Experimental Neurology最新文献

{"title":"Effects of cranial X-ray irradiation in Presymptomatic 3 × Tg-AD mice","authors":"Wei Cheng ,&nbsp;Yanxi Ma ,&nbsp;Feifei Gao ,&nbsp;Zheng Shi ,&nbsp;Dashan Zuo ,&nbsp;Cuixia Di ,&nbsp;Xiaodong Jin ,&nbsp;Weiqiang Chen ,&nbsp;Fei Ye ,&nbsp;Qiang Li","doi":"10.1016/j.expneurol.2025.115482","DOIUrl":"10.1016/j.expneurol.2025.115482","url":null,"abstract":"<div><h3>Background</h3><div>Recently, several animal studies have demonstrated the therapeutic potential of low-dose radiation therapy (LDRT) for Alzheimer's disease (AD), especially in decreasing amyloid-beta (Aβ) plaques. However, clinical concerns regarding the duration of efficacy and long-term safety of this treatment remain understudied. Additionally, LDRT has been shown to alleviate various neurological disorders. We hypothesize that the therapeutic mechanisms of LDRT in AD may extend beyond targeting Aβ and tau alone. In this study, we administered whole-brain X-ray irradiation (10 Gy in 5 fractions) to presymptomatic AD mice to re-examine its mechanism of action, duration of efficacy, and long-term safety profile.</div></div><div><h3>Results</h3><div>Two months after irradiation, the autonomous activity of 3 × Tg-AD mice was significantly enhanced, with specific improvements in the spatial learning and memory in females. Western blotting revealed reduced tau phosphorylation at Ser262 site in the hippocampus of females. SnRNA-seq demonstrated restored neuronal network in females. However, these therapeutic effects appeared exhibited transient characteristics. By ten months post-irradiation, no significant behavioral and AD-related pathological changes were detected across groups, except for the elevated Aβ1–42 in the hippocampus of females.</div></div><div><h3>Conclusions</h3><div>In conclusion, the effects of early X-ray intervention on 3 × Tg-AD mice were sex-specific and time-dependent. The short-term improvement observed in female mice may be attributed to attenuated tau hyperphosphorylation and restored neuronal networks. Longitudinal observation over ten consecutive months post-irradiation showed no evidence of severe adverse effects.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"395 ","pages":"Article 115482"},"PeriodicalIF":4.2,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148608","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":"Ellagitannin component punicalin prevents cognitive impairment by inhibiting metabolic disorders, TLR4/NF-kB/NLRP3 inflammasome signaling, and mitochondrial dysfunction in high-fat diet-fed mice","authors":"Peng Chen ,&nbsp;Jiexin Lei ,&nbsp;Rong Wang ,&nbsp;Changlin Li ,&nbsp;Benhong Zhou ,&nbsp;Ruhong Zhang","doi":"10.1016/j.expneurol.2025.115479","DOIUrl":"10.1016/j.expneurol.2025.115479","url":null,"abstract":"<div><div>Obesity linked to overnutrition can result in metabolic dysregulation and cognitive impairment. This study aimed to explore the protective role of punicalin (PUN), an ellagitannin with various biological activities, against cognitive impairment in high-fat diet (HFD)-fed mice and to examine the underlying mechanisms. PUN was orally administered at 50, 100, and 150 mg/kg for 8 weeks, resulting in a significant reduction in body weight, restoration of glucose tolerance, and normalization of lipid profiles in the serum and liver of HFD-fed mice. PUN notably enhanced spatial memory and improved depression-like symptoms across various behavioral assessments, which were associated with improved synaptic function by boosting synaptic protein levels and excitatory postsynaptic currents, while decreasing oxidative damage, balancing amyloidogenesis, and the cholinergic system in HFD-fed mice. PUN reduced the activation of the TLR4/NF-kB/NLRP3 inflammasome, which decreased microglia overactivation, engulfment of PSD95 in microglia and mediated neuroinflammation in mouse models of HFD-induced obesity. In addition, PUN improved the activity of tricarboxylic acid cycle enzymes, including PDH, CS, and OGDH; lowered 8-OHdG levels; elevated ATP and NAD+ levels; and disrupted mitochondrial structure. PUN modulates molecular pathways by reducing phosphorylated p53 levels and upregulating PGC-1α, thereby improving mitochondrial function. Therefore, PUN could help counteract cognitive impairment in HFD-fed mice by inhibiting neuroinflammation via the TLR4/NFkB/NLRP3 inflammasome and reinstating mitochondrial capabilities through the p53/PGC-1α pathway. PUN could serve as a new nutritional strategy for preventing obesity-related cognitive dysfunction via its metabolic regulation and anti-inflammatory effects.