[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"health-studies-list:{\"overallStatus\":[\"RECRUITING\",\"AVAILABLE\",\"NOT_YET_RECRUITING\"],\"leadSponsorName\":\"Neuromed IRCCS\",\"orderBy\":\"LastUpdateSubmitDate:desc\",\"size\":25,\"offset\":0}":3,"health-study-condition:":265},{"pageToken":4,"total":5,"offset":6,"count":5,"results":7},null,9,0,[8,60,87,115,142,170,196,220,246],{"id":9,"slug":10,"hasResults":11,"nctId":12,"briefTitle":13,"officialTitle":14,"acronym":4,"eligibilityCriteria":15,"healthyVolunteers":16,"sex":17,"minAge":18,"maxAge":4,"enrollmentInfo":19,"targetDuration":22,"studyType":23,"phases":4,"briefSummary":24,"conditions":25,"keywords":33,"overallStatus":47,"whyStopped":4,"lastUpdateSubmitDate":48,"lastUpdatePostDateStruct":49,"startDateStruct":52,"completionDateStruct":54,"leadSponsor":56,"locationsCount":59},"100633930","italian-validation-of-the-dna-scale-and-its-correlation-with-neurocognitive-variables-100633930",false,"NCT07533084","Italian Validation of the dNA Scale and Its Correlation With Neurocognitive Variables","Italian Validation of the Dynamic Neurocognitive Adaptation (dNA) Scale and Its Correlation With Neurocognitive Variables","Inclusion Criteria (Stage #1):\n\n* Individuals aged ≥ 65 years residing in Italy;\n* Cognitively healthy individuals (HC);\n* Individuals with subjective memory complaints (SMC);\n* Individuals with mild cognitive impairment (MCI);\n* Individuals with probable Alzheimer's disease (AD).\n\nInclusion criteria (Stage #2 \\& Stage #3):\n\n* Individuals aged ≥ 65 years residing in Italy;\n* Cognitively healthy individuals (HC);\n* Individuals with subjective memory complaints (SMC);\n* Individuals with mild cognitive impairment (MCI);\n* Individuals with probable Alzheimer's disease (AD);\n* Individuals with Alzheimer's disease or other forms of dementia;\n* Individuals suffering from mental disorders clinically diagnosed.\n\nCognitively healthy individuals (HC):\n\n* MMSE score ≥24, or alternatively MoCA score ≥26;\n* No diagnosis of depression, MCI or any form of dementia;\n* Episodic memory performance within the normal range (Wechsler Memory Scale Logical Memory II ≥9 for 16 years of schooling or more; ≥5 for 8-15 years of schooling, ≥3 for 0-7 years of schooling; or alternatively for Prose Memory Test with scores ≥9 for ≥16 years of schooling → ≥5 items in immediate or delayed recall; ≥5 for 8-15 years of schooling → ≥3-4 items in immediate or delayed recall; ≥3 for 0-7 years of schooling → ≥2 items in immediate or delayed recall)\n\nIndividuals with Subjective Memory Complaints (SMC):\n\n* MMSE score ≥24, or alternatively MoCA score ≥26;\n* A significant memory impairment, reported by the subject, a family member, or the clinician;\n* No diagnosis of depression, MCI or any form of dementia;\n* Episodic memory performance within the normal range on the Wechsler Memory Scale Logical Memory II adjusted for years of schooling (≥9 for 16+ years of schooling, ≥5 for 8-15 years of schooling, ≥3 for 0-7 years of schooling) or, alternatively, on the Prose Memory Test (with scores ≥9 for ≥16 years of schooling → ≥5 items in immediate or delayed recall; ≥5 for 8-15 years of schooling → ≥3-4 items in immediate or delayed recall; ≥3 for 0-7 years of schooling → ≥2 items in immediate or delayed recall)\n\nIndividuals with Mild Cognitive Impairment (MCI):\n\n* MMSE score between 19 and 23 inclusive (alternatively MoCA);\n* A decline in memory reported by the subject, a family member, or the clinician;\n* No diagnosis of depression or affected by any form of dementia, with preserved ability in activities of daily living;\n* Objective episodic memory loss on the Wechsler Memory Scale Logical Memory II adjusted for years of schooling.\n\nIndividuals with probable Alzheimer's disease (AD):\n\n* Insidious onset with atypical course: some criteria for probable AD are met, but the onset of symptoms may have been sudden, or there is a lack of objective evidence of progressive cognitive decline;\n* Mixed etiology presentation: All criteria for probable AD are met, with concomitant cerebrovascular disorders, or the presence of features typical of another dementia or the evidence of other neurological disorders or non-neurological comorbidities;\n* A decline in performance compared to the previous level of functioning is evident, as also described by a caregiver (often a family member)\n* Onset with memory disturbances, defined as difficulty learning new information or recalling it;\n* Onset with non-mnemonic symptoms (language symptoms, particularly difficulty finding the correct words; visuospatial symptoms: perceptual deficits characterized by failure to recognize objects, people, or written words; executive symptoms: difficulties with reasoning and critical thinking);\n* MMSE score \\\u003C 23 (alternatively MoCA \\\u003C 25);\n* Objective episodic memory loss on the Wechsler Memory Scale Logical Memory II adjusted for years of schooling.