{"title":"Modification of locomotion-respiration coupling in patients with obstructive sleep apnea syndrome.","authors":"Rémi Valentin, Baptiste Sandoz, Marie-Cécile Niérat, Thomas Similowski, Valérie Attali, Hélène Pillet","doi":"10.1159/ndd/aduag007","DOIUrl":"https://doi.org/10.1159/ndd/aduag007","url":null,"abstract":"<p><strong>Introduction: </strong>Locomotion is a complex motor task integrating sensory-motor and cognitive inputs through central pattern generator control. Locomotion-respiration coupling (LRC), defined as the synchronization between gait and breathing events, has been described during running and walking. Patients with obstructive sleep apnea syndrome (OSAS) exhibit altered gait patterns during wakefulness, which appear to be partially independent of nocturnal symptomatic treatment. While intermittent hypoxia may induce long-term (\"fixed\") central nervous system alterations, OSAS patients also display \"reversible\" adaptive mechanisms during wakefulness aimed at preventing upper airway (UA) collapse, involving changes in respiratory control and posture. Whether these adaptive mechanisms affect LRC and contribute to gait alterations remains unknown.</p><p><strong>Methods: </strong>Ten awake patients with controlled OSAS treated with a mandibular advancement device (MAD) and ten matched healthy controls performed a one-minute walking trial on an instrumented treadmill with motion capture. Ventilation was assessed via thoracic expansion, and spatiotemporal gait parameters were extracted from kinematic and force platform data. LRC was quantified using phase-locking values (PLV) between ventilatory events and sagittal-plane joint kinematics. OSAS patients were assessed both with and without their MAD.</p><p><strong>Results: </strong>Compared with controls, OSAS patients exhibited a longer double-stance phase and a shorter swing phase. Expiratory events occurred preferentially during double stance in OSAS patients, whereas controls showed a higher occurrence during swing. PLV analysis revealed increased synchronization between inspiratory events and hip and knee motion, as well as between expiratory events and trunk and hip motion in OSAS patients. These significative differences were no longer observed when patients wore their MAD. Logistic regression demonstrated that PLV metrics of inspiratory-hip and expiratory-trunk coupling effectively discriminated OSAS patients from controls, but not when UA stabilization was applied.</p><p><strong>Conclusion: </strong>Awake patients with controlled OSAS exhibit altered gait patterns characterized by increased locomotion-respiration coupling. This heightened synchronization likely reflects adaptive, reversible strategies aimed at limiting UA collapsibility during wakefulness rather than fixed hypoxia-related impairments alone. LRC may represent a functional marker of daytime motor alterations in OSAS and a potential target for interventions addressing UA mechanics beyond nocturnal treatment.</p>","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":" ","pages":"1"},"PeriodicalIF":4.0,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Setareh Ranjbar, Ruken Yaman-Deveci, Kevin Swierkosz-Lenar, Mohamed Hichem Lakhal, Alessia Donati, Pierre Vandel, Armin von Gunten, Beatriz Pozuelo Moyano
{"title":"Early Parental Attachment Style and Late-Life Depressive Symptoms: An Exploratory Analysis on the Moderating Role of Mild Cognitive.","authors":"Setareh Ranjbar, Ruken Yaman-Deveci, Kevin Swierkosz-Lenar, Mohamed Hichem Lakhal, Alessia Donati, Pierre Vandel, Armin von Gunten, Beatriz Pozuelo Moyano","doi":"10.1159/ndd/aduag005","DOIUrl":"https://doi.org/10.1159/ndd/aduag005","url":null,"abstract":"<p><strong>Background: </strong>Early relationships with caregivers shape emotional and cognitive development, colouring attitudes and behaviours across the lifespan. Secure attachment has consistently been associated with a lower risk of late-life depression (LLD). However, the extent to which parental (maternal or paternal) attachment contributes to late-life depressive symptoms and whether this association is influenced by cognitive impairment remains unclear.</p><p><strong>Objectives: </strong>We investigated whether mild cognitive impairment (MCI) moderates the association between parental (maternal/paternal) attachment style (secure vs. insecure) and late-life depressive symptoms.