Journal of neural transmission (Vienna, Austria : 1996)最新文献

{"title":"Celebrating the career of professor Zdravko Lacković: a life in neuroscience, pharmacology, and discovery.","authors":"Lidija Bach-Rojecky, Ivica Matak","doi":"10.1007/s00702-025-02977-1","DOIUrl":"https://doi.org/10.1007/s00702-025-02977-1","url":null,"abstract":"","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144661738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Movement disorders associated with diarrhoea.","authors":"Claudia Lazcano-Ocampo, Tobias Warnecke, Iro Boura, Daniele Urso, Valentina Leta, Karolina Poplawska-Domaszewicz, Lucia Batzu, Ece Bayram, Vanessa Raeder, Chin-Hsien Lin, Cristian Falup-Pecurariu, K Ray Chaudhuri","doi":"10.1007/s00702-025-02924-0","DOIUrl":"https://doi.org/10.1007/s00702-025-02924-0","url":null,"abstract":"<p><p>Although the bidirectional relationship between the central nervous system and the gut has gained increasing attention in neurodegenerative conditions and movement disorders, much of the focus seems to be on constipation and other symptoms related to gastrointestinal hypomotility. However, intestinal hypermotility-related symptoms, such as diarrhoea, are also frequently associated with movement disorders, representing a clinical and research gap that needs to be addressed. This narrative review aims to describe the movement disorders associated with diarrhoea as a gastrointestinal manifestation and provide a useful overview for routine clinical practice. A variety of acquired causes, such as infectious, toxic, metabolic, and autoimmune, as well as inherited conditions may present with diarrhoea; in fact, loosen stool may sometimes precede the onset of movement disorders. Furthermore, the characteristics and volume of diarrhoea may vary depending on the underlying condition, as different pathophysiological mechanisms affecting the central and peripheral nervous system may alter gastrointestinal function. Diarrhoea is a prominent clinical symptom across a wide range of conditions, particularly those manifesting with hyperkinetic movement disorders, such as ataxia, myoclonus and tremor. When occurring in conditions with predominant hypokinetic movement disorders, it is mostly drug-associated or presents as overflow diarrhoea. Further studies exploring the relationship between bowel hypermotility and neurological dysfunction are needed.</p>","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144661740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Approaching therapy of Alzheimer's disease via the antidiabetic drug liraglutide-a study with streptozotocin intracerebroventricularly treated Wistar rats.","authors":"Ana Knezovic, Michael Hosch, Catharina Sophia Hamann, Sandy Popp, Gabriela Ortega, Jelena Osmanovic-Barilar, Edna Grünblatt, Camelia Monoranu, Peter Riederer, Melita Salkovic-Petrisic, Angelika Schmitt-Böhrer","doi":"10.1007/s00702-025-02979-z","DOIUrl":"https://doi.org/10.1007/s00702-025-02979-z","url":null,"abstract":"<p><p>Risk factors for developing dementia include type 2 diabetes and obesity. Streptozotocin (STZ) intracerebroventricularly (icv) treated rats are a well-accepted animal model for the sporadic Alzheimer`s disease (sAD). STZ-icv treatment results in an insulin-resistant brain state, cognitive deficits, and reduced hippocampal adult neurogenesis (AN). As the antidiabetic drug liraglutide (LIR) has been shown to improve AN, and spatial learning in an AD mouse model, we have investigated the effects of LIR treatment on spatial and fear-motivated learning, AN, and gene expression profiles in STZ-icv treated rats. Male Wistar rats were injected icv with STZ (f.c. 3 mg/kg) or vehicle. Two months later, four weeks of subcutaneous treatment with LIR (0.3 mg/kg) began. Cognitive abilities were assessed with the Morris water maze (MWM) and passive avoidance (PA) test. We performed quantitative immunohistochemistry to evaluate AN, and quantitative real-time PCR to determine the expression levels of genes involved in insulin signaling, glucose uptake, and neuroinflammation. STZ-icv rats showed significantly impaired spatial learning performance in the MWM and fear-motivated memory deficits in the PA test accompanied by reduced AN, downregulated insulin system- and glucose metabolism-related genes in the hippocampus and prefrontal cortex. LIR treatment did not reverse these cognitive deficits of STZ-icv rats in the MWM, and did even worsen PA performance. However, LIR partially restored dysregulated gene expression, however, additionally stimulated neuroinflammation. Refined experimental designs, e.g., refined dosing, should help to further clarify the therapeutic potential of LIR in the future.