\n\nExclusion criteria (Stage #1):\n\n* Individuals aged \\\u003C 65 years;\n* Individuals not residing in Italy;\n* Individuals with depression or other psychiatric disorders;\n* Individuals with forms of dementia other than Alzheimer's disease.",true,"ALL","65 Years",{"count":20,"type":21},265,"ESTIMATED","1 Year","OBSERVATIONAL","The goal of this experimental multicentric intervention study is to validate, in Italian, the dynamic Neurocognitive Adaptation (dNA) Scale, which has already been validated in English, among a healthy elderly population (aged 65 and older) residing in Italy and patients with dementia or Alzheimer's Disease. dNA is a questionnaire designed to assess both current and past levels of engagement in physical, cognitive, creative, and social activities.\n\nThe study aims to recruit a total of 265 participants with mild cognitive impairment, subjective memory complaints, or dementia. These participants will be distributed among the 8 recruitment centers. Neuropsychological data, subjective measures, and MRI data will be collected and analyzed to address the following research questions: 1) Is there a positive correlation between scores on the dNA Scale and cognitive efficiency, as reflected in neuropsychological measures, such as episodic memory and executive functions? 2) Is there a correlation between dNA scores and improved functional connectivity within neural networks, such as the Default Network (DN)?\n\nParticipants recruited at the participating clinical centers will undergo:\n\n* A clinical interview, during which demographic and medical history information will be collected. The dNA Scale will be administered, along with a questionnaire assessing adherence to dietary habits typical of a Mediterranean diet (14-Item Mediterranean Diet Adherence Screener; MEDAS).\n* A neuropsychological assessment, aimed at evaluating general cognitive function with a particular focus on episodic memory and executive functions. The following tests will be administered: Mini-Mental State Examination (MMSE) or, alternatively, Montreal Cognitive Assessment (MoCA); Rey Auditory Verbal Learning Test (RAVLT); Trial Making Test (TMT) Form B; Digit Span Forward and Backward (WAIS or WAIS-III); and the Stroop Test.\n* Self-report questionnaires designed to assess depressive symptoms using the Geriatric Depression Scale (GDS) and anxiety symptoms using the Geriatric Anxiety Scale (GAS) (or alternatively the State-Trait Anxiety Inventory, STAI). Finally, the Cognitive Reserve Index Questionnaire will be administered to estimate Cognitive Reserve (CRIq).\n* Where available, MRI data previously acquired for clinical or diagnostic purposes will be included in the study and analyzed by the principal investigator.",[26,27,28,29,30,31,32],"Active Aging Individuals Aged 65 and Over","Aging","Mild Cognitive Impairment (MCI)","Dementia","Dementia Alzheimer Type","Subjective Memory Complaints","Probable Alzheimer's Disease",[34,35,36,37,38,39,40,41,42,43,44,45,46],"activities","habits","lifetime protective factors","adaptation","dynamic","neurocognitive","prevention","reserve","resilience","resistance","validation","well-being","aging","NOT_YET_RECRUITING","2026-06-09",{"date":50,"type":51},"2026-06-11","ACTUAL",{"date":53,"type":21},"2026-09",{"date":55,"type":21},"2027-11-27",{"name":57,"class":58},"Neuromed IRCCS","OTHER",8,{"id":61,"slug":62,"hasResults":11,"nctId":63,"briefTitle":64,"officialTitle":65,"acronym":4,"eligibilityCriteria":66,"healthyVolunteers":11,"sex":67,"minAge":68,"maxAge":69,"enrollmentInfo":70,"targetDuration":4,"studyType":23,"phases":4,"briefSummary":72,"conditions":73,"keywords":4,"overallStatus":77,"whyStopped":4,"lastUpdateSubmitDate":78,"lastUpdatePostDateStruct":79,"startDateStruct":81,"completionDateStruct":83,"leadSponsor":85,"locationsCount":86},"100470268","mediterranean-diet-on-pregnancy-and-foetus-development-100470268","NCT05403632","Mediterranean Diet on Pregnancy and Foetus Development","Influence of Mediterranean Dietary Habits on Pregnancy and Foetus Development: the Role of Epigenetics and Inflammation","Inclusion Criteria:\n\n* pregnant women attending the Units of Obstetrics and Gynecology at Neuromed Clinical Research Network\n* women within the first trimester of pregnancy\n* women who express the willing to deliver at the aforementioned operating units\n\nExclusion Criteria:\n\n* pregnancy with foetuses with known chromosomal or congenital malformation\n* history of inflammatory disease\n* use of immunosuppressant drugs\n* pre-existing diabetes or hypertension\n* conception by heterologous artificial insemination\n* malabsorptive bariatric surgery\n* eating disorders","FEMALE","18 Years","50 Years",{"count":71,"type":21},2000,"The Mediterranean-style diet has been associated with longevity, long-life wellbeing, lower risk of cardiovascular disease, cancer, obesity, and metabolic syndrome. Research is pointing to the benefits that MeD could have in pregnant. Pregnancy is a very complex period and recently, the attention has been focused on the possibility that healthy dietary patterns positively influence pregnancy and the development of organs in the offspring. The mechanisms through which MeD influences pregnancy and fetal growth may partly depend on its antinflammatory properties and possibly on changes in epigenetic mechanisms. Systemic inflammation might contribute to the association between maternal obesity and less favorable neurodevelopmental