</p><p><strong>Methods: </strong>We analysed data from 120 participants enrolled in a cross-sectional study conducted at the Old-Age Psychiatric Service of Lausanne University Hospital. Retrospective parental attachment was assessed using the Attachment Multiple Model Interview (AMMI), from which maternal and paternal secure and insecure attachment scores were derived. Late-life depressive symptoms were measured with the Cornell Scale for Depression in Dementia using both self- and informant-reports. MCI was defined using the Clinical Dementia Rating (CDR), with a global score equal to 0.5 indicating MCI. Associations and potential moderation by MCI were examined using multiple linear regression models.</p><p><strong>Results: </strong>Lower secure paternal attachment was significantly associated with higher self- and informant-reported depressive symptom severity, but only among participants with MCI. No significant associations were observed independently of the MCI for maternal attachment or insecure paternal attachment.</p><p><strong>Conclusions: </strong>Early paternal bonds may shape emotional vulnerability differently in the context of cognitive decline. These results suggest considering both attachment history and cognitive status in interventions for late-life depressive symptoms.</p>","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":" ","pages":"1"},"PeriodicalIF":4.0,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149128077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Can Music-induced brain plasticity delay Neurodegenerative Disorders in Musicians? Review and Cases.","authors":"Eckart Altenmüller","doi":"10.1159/ndd/aduag004","DOIUrl":"https://doi.org/10.1159/ndd/aduag004","url":null,"abstract":"<p><p>Musicians undergo early and intensive training to enhance auditory, sensorimotor, and emotional skills. These abilities are underpinned by brain plasticity, which allows adaptation to demanding and motivating tasks. Musical activity can boost cognitive reserve and slow neurodegenerative diseases; for example, rhythmic movement aids gait in Parkinson's patients, and musicians may develop dementia later, though more research is needed. The chapter also discusses two musicians, Maurice Ravel, likely affected by fronto-temporal dementia with corticobasal degeneration, and Aaron Copland, who probably had Alzheimer's disease.</p>","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":" ","pages":"1"},"PeriodicalIF":4.0,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149031296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nan Hu, Ning Su, Dingding Zhang, Jiangxia Zhang, Kai Wang, Yuming Xu, Zhenzhong Li, Lihua Wang, Bo Wu, Lan Chu, Yinzhou Wang, Hong Jiang, Zhengqi Lu, Jian Wu, Xiangmin Fan, Fei Han, Jing Yuan, Yicheng Zhu, Mingsheng Liu
{"title":"Gait Characteristics and Fall Risk in Amyotrophic Lateral Sclerosis: A 12-Month Prospective Cohort Study.","authors":"Nan Hu, Ning Su, Dingding Zhang, Jiangxia Zhang, Kai Wang, Yuming Xu, Zhenzhong Li, Lihua Wang, Bo Wu, Lan Chu, Yinzhou Wang, Hong Jiang, Zhengqi Lu, Jian Wu, Xiangmin Fan, Fei Han, Jing Yuan, Yicheng Zhu, Mingsheng Liu","doi":"10.1159/ndd/aduag003","DOIUrl":"https://doi.org/10.1159/ndd/aduag003","url":null,"abstract":"<p><strong>Background: </strong>Gait impairment in amyotrophic lateral sclerosis (ALS) substantially increases fall risk and accelerates functional decline. However, prospective data linking quantitative gait parameters to fall outcomes remain scarce. We aimed to identify gait parameters associated with falls and functional decline in ALS.</p><p><strong>Methods: </strong>In this single-center prospective cohort study, we enrolled 256 ALS patients and 256 matched healthy controls. Nineteen spatiotemporal gait parameters were captured using a 3D vision-based system at baseline. Falls, time to wheelchair use, and ALSFRS-R decline were recorded over 12 months. Multivariable logistic regression was used to identify independent fall predictors.