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

{"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}

{"title":"Determinants of clinical and neurophysiological features in essential tremor and essential tremor plus.","authors":"Takashi Tsuboi, Takashi Uematsu, Keito Sawada, Moeka Higuchi, Miki Hashida, Manabu Muto, Yoshiki Ito, Tomotaka Ishizaki, Sachiko Kato, Daisuke Nakatsubo, Takahiko Tsugawa, Satoshi Maesawa, Yuki Saito, Taiki Fukushima, Daigo Tamakoshi, Keita Hiraga, Masashi Suzuki, Ryuta Saito, Adolfo Ramirez-Zamora, Michael S Okun, Masahisa Katsuno","doi":"10.1007/s00702-025-02941-z","DOIUrl":"10.1007/s00702-025-02941-z","url":null,"abstract":"<p><p>The 2018 Movement Disorder Society classification introduced essential tremor plus (ETP) as a category for patients with essential tremor (ET) accompanied by additional features of uncertain significance. While earlier studies have characterized clinical features of ETP, the factors that characterize the phenotypic expression of ETP remain unclear. We prospectively evaluated 70 consecutive patients with ET or ETP. Clinical and neurophysiological assessments included tremor severity (Clinical Rating Scale for Tremor, CRST), cognitive functions (Addenbrooke's Cognitive Examination Revised, ACE-R), and accelerometric analysis. Statistical analyses examined between-group differences and factors influencing tremor characteristics. The prevalence of ETP (61%) exceeded that of ET. Among ETP patients, 77% exhibited two or more additional motor and/or cognitive features. Compared to ET patients, ETP patients demonstrated significantly higher tremor severity, lower tremor frequency, older age at assessment and onset, and poorer cognitive function, despite comparable disease duration. The accelerometric analysis revealed similar tremor patterns in both groups with quantitative differences in tremor amplitude and frequency. The propensity score matching and multiple regression analyses suggested that tremor severity and frequency are more influenced by age than by disease duration or diagnostic classification of ET/ETP. ACE-R score and the presence of resting tremor were also significant predictors of tremor severity. ETP represents a heterogeneous population with diverse neurological features, and age is likely a key determinant of severity and phenotypic expression. Comprehensive analysis is needed to identify other factors that may determine phenotype and treatment responsiveness.</p>","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":"1041-1050"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113251","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":"Co-occurrence of amyotrophic lateral sclerosis and multiple sclerosis: a rare but interesting association.","authors":"Kurt A Jellinger","doi":"10.1007/s00702-025-02975-3","DOIUrl":"https://doi.org/10.1007/s00702-025-02975-3","url":null,"abstract":"<p><p>Multiple sclerosis (MS) is an inflammatory demyelinating disease with highly variable clinical course and usual onset in younger age, caused by genetic and environmental factors. Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder that affects motor neurons in the brain and spinal cord, resulting in gradual loss of voluntary muscle and respiratory control. Both ALS and MS exhibit distinct underlying causes and disease mechanisms, despite some shared clinical effects. About 10% of ALS are linked to genetic factors, such as C9orf72, the remaining sporadic ones being potentially influenced by environmental, toxic and oxidative stress, while MS is an autoimmune disorder where the immune system leads to inflammation and attacks the myelin sheath, genetic predisposition and viral infections playing a role in its susceptibility. The co-occurrence of ALS and MS is extremely rare, with 46 cases being reported in the available literature from 1986 to 2024, while in the earlier literature, cases with coincidental muscular atrophy simulating ALS were described. In the overwhelming majority, ALS manifested between one and 41 years after the onset of MS; only in four cases was ALS present before detection of MS. The concurrence of MS and ALS can be explained by similarities in their pathogenesis related to neurodegeneration, inflammation, and/or genetic susceptibility. The role of rare genetic ALS forms in this comorbidity deserves further studies. The shared inflammatory component with a cascade of oxidative stress and other noxious mechanisms leads to progressive motor and bulbar or other symptoms that underscore the potential for cross-disease research to yield insights applicable to both conditions and their relations to immune-mediated disorders.</p>","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144532755","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":"Sensitivity to negative-feedback processing in people with Parkinson's disease and impulsive-compulsive behaviours.","authors":"Alice Martini, Nicola Edelstyn, Luca Weis, Stefano Tamburin, Roberta Schifano, Joseph L Brooks, Elisa Mantovani, James A Grange, Matteo Francesco Lauriola, Francesca Pistonesi, Giuseppe Leoni, Angelo Antonini, Roberta Biundo","doi":"10.1007/s00702-025-02967-3","DOIUrl":"https://doi.org/10.1007/s00702-025-02967-3","url":null,"abstract":"","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144487727","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":"Concomitant pathologies and their impact on Huntington's disease. A brief review of current evidence.","authors":"Kurt A Jellinger","doi":"10.1007/s00702-025-02957-5","DOIUrl":"10.1007/s00702-025-02957-5","url":null,"abstract":"","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340796","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}