outcomes. The investigators aim to define how maternal adhesion to MeD may affect pregnancy and new-born development, hence representing a notable burden from a public health and social perspective. Main objective of this project is to build up a birth cohort suitable to investigate the role of maternal dietary habits on maternal and new-born health, with special focus on MeD and its possible mechanism of action through epigenetic and inflammation changes. To establish a mother\u002Fnew-born cohort, collect detailed information on maternal dietary habits and set-up a biobank of biological samples to evaluate the association between dietary habits and pregnancy outcomes. The investigators will recruit 2000 pairs (mother, new-born) in different obstetrics departments. To investigate the association between maternal dietary habits, foetal growth and offspring development and possible mediation by the inflammation profile of the mother. To understand whether maternal dietary habits are associated with epigenetic changes in the offspring and if this process is driven by the inflammation profile of the mother. Venous blood samples will be obtained at the baseline and at each gestational period for ultrasound at 11-13 gestational weeks, 20-22 weeks and 30-32 weeks. Women will be followed-up with standard clinical and 2D ultrasound examinations at gestational weeks 11-13, 20-22 and 30-32 to evaluate the fetal growth. Offspring development will be assessed at 6, 12, 18, 24 months of age. After delivery, the investigators will collect umbilical cord blood and saliva samples from new-born using standard procedures. To understand if new-born epigenetics is associated with infant physical and neurocognitive development in the following 2 years.",[74,75,76],"Pregnancy Outcomes","Fetal Development","Infant Development","RECRUITING","2026-04-08",{"date":80,"type":51},"2026-04-09",{"date":82,"type":51},"2023-05-01",{"date":84,"type":21},"2027-12-31",{"name":57,"class":58},1,{"id":88,"slug":89,"hasResults":11,"nctId":90,"briefTitle":91,"officialTitle":92,"acronym":93,"eligibilityCriteria":94,"healthyVolunteers":16,"sex":17,"minAge":68,"maxAge":4,"enrollmentInfo":95,"targetDuration":97,"studyType":23,"phases":4,"briefSummary":98,"conditions":99,"keywords":103,"overallStatus":77,"whyStopped":4,"lastUpdateSubmitDate":107,"lastUpdatePostDateStruct":108,"startDateStruct":110,"completionDateStruct":112,"leadSponsor":114,"locationsCount":86},"100628885","precision-medicine-and-neurodegenerative-diseases-advanced-systems-for-the-diagnosis-and-treatment-of-parkinsons-disease-and-alzheimers-disease-100628885","NCT07467460","Precision Medicine and Neurodegenerative Diseases: Advanced Systems for the Diagnosis and Treatment of Parkinson's Disease and Alzheimer's Disease.","NEUROTECHNO: Precision Medicine and Neurodegenerative Diseases: Advanced Systems for the Diagnosis and Treatment of Parkinson's Disease and Alzheimer's Disease.","NEUROTECHNO","Inclusion Criteria:\n\n* -Inclusion Criteria:\n* Inclusion criteria for PD patients. For the IRCCS INM Neuromed, patients will be recruited from those affiliated with the Center for the Study and Treatment of Parkinson's Disease of the Neuromed Institute of Pozzilli.\n\nPresence of at least 2 of the 4 cardinal signs (tremor, rigidity, bradykinesia, asymmetric onset), one of which must be tremor or bradykinesia:\n\nAbsence of atypical symptoms such as: i) early postural instability, freezing episodes, cognitive decline, hallucinations, pathological involuntary movements, vertical gaze palsy; ii) confirmed causes of secondary parkinsonism (focal lesions, medications, toxic substances); Documented response to L-dopa or dopamine agonists (or lack of an adequate therapeutic trial with L-dopa or dopamine agonists).\n\n-Inclusion criteria forAD patients. For the University of Campania, patients will be selected at the Department of Advanced Medical and Surgical Sciences of the University of Campania \"L. Vanvitelli,\" located at Piazza Miraglia 2, Naples. The Department will establish a collaboration with the Alzheimer's day centers of ASL NA1 (Geriatric Facility \"Villa Walpole\" - Via Ponti Rossi, 118 - Naples, and Geriatric Facility \"Frullone\" - Via Comunale del Principe, 16\u002FA - Naples) to identify potential subjects for screening to verify the parameters required for recruitment. The Geriatrics and Internal Medicine Unit (UOC), AOU University of Campania, will also be involved.\n\nPatients with AD will be included following a diagnosis of probable Alzheimer's disease according to the McKhann criteria (2011), supported by positive biomarkers for amyloidopathy (amyloid PET or cerebrospinal fluid amyloid assay).