</p><p><strong>Results: </strong>During follow-up, 129 of 224 patients (57.6%) experienced at least one fall. Prolonged Timed Up and Go (TUG) time (OR=1.083 per second, 95%CI 1.036-1.133, p<0.001), younger age (OR=0.968 per year, 95%CI 0.940-0.996, p=0.024), and lower MRC sum score (OR=0.976 per point, 95%CI 0.954-0.998, p=0.035) independently predicted falls. The model showed moderate discrimination (AUC=0.665, 95%CI 0.594-0.736). Gait speed (rₛ=0.366) and TUG time (rₛ=-0.381) correlated most strongly with time to wheelchair use (both p<0.001), whereas no gait parameters correlated with ALSFRS-R decline rate.</p><p><strong>Conclusions: </strong>TUG time, younger age, and lower MRC score independently predict falls in ALS, though with modest predictive accuracy. The modest model performance underscores the multifactorial nature of falls and the need for multi-domain risk assessment. Gait speed and TUG time may warrant further investigation as candidate surrogate markers for functional decline. Future studies integrating cognitive evaluation, continuous monitoring, and attention to psychosocial factors may improve prediction and fall prevention strategies.</p>","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":" ","pages":"1"},"PeriodicalIF":4.0,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149025562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Physical Training in Parkinson's Disease: A Systematic Review of Neurobiological Mechanisms, Brain-Muscle Adaptations, and Implications for Personalized Rehabilitation.","authors":"Anthony Jannou, Marie-Laure Welter","doi":"10.1159/ndd/aduag002","DOIUrl":"10.1159/ndd/aduag002","url":null,"abstract":"<p><strong>Background: </strong>Physical Training (PT), defined a planned, structured, and long-term exercise intervention, is recognized as an important non-pharmacological therapy in Parkinson's disease (PD). Beyond its symptomatic benefits, experimental evidence suggests that PT may also modulate pathological mechanisms involved in dopaminergic neurodegeneration. This systematic review summarizes the neurobiological and neurophysiological adaptations induced by PT in animal models of PD and in patients with PD, and proposes mechanistically driven recommendations for personalized exercise prescription.</p><p><strong>Summary: </strong>MEDLINE and Web of Science were searched from January 1, 1974, to April 3, 2026. The PRISMA 2020 guidelines were followed, and two reviewers independently screened titles and abstracts to identify studies that reporting neurobiological or neurophysiological effects of PT performed for at least 4 weeks, in both animal models of PD or in patients with PD. Risk of bias were assessed using validated tools for animal studies (SYRCLE), and for randomized (RoB 2) or non-randomized controlled trials (ROBINS-I) in humans. A total of 78 studies were included, comprising 55 animal studies and 23 studies in patients with PD. In parkinsonian animals, PT consisted mainly of forced treadmill training, performed 20-60 min/day, 5 days/week, typically for 4 weeks. PT reduced oxidative stress and mitochondrial dysfunction, enhanced antioxidant defences, and regulated mitochondrial dynamics. Exercise also decreased α-synuclein accumulation, attenuated neuroinflammation, and increased neurotrophic factor expression. These adaptations promoted synaptic plasticity, neurogenesis, and preservation of nigrostriatal dopaminergic neurons. In patients with PD, aerobic training (AT), resistance training (RT) and balance training (BT) have been tested, and multimodal interventions have been investigated, most commonly involving 120-150 min/week for 6-12 weeks, sometimes combined with virtual reality or exergaming. PT induced structural and functional adaptations across the brain-muscle axis, including modulation of dopaminergic signalling, reorganization of cortico-striatal and cerebellar connectivity, improved cortical inhibitory control, enhanced corticospinal drive, and neuromuscular remodelling. AT mainly improved fatigability and cardiorespiratory fitness, whereas RT and BT appear to preferentially enhance muscle strength, rate of force development, gait automaticity, and balance control.</p><p><strong>Key messages: </strong>Current evidence indicates that PT acts as a multimodal intervention capable of inducing adaptations ranging from molecular pathways to large-scale motor networks in PD. These findings support the implementation of personalized multimodal programmes combining AT, RT and BT, with progressive intensity and long-term adherence. Future studies should better define dose-response relationships, identify biomarkers of responsi","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":" ","pages":"1"},"PeriodicalIF":4.0,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148897530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Patrick Stancu, Anna E Goodheart, Lisa Hentsch, Caroline Hertler, Gilles Allali, Frédéric Assal
