xinning Zhang ,&nbsp;Sushi Wang ,&nbsp;Weizheng Ran ,&nbsp;Wenyang Tian ,&nbsp;Ying Zhou ,&nbsp;Zhigang Chen","doi":"10.1016/j.nbd.2025.107213","DOIUrl":"10.1016/j.nbd.2025.107213","url":null,"abstract":"<div><h3>Background</h3><div>Dysfunction of the cholinergic system is implicated in the pathophysiology of Multiple System Atrophy (MSA). However, in vivo assessment of cholinergic pathways originating from the nucleus basalis of Meynert (NBM) and pedunculopontine nucleus (PPN), and their clinical relevance remains inadequately characterized.</div></div><div><h3>Objectives</h3><div>To utilize diffusion MRI and free-water (FW) image model to characterize cholinergic system degeneration in MSA and examine its association with clinical features.</div></div><div><h3>Methods</h3><div>We included 103 MSA patients and 44 healthy controls who underwent diffusion MRI. Probabilistic tractography reconstructed three major cholinergic pathways: a medial NBM projection via cingulum, a lateral NBM projection via external capsule, and PPN-thalamus pathway. FW imaging quantified microstructural integrity using FW fraction (FWf) and corrected axial diffusivity (cAxD). These DWI-based metric were analyzed to (1) differentiate patients from controls and (2) examine the associations with clinical features in MSA.</div></div><div><h3>Results</h3><div>Compared to controls, MSA patients showed higher FWf values in both the lateral NBM and PPN-thalamus pathways. Receiver operating characteristic analysis showed that the FWf-based model best differentiated MSA from controls (AUC = 0.89 [0.76–1.00]), with PPN-thalamus FWf being the most discriminative feature. Across all three cholinergic pathways, higher FWf values were associated with longer disease duration, and PPN-thalamus FWf values specifically correlated with total Unified Multiple System Atrophy Rating Scale scores.</div></div><div><h3>Conclusion</h3><div>Cholinergic pathway damage is a prominent pathological feature of MSA, with PPN-thalamus pathway showing particular vulnerability (as indicated by increased FWf) and strong clinical relevance. This FWf elevation likely related to neuronal degeneration or neuroinflammatory changes driven by α-synuclein pathology.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"218 ","pages":"Article 107213"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145678220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MAPK family members differentially regulate pThr175 tau-mediated pathogenicity","authors":"Neil Donison ,&nbsp;Matthew A. Hintermayer ,&nbsp;Jacqueline Palik ,&nbsp;Jessica Fisher ,&nbsp;Kathryn Volkening ,&nbsp;Michael J. Strong","doi":"10.1016/j.nbd.2025.107223","DOIUrl":"10.1016/j.nbd.2025.107223","url":null,"abstract":"<div><div>The phosphorylation of tau is a critical determinant of both its physiological function and the induction of pathological misfolding and aggregation. We have previously provided evidence that tau phosphorylation at Thr175 results in the exposure of the N-terminal phosphatase-activating domain (PAD) leading to the subsequent phosphorylation of Thr231, and formation of tau oligomers. A number of tauopathies, including chronic traumatic encephalopathy (CTE), amyotrophic lateral sclerosis with cognitive impairment (ALSci), and experimental traumatic brain injury (TBI) have been proposed to be associated with this cascade of events. However, the cellular mechanism by which Thr175 tau is phosphorylated remains unclear. In this study we identified ERK2, JNK1, and p38 as candidate kinases through molecular and histological analyses in a rodent model of TBI, where increased kinase activity and protein interaction were associated with pThr175 tau. We confirmed that both ERK2 and JNK1 are capable of phosphorylating Thr175 tau <em>in vitro</em>, but only ERK2-mediated phosphorylation of Thr175 tau induced the pathological cascade characterized by PAD exposure and the generation of oligomeric, truncated and neurofibrillary tau. Thr175 phosphorylation was also associated with an altered interaction between tau and the molecular chaperone protein DnaJC7, which regulates tau misfolding. Additionally, we observed that pThr175 and pThr231 tau were increased by oxidative stress, which was associated with the activation of the MAPK signaling pathways. These findings further clarify the mechanisms leading to Thr175 tau phosphorylation and its role in pathological tau formation by identifying ERK1 and JNK2 as important cellular mediators.