\n\nExclusion Criteria:\n\n* Pre-existing psychiatric disorders;\n* Neurodegenerative neurological diseases such as multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer's disease, neuromuscular disorders, epilepsy;\n* Diagnosis of dementia.",{"count":96,"type":21},500,"24 Months","In recent decades, advances in medicine have significantly improved both quality of life and life expectancy. However, these positive effects are also associated with a considerable increase in the prevalence of age-related diseases. Among these, Alzheimer's disease (AD), Parkinson's disease (PD), and type 2 diabetes (T2D) currently represent a major threat to human health. PD and AD are the most common neurodegenerative diseases in industrialized populations. In particular, AD accounts for 54% of all cases of dementia, with a prevalence of 4.4% among individuals over 65 years of age. PD has a prevalence of about 1% in people older than 60 years, reaching up to 4% in those over 80 years of age. AD and PD are highly disabling disorders with a slow but progressive course, caused by the degeneration and\u002For death of nerve cells. This results in impairments in the control of movement and balance, as in the case of PD, or in cognitive functioning, as in AD.\n\nTo date, neither effective treatments nor early diagnostic tools are available to address these conditions in the initial phase of neurodegeneration. Likewise, there are no tools capable of monitoring disease progression and improving patients' adaptation to therapy.\n\nMoreover, although the association between T2D and the risk of PD and\u002For AD has long been recognized, these conditions were historically considered unrelated. Recent evidence from clinical and epidemiological studies suggests the existence of shared pathophysiological mechanisms associated with insulin resistance and persistent inflammation in several metabolically relevant tissues, such as adipose tissue and the brain. However, the mechanisms that increase the risk of PD and\u002For AD in individuals with T2D remain poorly understood.\n\nThese data highlight how relevant these diseases are for the National Health System and demonstrate that they represent one of the most important priorities to be addressed, requiring substantial investments in both scientific research and early diagnostic strategies.\n\nTherefore, the present project proposal, which aims to develop new minimally invasive tools for the early prediction and monitoring of neurodegenerative diseases such as AD and PD, will help fill an important gap in the clinical and therapeutic management of these patients.",[100,101,102],"PARKINSON DISEASE (Disorder)","Alzheimer s Disease","Diabete Type 2",[104,105,106],"Identification of genetic and metabolic profiles associated with neurodegenerative diseases","Identification of epigenetic profiles associated with neurodegenerative diseases","Integration and analysis of omics and neuroimaging data","2026-03-09",{"date":109,"type":51},"2026-03-12",{"date":111,"type":51},"2026-02-17",{"date":113,"type":21},"2028-09-30",{"name":57,"class":58},{"id":116,"slug":117,"hasResults":11,"nctId":118,"briefTitle":119,"officialTitle":120,"acronym":4,"eligibilityCriteria":121,"healthyVolunteers":11,"sex":17,"minAge":4,"maxAge":4,"enrollmentInfo":122,"targetDuration":4,"studyType":124,"phases":125,"briefSummary":127,"conditions":128,"keywords":130,"overallStatus":47,"whyStopped":4,"lastUpdateSubmitDate":134,"lastUpdatePostDateStruct":135,"startDateStruct":137,"completionDateStruct":139,"leadSponsor":141,"locationsCount":4},"100591173","transcranial-static-magnetic-stimulation-tsms-in-huntingtons-disease-hd-100591173","NCT06976983","Transcranial Static Magnetic Stimulation (tSMS) in Huntington's Disease (HD)","Effects of Transcranial Static Magnetic Stimulation (tSMS) in the Treatment of Hyperkinetic Symptoms of Huntington's Disease","Inclusion Criteria:\n\n* Diagnosis of HD genetically confirmed (number of CAG triplets ≥36)\n* Presence of chorea movements quantified with a score ≥ 10 on the sum of the scores of the subscale of the Unified Huntington's Disease Rating Scale (UHDRS) for the evaluation of maximum chorea for the facial, oro-bucco-lingual, truncal, four limbs districts\n* Ability to provide written informed consent\n* No changes in drug therapy in the 8 weeks prior to the baseline visit\n* No changes in drug therapy for the entire duration of the study\n\nExclusion Criteria:\n\n* Contraindications to exposure to magnetic fields\n* Patients who are pregnant or breastfeeding\n* Presence of significant risk of suicidal behavior\n* Patients who have received an investigational drug in a clinical trial within 30 days of the baseline visit or have planned to use such an investigational drug during the study",{"count":123,"type":21},30,"INTERVENTIONAL",[126],"NA","Huntington's disease (HD) is a neurodegenerative pathology characterized by choreic hyperkinesias which represent the typical motor symptom and are represented by involuntary, aimless, irregular, recurrent, unpredictable and non-rhythmic movements of the trunk, face and limbs.\n\nNon-invasive brain neuromodulation has been proposed as a possible treatment for involuntary movements in several clinical conditions including HD.