</p>","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144621741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of neuro-imaging in multiple system atrophy.","authors":"Florian Krismer, Klaus Seppi, Werner Poewe","doi":"10.1007/s00702-025-02964-6","DOIUrl":"https://doi.org/10.1007/s00702-025-02964-6","url":null,"abstract":"<p><p>Neuroimaging plays a crucial role in diagnosing multiple system atrophy and monitoring progressive neurodegeneration in this fatal disease. Advanced MRI techniques and post-processing methods have demonstrated significant volume loss and microstructural changes in brain regions well known to be affected by MSA pathology. These observations can be exploited to support the differential diagnosis of MSA distinguishing it from Parkinson's disease and progressive supranuclear palsy with high sensitivity and specificity. Longitudinal studies reveal aggressive neurodegeneration in MSA, with notable atrophy rates in the cerebellum, pons, and putamen. Radiotracer imaging using PET and SPECT has shown characteristic disease-related patterns, aiding in differential diagnosis and tracking disease progression. Future research should focus on early diagnosis, particularly in prodromal stages, and the development of reliable biomarkers for clinical trials. Combining different neuroimaging modalities and machine learning algorithms can enhance diagnostic precision and provide a comprehensive understanding of MSA pathology.</p>","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144621742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A call to action: revitalizing the German parkinson's research ecosystem post-pandemic.","authors":"Günter Höglinger, Wolfgang H Jost","doi":"10.1007/s00702-025-02980-6","DOIUrl":"https://doi.org/10.1007/s00702-025-02980-6","url":null,"abstract":"","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144593778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Are we still treading water, or are we already moving ahead again?","authors":"Wolfgang H Jost","doi":"10.1007/s00702-025-02981-5","DOIUrl":"https://doi.org/10.1007/s00702-025-02981-5","url":null,"abstract":"","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144586190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between alcohol consumption and mortality in Parkinson's disease.","authors":"You Hyun Park, Yong Wook Kim, Dae Ryong Kang, Seo Yeon Yoon","doi":"10.1007/s00702-025-02976-2","DOIUrl":"https://doi.org/10.1007/s00702-025-02976-2","url":null,"abstract":"<p><p>Previous studies on the association between alcohol consumption and risk of Parkinson's disease (PD) have produced controversial results. However, the relationship between alcohol consumption and mortality in PD has scarcely been investigated. Among the nationwide population data from Korea National Health Insurance Service, newly diagnosed PD (ICD-10 code: G20 and a rare intractable disease registration code: V124), between 2009 and 2017, were selected. Alcohol consumption habit was obtained from a self-reported questionnaire on the National Health Screening Program. 32,419 individuals with PD were followed-up longitudinally until December 31, 2017, and all-cause mortality was evaluated. During the follow-up period (mean 4.37 ± 2.67 years), 9,049 deaths occurred. When nondrinkers are used as a reference group, there were significant associations between alcohol consumption and all-cause mortality in mild (hazard ratio [HR] 0.78, 95% confidence interval [CI] 0.71-0.84) and moderate drinkers (HR 0.69, 95% CI 0.58-0.82), but not in heavy drinkers (HR 0.84, 95% CI 0.69-1.02). In the sensitivity analysis using never drinkers as the reference group, the results also showed an overall 20% reduced mortality risk among drinkers with PD. Regarding changes in alcohol consumption behavior before and after diagnosis, the mortality rate was higher in former drinkers (HR 1.20, 95% CI 1.02-1.41) and lower in constant drinkers (HR 0.74, 95% CI 0.65-0.83) than in never drinkers. Alcohol consumption appears to be associated with reduced all-cause mortality in PD, suggesting potential neuroprotective effects on disease progression. Although drinking does not appear to be detrimental to all-cause mortality in individuals with PD, alcohol consumption in PD requires attention considering individual motor and non-motor symptoms. Future studies in other ethnic groups are warranted to validate the association between alcohol consumption and disease progression, including mortality, in PD.