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"218 ","pages":"Article 107223"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145757099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glymphatic activity is linked to the synaptic vesicle cycle pathway in frontotemporal dementia: A metabolomics study","authors":"Min Chu,&nbsp;Ailing Yue,&nbsp;Haitian Nan,&nbsp;Hong Ye,&nbsp;Miao Qu,&nbsp;Liyong Wu","doi":"10.1016/j.nbd.2025.107135","DOIUrl":"10.1016/j.nbd.2025.107135","url":null,"abstract":"<div><h3>Background</h3><div>Emerging evidence implicating glymphatic dysfunction contributes to the pathogenesis of frontotemporal dementia (FTD). However, the pathway correlated to glymphatic function in FTD remains poorly understood. We aimed to explore potential underlying metabolic pathways associated with glymphatic dysfunction in FTD.</div></div><div><h3>Methods</h3><div>We enrolled 37 behavior FTD (bvFTD) patients and 40 healthy controls. Glymphatic activity was assessed using diffusion tensor imaging data. Plasma metabolomic profiling was performed to identify glymphatic-associated metabolites, followed by pathway enrichment analysis. Additionally, the plasma biomarker was tested in a subset of 25 patients to validate the metabolite findings.</div></div><div><h3>Results</h3><div>Patients with bvFTD exhibited significantly altered metabolite profiles compared to controls. The glymphatic-associated metabolites were predominantly enriched in the synaptic vesicle cycle pathway (FDR <em>p</em> &lt; 0.05). Furthermore, plasma neuropentraxin-2 (NPTX2) levels positively correlated with anterior glymphatic indices (<em>r</em> = 0.46, <em>p</em> = 0.027).</div></div><div><h3>Conclusion</h3><div>Our findings demonstrate the association between the glymphatic system and synaptic function in bvFTD.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"218 ","pages":"Article 107135"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145252261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-cell autonomous autophagy in amyotrophic lateral sclerosis: A new promising target?","authors":"Francesca Rosso ,&nbsp;Rocio Magdalena ,&nbsp;Carola Torazza ,&nbsp;Francesca Bacchetti ,&nbsp;Marco Milanese ,&nbsp;Angelo Poletti ,&nbsp;Giambattista Bonanno ,&nbsp;Riccardo Cristofani ,&nbsp;Tiziana Bonifacino","doi":"10.1016/j.nbd.2025.107203","DOIUrl":"10.1016/j.nbd.2025.107203","url":null,"abstract":"<div><div>Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative non-cell-autonomous disease with no cure, thus research is intensely focused on identifying pharmacological targets. Several studies aimed to clarify the pathogenic mechanisms and involvement in various cell types. A crucial factor in ALS is autophagy, which plays a key role in degrading intracellular protein aggregates. The connection between ALS and autophagy is reinforced by the fact that several genes mutated in ALS are linked to fundamental aspects of autophagy. The blockage of the autophagic flux was observed in ALS motor neurons, where it occurs earlier than in glia. However, the inconsistent effects of autophagy modulators in preclinical and clinical studies indicate the need for a deeper understanding of the role of autophagy in other cell types, such as astrocytes, microglia, and oligodendrocytes. Astrocytes and microglia are significantly impacted by autophagy dysregulation, contributing to neurodegeneration in both mouse and human-derived models. Autophagy is overactivated early in the disease, even before symptoms appear. This overactivation is influenced by the timing and specific tissue involved. It can alter cells' immunophenotype, favouring proinflammatory responses and affecting the cellular environment and autophagy in the surrounding cells. In contrast, oligodendrocytes show mild autophagic alterations. Additionally, sex hormones may affect proper autophagy function and ALS progression. The lack of information on how sex influences autophagy in glia highlights the need for more nuanced investigation into this mechanism. Future research should focus on these aspects, paving the way for personalised pharmacological approaches that consider the roles of cell types, time of intervention, and sex.