\n\nThe objective of the study is to evaluate the effect of home treatment with repeated sessions of transcranial static magnetic field stimulation (tSMS) in safely reducing choreic hyperkinesis in HD patients.",[129],"Huntington Disease",[131,132,133],"huntington disease","transcranial stimulation with static magnetic field","hyperckinesia","2025-05-10",{"date":136,"type":51},"2025-05-16",{"date":138,"type":21},"2025-09-01",{"date":140,"type":21},"2026-04-30",{"name":57,"class":58},{"id":143,"slug":144,"hasResults":11,"nctId":145,"briefTitle":146,"officialTitle":147,"acronym":148,"eligibilityCriteria":149,"healthyVolunteers":11,"sex":17,"minAge":68,"maxAge":150,"enrollmentInfo":151,"targetDuration":4,"studyType":124,"phases":153,"briefSummary":154,"conditions":155,"keywords":157,"overallStatus":47,"whyStopped":4,"lastUpdateSubmitDate":162,"lastUpdatePostDateStruct":163,"startDateStruct":165,"completionDateStruct":167,"leadSponsor":169,"locationsCount":86},"100585330","transcranial-static-field-stimulation-tsms-and-transcranial-direct-current-stimulation-tdcs-for-the-treatment-of-neurological-symptoms-100585330","NCT06900959","Transcranial Static Field Stimulation (tSMS) and Transcranial Direct Current Stimulation (tDCS) for the Treatment of Neurological Symptoms.","Transcranial Static Field Stimulation (tSMS) and Transcranial Direct Current Stimulation (tDCS) for the Treatment of Neurological Symptoms","NIBS-tSMS\u002FtDCS","Inclusion Criteria:\n\n* Males or females aged between 18 and 80 years;\n* Presence of a neurological disorder, specifically the following conditions will be considered: MS, ALS, PD, AD, Dementias, TBI, neurosurgical interventions, stroke, fibromyalgia, epilepsy, headache, migraine, with at least one of the following symptoms: pain, neuropathic pain, neuralgias, depression, anxiety, apathy, fatigue, cognitive decline, aphasia, functional motor disorders (FMD), neuromuscular tone alterations, hyposthenia, involvement of multiple cognitive functions (including decision-making, problem-solving, learning, memory, executive functions, social and emotional cognition);\n* Patients must be able to follow the protocol instructions for the duration of the study;\n* Be able to understand the purposes and risks of the study;\n* Be able to understand and provide written informed consent to the study.\n\nExclusion Criteria:\n\n* Partial or total inability to understand or make decisions, inability to provide written informed consent for the study;\n* Patients with a history or presence of any unstable medical condition, such as neoplasms or infections;\n* Women with a positive pregnancy test at baseline or planning to become pregnant. Women who are breastfeeding or have given birth within the last three months prior to the start of the study;\n* Use of medications that increase the risk of seizures (e.g., Fampridine, 4-aminopyridine);\n* Concurrent use of medications that may alter synaptic transmission and plasticity (L-dopa, antiepileptics);\n* In the case of using NIBS techniques, subjects should not have any contraindications specific to this method (for further details, see the \"Methods\" and the \"Stimulation Assessment Questionnaire\" attached to this proposal).","80 Years",{"count":152,"type":21},40,[126],"The presence of damage to the central and\u002For peripheral nervous system resulting from various pathologies, such as Multiple Sclerosis (MS), Amyotrophic Lateral Sclerosis (ALS), Parkinson's disease (PD), Alzheimer's disease (AD), dementia, traumatic brain injury (TBI), stroke, or other neurological syndromes, is commonly a cause of both physical and mental disability. This leads to symptoms in the patient, including: pain, migraines, headaches, neuropathic pain, trigeminal neuralgia, depression, anxiety, apathy, fatigue, cognitive decline, aphasia, functional motor disorders (FMD), neuromuscular tone alterations, and hyposthenia, in addition to involvement of various cognitive functions, such as decision-making, problem-solving, learning, memory, executive functions, social cognition, and emotional cognition. The presence of these neurological symptoms is often evident in a first clinical examination and is one of the main reasons for further healthcare consultations. These difficulties have a profound impact on the quality of life, affecting work, social, and family functioning.\n\nIn recent years, several non-invasive brain stimulation (NIBS) techniques have emerged, aimed at eliciting brain neural networks, such as transcranial static magnetic field stimulation (tSMS) and transcranial direct current stimulation (tDCS).\n\ntSMS is an NIBS technique that involves the application of a neodymium magnet on the scalp. Since the first study proposing this method, several others have confirmed that tSMS can reduce corticospinal excitability. tDCS involves the application of weak electrical currents capable of generating an electric field that can modulate neural activity in an excitatory or inhibitory manner. NIBS techniques can be used experimentally to modulate cortical activity.\n\nThe primary aim of this proposal is to address the impact of neurological symptoms through the combination of tSMS with tDCS and rehabilitation techniques. Specifically, it aims to understand whether the combination of these neuromodulatory therapeutic NIBS methods can enhance symptom improvement in patients with neurological conditions.\n\nTo assess the impact of this intervention, a series of tests and questionnaires, described in detail below, will be used to evaluate the severity of the reported symptoms and secondary outcomes.