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"395 ","pages":"Article 115479"},"PeriodicalIF":4.2,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137046","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":"Therapeutic doses of methylphenidate following repetitive mild traumatic brain injury transiently disrupts risk/reward decision making in a sex dependent manner.","authors":"Eleni Papadopoulos ,&nbsp;Samantha Walkow ,&nbsp;Anna Abrimian ,&nbsp;Christopher P. Knapp ,&nbsp;Jessica A. Loweth ,&nbsp;Barry D. Waterhouse ,&nbsp;Rachel L. Navarra","doi":"10.1016/j.expneurol.2025.115478","DOIUrl":"10.1016/j.expneurol.2025.115478","url":null,"abstract":"<div><div>Mild traumatic brain injury (mTBI) can often impair prefrontal cortex (PFC)-mediated higher-order decision making processes that lead to increased risk-taking behaviors, and repetitive mTBIs (rmTBIs) increase susceptibility to more severe and lasting symptoms. The catecholamine transmitters, dopamine and norepinephrine, modulate neural activity within the PFC and catecholamine dysregulation associated with TBI may underly aberrant decision making. The psychostimulant, methylphenidate (MPH), elevates catecholamine levels by blocking their reuptake transporters and is often used off-label to treat post-injury cognitive symptoms. However, to establish a treatment regimen, it is necessary to characterize how chronic therapeutic doses of MPH affect rmTBI-induced disruptions of decision making. Here, male and female rodents were trained on the probabilistic discounting task (PDT) prior to receiving rmTBI induced by the closed head-controlled cortical impact model. Rats then received daily administration of saline or low-dose MPH (0.5 or 2 mg/kg, i.p.) upon return to the PDT to assess their risk/reward decision-making behavior for 4 weeks post-surgery. The combination of rmTBI and MPH treatment significantly increased risky choice preference in males for 2 weeks. In contrast, MPH (2 mg/kg) disrupted choice preference only in uninjured females within the first week post-surgery. Upon completion of chronic MPH treatment and PDT testing, no changes in catecholamine transporter protein levels within subregions of the PFC were observed. These results indicate MPH treatment transiently exacerbates risky behavior in males, but not females, following rmTBI. These sex-specific responses advise caution for males exposed to making decisions that involve uncertain risk/reward outcomes when considering MPH to treat post-rmTBI cognitive symptoms.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"395 ","pages":"Article 115478"},"PeriodicalIF":4.2,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137092","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":"Animal models of Chiari malformation types 1 and 2: Mechanistic insights and translational challenges","authors":"William Davalan ,&nbsp;Qiang Li ,&nbsp;Andrew T. Hale ,&nbsp;Baojian Fan ,&nbsp;Phan Q. Duy ,&nbsp;Neel H. Mehta ,&nbsp;Seth L. Alper ,&nbsp;Adam J. Kundishora ,&nbsp;William Muñoz ,&nbsp;Evan Dennis ,&nbsp;Garrett Allington ,&nbsp;Kedous Y. Mekbib ,&nbsp;William E. Butler ,&nbsp;Kristopher T. Kahle","doi":"10.1016/j.expneurol.2025.115473","DOIUrl":"10.1016/j.expneurol.2025.115473","url":null,"abstract":"<div><div>Chiari malformation (CM) types 1 and 2 are common congenital hindbrain disorders characterized by varying degrees of cerebellar herniation and association with neural tube defects. Knowledge of CM pathogenesis has thus far relied on preclinical animal models. Here, we provide a comprehensive review of animal models (genetic, teratogen-induced, surgical, and spontaneous) of CM1 and CM2, highlighting their construct validity, pathophysiological insights, and translational