</p>","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144577592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From stress to anhedonia: differential gene expression, behavioural and biochemical modulations in resilient versus susceptible mice in an ultrasound model of juvenile depression.","authors":"Tatyana Strekalova, Johannes de Munter, Anna Gorlova, Raymond Cespuglio, Alexei V Deykin, Alexei Lyundup, Alisa Burova, Elina Kochina, Kseniia Sitdikova, Aleksey Umriukhin, Boris Shulgin, Edna Grünblatt, Susanna Walitza","doi":"10.1007/s00702-025-02974-4","DOIUrl":"https://doi.org/10.1007/s00702-025-02974-4","url":null,"abstract":"","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144556522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fluid biomarkers in atypical Parkinsonism: current state and future perspectives.","authors":"Anastasia Bougea, Carlo Colosimo, Cristian Falup-Pecurariu, Giovanni Palermo, Yildiz Degirmenci","doi":"10.1007/s00702-025-02930-2","DOIUrl":"10.1007/s00702-025-02930-2","url":null,"abstract":"<p><p>Diagnosing Atypical Parkinsonian Syndromes (APS) may be challenging due to overlapping clinical features of Parkinson's disease (PD), and the lack of pathognomonic diagnostic tests. Fluid biomarkers can be useful tools that make it easier to identify and track different APS. Objectives: this narrative review aim to update the current state of fluid biomarker research in APS and their potential implications in clinical practice. A comprehensive literature search was conducted in PubMed and Scopus using the following terms: \"Aβ42 amyloid beta with 42 amino acids'', \" alpha-synuclein'', \"Atypical Parkinsonian Syndromes'', \"corticobasaldegeneration'', \"C reactive protein'', \"cerebrospinal fluid'', \"dementia with Lewy bodies'', \"multiple system atrophy'', \"neurofilament light, oligomericαsyn, phosphorylated α -syn'', \"tau phosphorylated at threonine 181'', \"progressive supranuclear palsy'', \"Seeding Amplification Assay'', \"t-tau; total tau\". The lack of high-affinity α-syn antibodies and ligands may contribute to α-syn's low efficacy as a diagnostic biomarker of APS. Cerebrospinal fluid (CSF) biomarkers reflecting Alzheimer pathology, axonal damage (neurofilament light chain) add valuable diagnostic and prognostic information in the neurochemical characterization of APS. Inflammatoryand microRNAs markers need to be further validated before their clinical use. Seeding Amplification Assays (SAA), despite their high sensitivity and specificity, are at this point used only as a research tool, and they are not quantitative or reflective of disease severity. Biomarker research for early identification and prognosis of APS patients requires multicenter collaboration, validation, and AI-based diagnostics, despite immature biological classification systems.</p>","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":"921-941"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vascular parkinsonism: an update.","authors":"Kurt A Jellinger","doi":"10.1007/s00702-025-02960-w","DOIUrl":"10.1007/s00702-025-02960-w","url":null,"abstract":"<p><p>Vascular parkinsonism (VP), resulting from cerebrovascular disease, is a rare disorder with a characteristic motor and non-motor clinical profile distinct from sporadic/idiopathic Parkinson disease (PD) and other parkinsonian disorders. It accounts for 3-6% of all parkinsonian syndromes and may overlap with other parkinsonisms. Clinical features of VP are heterogenous and include bilateral rigidity with lower body predominance, bradykinesia, postural instability, shuffling gait, falls, corticospinal symptoms and cognitive impairment, tremor being rare or absent. An international working group recommended three VP subtypes: (1) the acute or subacute poststroke type: asymmetric parkinsonism due to involvement of the nigrostriatal system and response to dopaminergic drugs, (2) the more frequent insidious onset subtype due to ischemic deep white matter lesions and/or lacunar infarcts presents with progressive, symmetrical parkinsonism, prominent postural instability, gait impairment, corticospinal, pseudobulbar, urinary and cognitive symptoms, and poor levodopa response; (3) mixed VP/PD and other neurodegenerative parkinsonisms showing overlaps between these forms, with upper and lower body rigidity, resting tremor, dementia and positive levodopa response. Neuroimaging shows brain atrophy, widespread deep white matter lesions, lacunar infarcts and rare direct damage to nigrostriatal areas. Advanced MRI techniques and dopamine transporter imaging may be useful in the differentiation of VP with PD and other neurodegenerative parkinsonian syndromes. Neuropathology of VP reveals multiple subcortical ischemic lesions due to small vessel disease in basal ganglia and deep white matter, less often lesions of striatum, and substantia nigra involving cortico-basal ganglia-cortical and other neuronal circuits. Lewy pathology is usually absent. New molecular biomarkers will help to differentiate VP from other parkinsonian syndromes. The response of VP to different therapeutic strategies is modest. Further studies are warranted to explore the role of vascular lesions in the pathogenesis of VP and to demonstrate the efficacy of new therapy options.</p>","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":"899-919"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144228401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}