\n\nMoreover, the contribution of specific brain areas to the symptom will be evaluated through the direct modulation of brain activity. This modulation will be achieved using an additional NIBS technique, such as Transcranial Magnetic Stimulation (TMS). TMS, in particular, is a non-invasive method for stimulating neurons in the brain's superficial areas, which has been frequently used in neurology as a diagnostic and research tool since its introduction. TMS uses magnetic fields to induce electrical currents capable of facilitating or inhibiting cortical activity.",[156],"Neurological Diseases or Conditions",[158,159,160,161],"neuromodulation","non-invasive brain stimulation","transcranial direct current stimulation tDCS","transcranial static field stimulation tSMS","2025-03-22",{"date":164,"type":51},"2025-03-28",{"date":166,"type":21},"2025-05-11",{"date":168,"type":21},"2026-02-11",{"name":57,"class":58},{"id":171,"slug":172,"hasResults":11,"nctId":173,"briefTitle":174,"officialTitle":174,"acronym":4,"eligibilityCriteria":175,"healthyVolunteers":16,"sex":17,"minAge":176,"maxAge":4,"enrollmentInfo":177,"targetDuration":4,"studyType":23,"phases":4,"briefSummary":179,"conditions":180,"keywords":185,"overallStatus":77,"whyStopped":4,"lastUpdateSubmitDate":188,"lastUpdatePostDateStruct":189,"startDateStruct":191,"completionDateStruct":193,"leadSponsor":195,"locationsCount":86},"100577860","discovery-and-validation-of-protein-structural-complexes-in-circulating-biofluids-as-novel-biomarkers-for-early-diagnosis-prognosis-and-therapeutic-management-of-patients-affected-by-neurodegenerative-disorders-100577860","NCT06803784","Discovery and Validation of Protein Structural Complexes in Circulating Biofluids As Novel Biomarkers for Early Diagnosis, Prognosis and Therapeutic Management of Patients Affected by Neurodegenerative Disorders","* Inclusion Criteria:\n* Inclusion criteria for PD patients.\n\nFor the IRCCS INM Neuromed, patients will be recruited from those affiliated with the Center for the Study and Treatment of Parkinson's Disease of the Neuromed Institute of Pozzilli. Affected subjects will be selected according to the criteria proposed by Gelb et al in 1999. This is a very pragmatic scheme based on the presence of four cardinal signs, the response to a test administration of Levodopa and the absence of atypical signs:\n\nA) Presence of at least 2 of the 4 cardinal signs (tremor, rigidity, bradykinesia, asymmetric onset) one of which must be tremor or bradykinesia; B) Absence of atypical symptoms such as: i) early postural instability, freezing phenomena, cognitive deterioration, hallucinations, pathological involuntary movements, vertical gaze paralysis; ii) proven causes of secondary parkinsonism (focal lesions, drugs, toxic substances); C) Documented response to the use of L-dopa or dapamine agonists (or lack of an adequate therapeutic attempt with L-dopa or dopamine agonists).\n\n* Inclusion criteria forAD patients. Patients will be selected at the Center for Cognitive Disorders and Dementias (CDCD) SCDU Neurology, AOU Maggiore della Carità, Novara. Patients with AD will be included after diagnosis of probable Alzheimer's disease according to the McKhann criteria (2011) and supported by positive biomarkers for amyloidopathy (PET with amyloid tracer or amyloid cerebrospinal fluid dosage).\n* Inclusion criteria for FTD\u002FALS patients. For UPO, patients will be selected at the tertiary center Amyotrophic Lateral Sclerosis - SCDU Neurology, AOU Maggiore della Carità, Novara. Patients with amyotrophic lateral sclerosis will be included following a diagnosis according to the El Escorial criteria - revised (2015): in this regard, only patients with a definite or probable diagnosis supported by laboratory will be included. For patients with FTD, they will be selected at both centers mentioned above with a diagnosis according to the Rascovsky criteria (2011). In this group, the diagnosis will be supported by negative biomarkers for amyloidopathy (PET with amyloid tracer or amyloid cerebrospinal fluid dosage). For patients with concomitant ALS and FTD, the El Escorial criteria (2015) associated with the Strong criteria (2017) will be used.\n\nExclusion Criteria:\n\n* PD PATIENTS\n\n  * pre-existing psychiatric pathologies;\n  * neurodegenerative neurological diseases such as multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer's, neuromuscular diseases, epilepsy;\n  * diagnosis of dementia;\n* AD\u002FFTD\u002FALS PATIENTS\n\n  * pre-existing psychiatric pathologies;\n  * previous diagnosis of other neurodegenerative neurological diseases;\n  * patients unable to sign informed consent.