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"218 ","pages":"Article 107203"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145661496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemogenetic activation of oxytocinergic neurons rescues neural correlates of encephalopathy of prematurity in mice","authors":"Marit Knoop ,&nbsp;Marie-Laure Possovre ,&nbsp;Ece Trak ,&nbsp;Jean-Luc Pitetti ,&nbsp;Yohan van de Looij ,&nbsp;Eduardo Sanches ,&nbsp;Stergios Tsartsalis ,&nbsp;Julien Pansiot ,&nbsp;Gabriel Schirmbeck ,&nbsp;Olivier Baud","doi":"10.1016/j.nbd.2025.107250","DOIUrl":"10.1016/j.nbd.2025.107250","url":null,"abstract":"<div><div>Every year, 15 million babies are born preterm, putting them at increased risk of encephalopathy of prematurity (EoP). EoP is characterized by microglia-induced neuroinflammation, which can aggravate injury mechanisms leading to neuronal disorders, myelination delay, and subsequent functional consequences. While effective neuroprotective strategies in the preterm brain remain elusive, interventions such as skin-to-skin, developmental care, and music therapy have a positive impact on newborn brain development, potentially related to the oxytocinergic system. Endogenous oxytocin is recognized as a regulator of maternal-child social bonding, but its neuroprotective effect in the injured brain remains to be elucidated. Here, we investigated the effects of chemogenetic activation of oxytocinergic neurons on the neural correlates of EoP. Using a well-established mouse model of systemic interleukin-1β to induce EoP, we showed that neonatal chemogenetic activation of oxytocinergic neurons has anti-inflammatory effects in microglia, improving microstructural development of the corpus callosum and motor cortex, and rescuing typical social behavior. These neuroprotective effects were more pronounced in females, who showed a greater reduction in microgliosis and improved social behavior compared to males. This study provides a biological explanation for how developmental care and early interventions, linked to the oxytocinergic system, may induce neuroprotection in the developing brain.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"218 ","pages":"Article 107250"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145850454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protrudin acts at ER-endosome contacts to promote KIF5-mediated endosomal tubule fission","authors":"Julia Kleniuk ,&nbsp;Aishwarya G. Nadadhur ,&nbsp;Catherine Rodger ,&nbsp;Emily Wolfenden ,&nbsp;Isabelle A. Hall ,&nbsp;Samuel R. Cheers ,&nbsp;Eliska Zlamalova ,&nbsp;Evan Reid","doi":"10.1016/j.nbd.2025.107231","DOIUrl":"10.1016/j.nbd.2025.107231","url":null,"abstract":"<div><div>Defective endosomal sorting and trafficking are increasingly recognised as key drivers of neurodegeneration, including hereditary spastic paraplegia (HSP) and other motor neuron disorders. Early endosomal tubule fission (ETF) is essential for sorting cargoes for recycling and retrograde transport, yet the mechanisms coordinating this process are incompletely defined. Here, we identify the endoplasmic reticulum (ER)–resident protein protrudin—previously shown to promote axonal regeneration after injury—as a key regulator of ETF. Using CRISPR interference in human cells, we show that loss of protrudin causes marked accumulation of elongated endosomal tubules, caused by defective fission. Protrudin-mediated ETF required its ability to interact with ER-localised VAP proteins, endosomal phosphoinositides, and the kinesin motor KIF5, indicating a function at ER–endosome contact sites. The endosomal tubulation phenotype depended on dynamic microtubules and dynein and was phenocopied by KIF5 depletion, suggesting that protrudin coordinates opposing microtubule motor forces to drive fission. Beyond this direct role, protrudin connects multiple ETF machineries implicated in lipid transfer, actin regulation, and ER shaping, positioning it as a central scaffold for ETF. Importantly, depletion of protrudin or the HSP-associated kinesin KIF5A produced similar endosomal tubulation defects in human cortical neurons, underscoring the neurophysiological and disease relevance of this pathway. These findings identify protrudin as a key molecular link between ER–endosome communication, neuronal membrane trafficking, and axonal maintenance—processes whose disruption underlies neurodegenerative disease.