{"title":"When Walking Outlasts Cognition: Rethinking the Late-Stage of Lewy Body Dementia.","authors":"Patrick Stancu, Anna E Goodheart, Lisa Hentsch, Caroline Hertler, Gilles Allali, Frédéric Assal","doi":"10.1159/ndd/aduag001","DOIUrl":"10.1159/ndd/aduag001","url":null,"abstract":"<p><strong>Background: </strong>Lewy body dementia (LBD) is characterized by pervasive cognitive, motor, and neuropsychiatric symptoms. Although cognitive decline has traditionally shaped staging and prognosis, accumulating evidence indicates that gait and postural disturbances follow partially independent trajectories and may remain preserved even as cognition deteriorates. These observations challenge conventional assumptions about late-stage decline and suggest that locomotor function may complement cognitive measures when assessing late-stage transition in LBD.</p><p><strong>Summary: </strong>This review synthesizes current evidence on gait disturbances across the LBD spectrum and their neural substrates, in comparison with Alzheimer's disease (AD) and Parkinson's disease (PD). Gait impairment in LBD arises from distributed network dysfunction involving dopaminergic and cholinergic pathways, fronto-striatal, parietal, and cerebellar contributions, resulting in greater gait variability, reduced automaticity, and heightened dual-task costs relative to AD and PD. Despite this vulnerability, preserved procedural memory, brainstem locomotor circuits, and cerebellar-cortical compensation may allow walking to persist longer than cognition in some individuals. In advanced disease, rapid gait deterioration has been described near the end of life, suggesting that gait trajectories may capture aspects of late-stage decline that cognitive measures, affected by fluctuations and attentional instability, may not reliably reflect.</p><p><strong>Key messages: </strong>Gait and cognition do not decline in parallel in LBD; in some individuals, walking may outlast cognitive abilities. Gait disturbances reflect distributed network dysfunction rather than isolated motor system degeneration. In late stages, gait performance may offer a clinically useful indicator of disease transition when cognitive testing becomes less reliable. Integrating gait assessment into clinical evaluation may enhance prognostication and support palliative care planning in LBD.</p>","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":" ","pages":"1"},"PeriodicalIF":4.0,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13668057/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148760812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tshibambe N Tshimbombu, Kyle E Thurmann, Boris Decourt, Arsene Daniel Nyalundja, Samira Braimah Shardow, Melissa Ewurakua Amoako, Gates Mulume Iragi, Josué Aganze Mwambali, Marwan N Sabbagh
{"title":"Autophagy in Alzheimer's Disease: Mechanisms, Clinical Trials, and Horizons.","authors":"Tshibambe N Tshimbombu, Kyle E Thurmann, Boris Decourt, Arsene Daniel Nyalundja, Samira Braimah Shardow, Melissa Ewurakua Amoako, Gates Mulume Iragi, Josué Aganze Mwambali, Marwan N Sabbagh","doi":"10.1159/000553506","DOIUrl":"10.1159/000553506","url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease (AD) is an incurable progressive neurodegenerative disorder characterized by the pathological accumulation of amyloid beta (Aβ) plaques and neurofibrillary tangles in the brain. Recent findings have identified dysregulation of autophagy, a cellular mechanism for degradation and recycling, as a crucial contributor to the pathogenesis of AD. This narrative review examines the role of autophagy in the metabolism of Aβ and tau and evaluates current therapeutic strategies aimed at modulating autophagic pathways.