\n* CONTROLS\n\n  * pre-existing psychiatric pathologies;\n  * neurodegenerative neurological diseases such as Parkinson's, multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer's, neuromuscular diseases, epilepsy;\n  * diagnosis of dementia;\n  * depression;\n  * prolonged intake of anxiolytic, antidepressant, antipsychotic, sleep-inducing, cognitive stimulant drugs.","20 Years",{"count":178,"type":21},110,"Neurodegenerative disorders (NDDs), such as Parkinson¿s disease (PD), Alzheimer¿s disease (AD), Frontotemporal dementia (FTD) and Amyotrophic Lateral Sclerosis (ALS) are characterized by aggregation and intracellular accumulation of misfolded proteins, which are believed to play a key role in synaptic dysfunction and neuronal death. Protein structural complexes in biofluids have been proposed to mirror pathological conditions suggesting their use as biomarkers for NDDs characterized by protein aggregation. In this framework, we plan to: i) collect a large cohort of NDD and prodromal patients and healthy subjects using standardized clinical and genetics procedures; ii) apply a novel method based on genomics, proteomics and bioinformatic analysis to map protein complexes in biofluids; iii) identify novel circulating biomarkers and correlate them to genetic profiling and disease endophenotypes, and; iv) validate the biological properties in human brain tissue and dopaminergic cultures.",[181,182,183,184],"Parkinson Disease","Amyotrophic Lateral Sclerosis (ALS)","Frontotemporal Dementia (FTD)","Alzheimer's Disease (AD)",[186,187],"protein structural complexes in Neurodegenerative diseases","circulating biomarkers for neurodegenerative diseases","2025-03-17",{"date":190,"type":51},"2025-03-18",{"date":192,"type":51},"2025-02-04",{"date":194,"type":21},"2026-12",{"name":57,"class":58},{"id":197,"slug":198,"hasResults":11,"nctId":199,"briefTitle":200,"officialTitle":200,"acronym":4,"eligibilityCriteria":201,"healthyVolunteers":11,"sex":17,"minAge":68,"maxAge":18,"enrollmentInfo":202,"targetDuration":4,"studyType":124,"phases":203,"briefSummary":204,"conditions":205,"keywords":207,"overallStatus":77,"whyStopped":4,"lastUpdateSubmitDate":212,"lastUpdatePostDateStruct":213,"startDateStruct":215,"completionDateStruct":217,"leadSponsor":219,"locationsCount":86},"100501573","effects-of-transcranial-static-magnetic-field-stimulation-tsms-in-progressive-multiple-sclerosis-100501573","NCT05811013","Effects of Transcranial Static Magnetic Field Stimulation (tSMS) in Progressive Multiple Sclerosis","Inclusion Criteria:\n\n* Ability to give written informed consent to the study\n* Age range 18-65 years\n* Diagnosis of primary of secondary progressive MS according to 2017 revised Macdonald's criteria (Thompson et al., 2017), presenting with signs of symptoms of progressive dysfunction of the corticospinal tract\n* EDSS ≤ 6,5\n* Ability to participate to the study protocol\n* No or stable (at least six months) DMT or rehabilitative treatments before study entry, and willingness not to change these therapies (including cannabinoids, SSRI, baclofen) during the study.\n\nExclusion Criteria:\n\n* Relapsing-remitting MS or progressive MS presenting with signs of symptoms other than those typical of the ascending myelopathy phenotype (i.e. progressive cerebellar or cognitive involvement)\n* Female with positive pregnancy test at baseline or having active pregnancy plans\n* Comorbidities for which synaptic plasticity may be altered (i.e., Parkinson's disease, Alzheimer's disease, stroke)\n* Contraindications to TMS\n* History or presence of any unstable medical condition such as malignancy or infection\n* Use of medications with increased risk of seizures (i.e. Fampridine, 4-Aminopyridine)\n* Concomitant use of drugs that may alter synaptic transmission and plasticity (L-dopa, antiepileptics)",{"count":152,"type":21},[126],"In multiple sclerosis (MS) brains, inflammation induces specific abnormalities of synaptic transmission, collectively called inflammatory synaptopathy. Such synaptopathy consists in unbalanced glutamatergic and GABAergic transmission and in remarkable changes in synaptic plasticity, causing excitotoxic neurodegeneration and impairing the clinical compensation of the ongoing brain damage, thereby exacerbating the clinical manifestation of the disease. In progressive MS (PMS), synaptopathy is characterized by pathological potentatiation of glutamate-mediated synaptic up-scaling (Centonze et al., 2008; Rossi et al., 2013) and loss of long-term synaptic potentiation \\[LTP (Weiss et al., 2014)\\], both caused by proinflammatory molecules (released by microglia, astroglia, and infiltrating T and B lymphocytes) (Malenka et al., 2004; Di Filippo et al., 2017; Stampanoni Bassi et al., 2019). The combination of increased up-scaling and decreased LTP has a significant impact on the clinical manifestations of PMS, often presenting with signs and symptoms indicating length-dependent degeneration of neurons of the corticospinal tract. Altered LTP expression impairs brain ability to compensate ongoing neuronal loss (Stampanoni Bassi et al., 2020), and pathological TNF-mediated up-scaling may directly promote excitotoxic damage and neurodegeneration (Rossi et al., 2014). In addition, up-scaling and LTP are mutually exclusive at a given synapse through a mechanism of synaptic occlusion (i.e., pre-existing up-scaling saturates and prevents subsequent LTP expression), further promoting neurodegeneration by preventing the pro-survival effect of LTP, the induction of which activates intracellular anti-apoptotic pathways (Bartlett \\& Wang, 2013). It follows that a neuromodulation approach that can chronically (over several months) dampen up-scaling expression in the primary motor cortex (M1) of PMS patients could be beneficial by preventing excitotoxic neurodegenerative damage triggered by up-scaling