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"218 ","pages":"Article 107231"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145810708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Review on the role of hippocampus in autism spectrum disorder: Recent insights into neuropathology, genetics, and emerging therapeutic strategies","authors":"Poorna Manasa Bhamidimarri ,&nbsp;Khalood Alhosani ,&nbsp;Heng Cai ,&nbsp;Haya Al-Ali ,&nbsp;Yara Marwan Abukhaled ,&nbsp;Hasan Tawamie ,&nbsp;Sahar Abdelaziz ,&nbsp;Mouna Fawaz ,&nbsp;Junaid Kashir ,&nbsp;Yasmin Sajjad ,&nbsp;Lamiya Mohiyiddeen ,&nbsp;Michael Fakih ,&nbsp;Hamdan Hamdan","doi":"10.1016/j.nbd.2025.107227","DOIUrl":"10.1016/j.nbd.2025.107227","url":null,"abstract":"<div><div>The hippocampus, central to learning, memory, and social behavior, is increasingly implicated in the pathophysiology of autism spectrum disorder (ASD). Structural and functional disruptions in this region contribute to core ASD traits through impaired neurogenesis, abnormal dendritic morphology, excitatory/inhibitory imbalance, and altered connectivity with large-scale brain networks. Neuroimaging studies revealed changes in hippocampal volume, subfield-specific anomalies in the CA1 and dentate gyrus, and reduced functional connectivity within these regions. Genetic mutations in <em>Shank3</em>, <em>Syngap1</em>, <em>Fmr1</em>, and <em>Nlgn3</em> disrupt synaptic plasticity and social memory circuits, while epigenetic alterations and environmental exposures further impair regulatory processes. Neuroinflammation exacerbates ASD pathology through microglial activation and cytokine release. Collectively, current evidence positions hippocampal dysfunction as central to ASD, emphasizing its relevance as both a biomarker and a therapeutic target to improve clinical outcomes.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"218 ","pages":"Article 107227"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145781533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemogenetic control of GABAergic neurons within the interpeduncular nucleus reveals dissociable behavioral components of the nicotine withdrawal phenotype","authors":"Anabel M.M. Miguelez Fernández,&nbsp;Shana Netherton,&nbsp;Seshadri B. Niladhuri,&nbsp;Alexander C. Brown,&nbsp;Patricia Rivera,&nbsp;Kuei Y. Tseng,&nbsp;Christian J. Peters","doi":"10.1016/j.nbd.2025.107240","DOIUrl":"10.1016/j.nbd.2025.107240","url":null,"abstract":"<div><div>Chronic exposure to nicotine results in the development of a dependent state such that a withdrawal syndrome is elicited upon cessation of nicotine. The interpeduncular nucleus (IPN) contains a high concentration of nicotinic acetylcholine receptors (nAChRs) and has been identified as a key brain region involved in nicotine withdrawal. Here we investigated the contribution of two distinct subpopulations of IPN GABAergic neurons to nicotine withdrawal behaviors. Withdrawal was induced in mice by implantation of osmotic pumps containing nicotine, followed by precipitation by intraperitoneal injections of mecamylamine. Using a chemogenetic approach to specifically target Amigo1-expressing or Epyc-expressing neurons within the IPN, we found that activity of the Amigo1 subpopulation of GABAergic neurons is critical for anxiety-like behaviors both in naïve mice and in those undergoing nicotine withdrawal. Moreover, data revealed that stimulation of Amigo1 neurons in nicotine-naïve mice elicits opposite effects on affective and somatic behaviors. Taken together, these results suggest that somatic and affective behaviors constitute dissociable components of the nicotine withdrawal phenotype and are likely supported by distinct subpopulations of neurons within the IPN.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"218 ","pages":"Article 107240"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145827989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Notice to “Hypercholesterolemia-induced A<beta> accumulation in rabbit brain is associated with alteration in IGF-1 signaling” [Neurobiology of Disease 32 (2008) 426–432]","authors":"Sunita Sharma,&nbsp;R.P. Jaya Prasanthi,&nbsp;Eric Schommer,&nbsp;Gwen Feist,&nbsp;Othman Ghribi","doi":"10.1016/j.nbd.2025.107204","DOIUrl":"10.1016/j.nbd.2025.107204","url":null,"abstract":"","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"218 ","pages":"Article 107204"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145669071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}