relevance. Genetic models exhibit defects in cranial base development, cerebrospinal fluid (CSF) flow, and neural tube closure. Teratogenic and surgical models have been informative for understanding the consequences of CSF leakage and validating prenatal treatments, especially in fetal sheep and chick embryos. Spontaneous models in dogs, cattle, and primates have offered complementary insights but the heterogeneity arising from species-specific differences obscures further understanding. Despite these advances, translational challenges persist, including species-specific differences in skull anatomy, CSF physiology, and symptomatology. We highlight the need for a patient-first approach, emphasizing the translational importance of large-scale gene discovery research in human patients to inform and prioritize dowstream functional investigations in animal models to enhance mechanistic understanding and support the development of etiology-specific therapies for CM.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"395 ","pages":"Article 115473"},"PeriodicalIF":4.2,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137079","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":"Dosing parameters for grafting human neural stem cells into sites of spinal cord injury","authors":"J.H. Brock ,&nbsp;C.A. Shevinsky ,&nbsp;L. Graham ,&nbsp;E. Staufenberg ,&nbsp;K.R. Limon ,&nbsp;T.J. Vokes ,&nbsp;K. Archuleta ,&nbsp;A. Blesch ,&nbsp;P. Lu ,&nbsp;M.H. Tuszynski","doi":"10.1016/j.expneurol.2025.115480","DOIUrl":"10.1016/j.expneurol.2025.115480","url":null,"abstract":"<div><div>Grafts of neural stem cells into sites of spinal cord injury (SCI) in animal models support functional improvement by forming new synaptic relays across the lesion site. Efficacy has been demonstrated in mouse, rodent and rhesus monkey models of SCI after both thoracic and cervical level injury. In preparation for the initiation of clinical trials, it is important to establish the minimum effective dose and maximal tolerated dose of neural stem cells implanted into lesion sites. Accordingly, we grafted our human embryonic stem cell-derived spinal cord neural progenitor cells into sites of rat thoracic spinal cord contusion at five different doses ranging from 10,000 to 400,000 cells/μl. 12-weeks post-grafting, spinal cord tissue was assessed for graft filling, neuronal differentiation, graft axonal outgrowth and host axonal ingrowth. We now report that in rats; the minimum effective dose is 100,000 cells/μl and the maximum tolerated dose is 400,000 cells/μl. These cell concentrations constitute a potential cell dose range for testing in human clinical trials.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"395 ","pages":"Article 115480"},"PeriodicalIF":4.2,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137096","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":"Evaluating the impact of age and treatment on neuroinflammation-related proteins in mouse models of proteinopathies","authors":"Amelia D. Dahlén,&nbsp;Sahar Roshanbin,&nbsp;Nadja M. Bucher,&nbsp;Dag Sehlin,&nbsp;Stina Syvänen","doi":"10.1016/j.expneurol.2025.115475","DOIUrl":"10.1016/j.expneurol.2025.115475","url":null,"abstract":"<div><div>Neuroinflammation plays a key role in Alzheimer's disease (AD), but the actions of microglial mediators may vary across stages of amyloid-beta (Aβ) pathology. While drugs targeting brain immune responses are advancing to clinical trials, biomarkers to monitor their effects are lacking. This study investigated proteins expressed by activated microglia in three mouse models of Aβ pathology and α-synuclein, both during disease progression and after treatment, to evaluate their potential as <em>in vivo</em> biomarkers. Immunofluorescent staining was performed on cortical sections from App^NL-G-F, tg-ArcSwe, and wild-type (WT) mice. TREM2, Axl, galectin-3, Aβ, and cytokines were measured by immunoassays in brain homogenates from WT, App^NL-G-F, tg-ArcSwe, and tg-UppSwe mice across four age groups and from mice subjected to three treatment strategies targeting Aβ (beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhibitor NB-360 and antibody RmAb158) or α-synuclein (antibody RmAb38E2). TREM2 and Axl colocalized with Iba1 and Aβ in App^NL-G-F and tg-ArcSwe mice, with age-dependent increases observed in both models but not in tg-UppSwe. The lectin galectin-3 increased with age across all genotypes, including WT. Aβ correlated with elevated TREM2, Axl, and Galectin-3. Two months of BACE1-inhibition reduced TREM2, Axl, and galectin-3 in tg-ArcSwe mice and TREM2 and Axl in App^NL-G-F mice. In summary, microglial TREM2, Axl, and galectin-3 are promising biomarkers for tracking AD-related neuroinflammation. Microglial interactions with Aβ likely influence the outcomes of Aβ-targeting therapies, and characterizing their dynamic states will inform the development of diagnostic tools and treatments relying on microglial activation to alleviate pathologies associated with neurodegenerative diseases.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"395 ","pages":"Article 115475"},"PeriodicalIF":4.2,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137077","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":"Elevated ESM1 facilitates peripheral nerve regeneration via enhancing Schwann cell activity and developing a pro-regenerative microenvironment","authors":"Zhixian Ren ,&nbsp;Yang Miao ,&nbsp;Yunsong Zhang ,&nbsp;Lili Zhao","doi":"10.1016/j.expneurol.2025.115476","DOIUrl":"10.1016/j.expneurol.2025.115476","url":null,"abstract":"<div><div>Nerve injury often results in restricted regenerative capacity, leading to long-term functional disability. Growth factors are essential mediators of tissue repair and hold therapeutic promise for enhancing nerve regeneration. Identifying differentially expressed growth factors in injured nerves may reveal key promoters of nerve regeneration. In this study, through transcriptomic profiling of injured sciatic nerves in young and aged rats, we revealed dynamic dysregulation of growth factors, and identified endothelial cell-specific molecule 1 (ESM1) as an up-regulated growth factor following injury. Recombinant ESM1 protein enhanced Schwann cell viability, proliferation, and migration both in vitro and in vivo. Furthermore, the administration of ESM1 supports angiogenesis, reduces apoptosis, and accelerates axon regeneration in the injury site. Mechanistically, ESM1 elevated phosphorylated MEK1/2 and ERK1/2 levels and hence established a regenerative-permissive microenvironment. Our findings reveal the beneficial role of ESM1 in nerve regeneration and hence underscore its potential as a promising therapeutic avenue for peripheral nerve injury.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"395 ","pages":"Article 115476"},"PeriodicalIF":4.2,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137051","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":"Gene therapy device-based delivery of progranulin, prosaposin, and GDNF as a combined precision and neurorestorative therapy in the rat 6-OHDA model of parkinsonism","authors":"Chiara Bertasini ,&nbsp;Marco Rossini ,&nbsp;Jacopo Grisotto ,&nbsp;Dwaine Emerich ,&nbsp;Matteo Brunelli ,&nbsp;Serena Pedron ,&nbsp;Cristina Parrado ,&nbsp;Lars U. Wahlberg ,&nbsp;Johan Lundkvist ,&nbsp;Giovanna Paolone","doi":"10.1016/j.expneurol.2025.115474","DOIUrl":"10.1016/j.expneurol.2025.115474","url":null,"abstract":"<div><div>Parkinson's disease (PD) is a complex, multifactorial neurodegenerative disorder, characterized by a progressive degeneration of dopaminergic neurons, leading to significant motor impairments frequently associated with cognitive dysfunction and comorbidities in the elderly. Current treatments of PD are primarily symptomatic, highlighting the urgent need for disease-modifying therapies. An increasing body of evidence supports the pivotal role of lysosomal dysfunction in PD pathogenesis, providing new targets for therapeutic approaches. Particularly, recent studies suggest that among the genes implicated in PD are <em>GRN</em> and <em>PSAP</em>, encoding for progranulin (PGRN) and prosaposin (PSAP), respectively.</div><div>We proved that conditioned media from a Gene Therapy Device-based delivery system (GTD)-PGRN, -PSAP, and -PGRN+PSAP were internalized by primary cortical neurons, leading to enhanced glucocerebrosidase (GCase) activity.