</p><p><strong>Summary: </strong>Autophagy is governed by the key molecular regulators mammalian target of rapamycin, adenosine monophosphate-activated protein kinase, Beclin-1, and transcription factor EB, which collectively control the clearance of protein recycling, including aggregates, inside cells. Pharmacological agents such as rapamycin, resveratrol, and trehalose, alongside sigma-1 receptor agonists and gene therapy approaches, have demonstrated potential in modulating autophagy in preclinical and clinical studies. Despite these advances, significant challenges persist, namely, neuronal heterogeneity, optimal timing for therapeutic intervention, and the absence of reliable biomarkers to monitor autophagic activity and treatment efficacy.</p><p><strong>Key messages: </strong>Targeting autophagy offers a promising and potentially safe avenue for slowing AD progression. Future investigations should prioritize the development of selective autophagy modulators and personalized treatment strategies to restore autophagic flux and enhance clinical outcomes in patients with AD.</p>","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":" ","pages":"1-16"},"PeriodicalIF":4.0,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13493059/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148422925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mohammad Ali Rafiei, Sara Sadeghzadeh, Mehri Salari, Masoud Etemadifar
{"title":"Spinocerebellar Ataxia Type 12: Spectrums of Movement Disorders and Clinical Features.","authors":"Mohammad Ali Rafiei, Sara Sadeghzadeh, Mehri Salari, Masoud Etemadifar","doi":"10.1159/000553488","DOIUrl":"10.1159/000553488","url":null,"abstract":"<p><strong>Background: </strong>Spinocerebellar ataxia type 12 (SCA12) is a neurodegenerative disorder caused by a CAG repeat expansion in the PPP2R2B gene. It is characterized by tremor, cerebellar ataxia, and a wide range of neurological symptoms. The heterogeneity of SCA12 symptoms, particularly in movement presentation, highlights the need for standardized studies to better define its clinical spectrum.</p><p><strong>Summary: </strong>This review evaluates the spectrum of movement disorder symptoms, focusing on their type, age of onset, and progression, and highlights areas requiring further research. Tremor, typically action or postural, is often the initial symptom, followed by progressive cerebellar dysfunction, including gait instability, dysmetria, and dysdiadochokinesia, supported by neuroimaging evidence of cerebellar atrophy. Other movement-related features, such as dystonia and parkinsonism, further complicate the clinical picture. Psychiatric manifestations, including cognitive decline and depression, are also reported, though their prevalence varies. A clear characterization of the movement symptoms of SCA12 will guide future research into targeted therapeutic strategies, addressing the significant unmet needs of affected patients. This review underscores the importance of a multidisciplinary approach to studying SCA12, combining all relevant clinical data to advance knowledge and improve patient outcomes.</p><p><strong>Key messages: </strong>SCA12 presents predominantly with tremor, often preceding cerebellar signs by years. The clinical phenotype is broader than previously recognized, including dystonia, parkinsonism, and neuropsychiatric symptoms. Clinical variability may delay suspicion of SCA12, supporting early genetic testing. Systematic clinical characterization is critical for improving patient management.</p>","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":" ","pages":"1-12"},"PeriodicalIF":4.0,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13461124/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148422914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Eric Morel, Jenny C Kienzler, Giulia Bommarito, Alessandra Griffa, Mirco Nasuti, Noemi Di Fiore, Sabrina Carlier, Andrea Brioschi-Guevara, Gregoire Eberle, Katrien Van Den Keybus Deglon, Giulia Cossu, Mahmoud Messerer, Gilles Allali