</div><div>Furthermore, we developed a GTD-delivered therapy to target lysosomal dysfunction and support the dopaminergic system, combining the lysosomal factors PGRN and PSAP with the neurorestorative glial cell line-derived neurotrophic factor (GDNF). Interestingly, each factor provided neuroprotection to dopaminergic neurons and preserved motor function in a 6-hydroxydopamine (6-OHDA)-induced neurotoxicity model. Furthermore, eight-month treatments with GTD-PSAP and PSAP+GDNF resulted in significant neurorecovery effects on dopaminergic neurons and motor deficits following 6-OHDA injection.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"395 ","pages":"Article 115474"},"PeriodicalIF":4.2,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137003","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":"Progressively reduced cerebral oxygen metabolism and elevated plasma NfL levels in the zQ175DN mouse model of Huntington's disease","authors":"Qian Wu ,&nbsp;Minmin Yao ,&nbsp;Hongshuai Liu ,&nbsp;Aaron Kakazu ,&nbsp;Yuxiao Ouyang ,&nbsp;Chang Liu ,&nbsp;Ruoxuan Li ,&nbsp;Fan Yang ,&nbsp;Anqi Wang ,&nbsp;Sharmane Surasinghe ,&nbsp;Damien Gerochi ,&nbsp;Barbara Baldo ,&nbsp;Stefanie Jahn ,&nbsp;Haiying Tang ,&nbsp;Hanzhang Lu ,&nbsp;Zhiliang Wei ,&nbsp;Wenzhen Duan","doi":"10.1016/j.expneurol.2025.115461","DOIUrl":"10.1016/j.expneurol.2025.115461","url":null,"abstract":"<div><div>Huntington's disease (HD) is a progressive neurodegenerative disorder caused by a CAG-repeat expansion in exon-1 of the <em>huntingtin</em> gene. Currently, no disease-modifying therapies are available, with a significant challenge in evaluating therapeutic efficacy before clinical symptoms emerge. This highlights the need for early biomarkers and intervention strategies. Therefore, it is essential to develop and characterize accurate mouse models and identify early biomarkers for preclinical therapeutic development. In this study, we characterized the pathological progression of the heterozygous zQ175 neodeleted knock in (zQ175DN) mouse model across four age groups: 3, 6, 10, and 16 months to identify human translatable outcome measures. T2-relaxation-under-spin-tagging (TRUST) MRI was used to assess global CMRO₂, while T2-weighted MRI was used to analyze regional brain volumes. Significant striatal volume loss was detected as early as 6 months of age, worsening progressively with age in the zQ175 DN mice, resembling HD progressive striatal atrophy. A decline in CMRO₂ was observed in 6-month-old zQ175 DN mice, with significant and progressive reductions in 10- and 16- months old HD mice. Additionally, PHP1-positive mutant huntingtin (mHTT) aggregates were detectable in the striatum and cortex of zQ175 DN mice at all four ages, with intranuclear localization prior to 6 months, transitioning to co-exist of intranuclear and increased extracellular aggregates in older zQ175 DN mice, suggesting that the localization of mHTT aggregates may reflect the severity of HD pathogenesis. Interestingly, plasma neurofilament light chain (NfL) protein levels were significantly elevated at 6 months of age and older zQ175DN mice. These findings provide valuable insights for selecting outcome measures in preclinical evaluations of HD therapies using the zQ175 DN mouse model.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"394 ","pages":"Article 115461"},"PeriodicalIF":4.2,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145058497","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 “Cerebrospinal fluid of Alzheimer's disease and dementia with Lewy bodies patients enhances <alpha>-synuclein fibril formation in vitro” [Experimental Neurology 203 (2007) 579–583]","authors":"Kenjiro Ono ,&nbsp;Moeko Noguchi-Shinohara ,&nbsp;Mitsuhiro Yoshita ,&nbsp;Hironobu Naiki ,&nbsp;Masahito Yamada","doi":"10.1016/j.expneurol.2025.115456","DOIUrl":"10.1016/j.expneurol.2025.115456","url":null,"abstract":"","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"394 ","pages":"Article 115456"},"PeriodicalIF":4.2,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039526","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}