{"title":"Standardizing Normal Pressure Hydrocephalus Diagnosis: The Interdisciplinary Lausanne's Protocol.","authors":"Eric Morel, Jenny C Kienzler, Giulia Bommarito, Alessandra Griffa, Mirco Nasuti, Noemi Di Fiore, Sabrina Carlier, Andrea Brioschi-Guevara, Gregoire Eberle, Katrien Van Den Keybus Deglon, Giulia Cossu, Mahmoud Messerer, Gilles Allali","doi":"10.1159/000553392","DOIUrl":"10.1159/000553392","url":null,"abstract":"<p><strong>Introduction: </strong>Idiopathic normal pressure hydrocephalus (iNPH) is a reversible neurological condition characterized by gait disorders, cognitive impairment, and urinary incontinence with ventriculomegaly at brain imaging. Due to the diagnostic complexity, we developed a structured multidisciplinary protocol to improve iNPH diagnosis. We present here the results of the first year after its implementation.</p><p><strong>Methods: </strong>A multidisciplinary team involving neurosurgeons, physical therapists, neuropsychologists, and neurologists at the Lausanne University Hospitals (Switzerland) organized a diagnostic path with the following steps: first neurological assessment at the Leenaards Memory Center, neuropsychological assessment, CSF tap test with physiotherapeutic evaluation before and 24 h after the CSF tap-test, post-CSF tap test interdisciplinary consultation with a neurosurgeon and a neurologist, and an interdisciplinary board. In case of neurosurgical treatment, interdisciplinary consultations took place at 6 weeks, 6 and 12 months.</p><p><strong>Results: </strong>This retrospective analysis included 86 patients (mean age: 76.26 ± 9.08 years; 32.6% female) evaluated between June 2024 and May 2025. Gait disorders were the most common complaint (94.2% of the patients) followed by cognitive (75.6%) and urinary (60.5%) complaints. After initial investigations, the Board evaluated 44 candidates and recommended ventriculoperitoneal shunting for 27 patients. So far, 16 patients have been operated. A total of 92% reported gait improvement at 6 weeks postoperative control. Patients above 80 years of age reported more often gait improvement than patients below 80 years.</p><p><strong>Conclusion: </strong>The Lausanne's protocol demonstrates a feasible, structured, simplified, and efficient diagnostic pathway for iNPH, especially for the oldest patients.</p>","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":" ","pages":"1-11"},"PeriodicalIF":4.0,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13461114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148397410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Alice Accorroni, Christine Clavien, Giovanni B Frisoni
{"title":"Just Semantics? How Diagnostic Criteria Influence Physician-Patient Narratives in Alzheimer's Disease.","authors":"Alice Accorroni, Christine Clavien, Giovanni B Frisoni","doi":"10.1159/000552764","DOIUrl":"10.1159/000552764","url":null,"abstract":"<p><strong>Introduction: </strong>The current diagnosis of Alzheimer's disease (AD) is shaped by the Alzheimer's Association (AA) and the International Working Group (IWG) criteria. While both frameworks lead to similar physician-patient conversations when disclosing biomarker results to patients with cognitive impairment, they diverge significantly for cognitively unimpaired individuals. The aim of this paper is to explore these differences and their associated epistemological and ethical implications, through simulated, case-based physician-patient conversations.</p><p><strong>Methods: </strong>The conversations were developed on the basis of clinical experience, exchanges with patients and carers, insights from a targeted narrative literature review and were subsequently refined with large language model assistance.</p><p><strong>Results: </strong>Our analysis highlights that the AA framework reinforces a deterministic narrative by equating amyloid biomarker positivity with disease and raising a misunderstanding of illness. In contrast, the IWG framework is consistent with the incomplete penetrance of AD pathology and frames biomarker positivity in cognitively unimpaired individuals as a risk condition. We acknowledge that the IWG framework enables more complex but also more realistic physician-patient conversations.</p><p><strong>Conclusion: </strong>Physician-patient conversations employing a carefully selected lexicon, reflecting patient-centred outcomes, may promote patient engagement, compliance with medical recommendations, and, ultimately, societal trust in medicine and physicians.</p>","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":" ","pages":"1-17"},"PeriodicalIF":4.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13557707/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148331424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}