itself (Centonze et al. 2008, Rossi et al. 2014), and also by promoting LTP induction and LTP-dependent functional compensation of deficits, thereby reducing the speed of the neurodegeneration process through increased LTP-dependent neuronal survival and preservation of dendritic spines (Ksiazek-Winiarek et al., 2015). Our study aims to test whether transcranial static magnetic field stimulation (tSMS) could represent such a therapeutic approach, as recently proposed in patients with amyotrophic lateral sclerosis (ALS) (Di Lazzaro et al, 2021). Forty (40) ambulatory patients with PMS, presenting with the ascending myelopathy phenotype of the disease, will be recruited at the MS Center of the Unit of Neurology of the IRCCS Neuromed in Pozzilli (IS). In this randomized, sham-controlled, double-blind, within-subjects, cross-over study (allocation ratio 1:1), we will test the ability of repeated sessions of tSMS applied bilaterally over the M1 to safely reduce disability progression in patients with PMS. Patients will be randomly assigned to either real or sham tSMS. Each patient will participate in two experimental phases (real or sham stimulation). Each patient will self-administer tSMS over right and left M1, two session per day, 60 minutes each. The order will be randomly established and counterbalanced across participants. Both investigators and participants will be blinded to stimulation parameters. In the \"real stimulation\" phase, tSMS will be applied for 120 minutes each day, at home, for 12 consecutive months. In the \"sham stimulation\" phase, sham tSMS will be delivered with non-magnetic metal cylinders, with the same size, weight and appearance of the magnets. Clinical evaluations, including the Multiple Sclerosis Functional Composite measure (MSFC) will be performed before, during and after each experimental phase (\"real\" and \"sham\"). In addition, blood levels of neurofilaments, excitability and plasticity of M1, and MRI measures of cortical thickness will be measured before, during and after each stimulation phase.",[206],"Progressive Multiple Sclerosis",[206,208,209,210,211],"transcranial Static Magnetic Field Stimulation","disability progression","cortical hyperexcitability","cortical plasticity","2024-10-14",{"date":214,"type":51},"2024-10-16",{"date":216,"type":51},"2023-05-27",{"date":218,"type":21},"2026-05-27",{"name":57,"class":58},{"id":221,"slug":222,"hasResults":11,"nctId":223,"briefTitle":224,"officialTitle":225,"acronym":4,"eligibilityCriteria":226,"healthyVolunteers":11,"sex":17,"minAge":68,"maxAge":18,"enrollmentInfo":227,"targetDuration":4,"studyType":23,"phases":4,"briefSummary":229,"conditions":230,"keywords":234,"overallStatus":77,"whyStopped":4,"lastUpdateSubmitDate":238,"lastUpdatePostDateStruct":239,"startDateStruct":241,"completionDateStruct":243,"leadSponsor":245,"locationsCount":86},"100302458","biomarkers-of-synaptic-damage-in-multiple-sclerosis-100302458","NCT03217396","Biomarkers of Synaptic Damage in Multiple Sclerosis","Identification of New Biomarkers Useful to Define the Course of Multiple Sclerosis and Study of the Mechanisms That Promote Synaptic Damage","Inclusion Criteria:\n\n1. Male and female patients (age between 18 and 65 years)\n2. Diagnosis of MS in accordance with McDonald's (2010 rev) criteria,\n3. EDSS between 0 and 5.5 (included),\n4. Patients able to provide informed consent to participation in the study\n\nExclusion Criteria:\n\n1. Inability to provide informed written consent\n2. Altered basal blood count\n3. Pregnancy or lactation\n4. Contraindications for the execution of magnetic resonance imaging with gadolinium\n5. Significant clinical conditions in addition to SM or other chronic neurodegenerative diseases including latent viral infections",{"count":228,"type":21},300,"A prospective and retrospective cohort study of about five years will be performed on blood and cerebrospinal fluid samples taken for diagnostic reasons from recruited patients within the Neuromed Neurology Unit. Subjects with other chronic neurodegenerative diseases such as Amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD) and Parkinson's disease (PD), and healthy subjects subjected to blood sampling and \u002F or lumbar puncture for clinical reasons will be recruited As control groups.",[231,181,232,233],"Multiple Sclerosis","Amyotrophic Lateral Sclerosis","Alzheimer Disease",[235,236,237],"synaptic plasticity","neuroinflammation","neurodegeneration","2022-10-27",{"date":240,"type":51},"2022-10-28",{"date":242,"type":51},"2017-11-22",{"date":244,"type":21},"2027-09-30",{"name":57,"class":58},{"id":247,"slug":248,"hasResults":11,"nctId":249,"briefTitle":250,"officialTitle":251,"acronym":4,"eligibilityCriteria":252,"healthyVolunteers":11,"sex":17,"minAge":4,"maxAge":4,"enrollmentInfo":253,"targetDuration":4,"studyType":23,"phases":4,"briefSummary":255,"conditions":256,"keywords":4,"overallStatus":77,"whyStopped":4,"lastUpdateSubmitDate":258,"lastUpdatePostDateStruct":259,"startDateStruct":261,"completionDateStruct":262,"leadSponsor":264,"locationsCount":86},"100474529","functional-study-of-inhibitory-neurotransmission-in-the-human-epileptic-brain-100474529","NCT05459090","Functional Study of Inhibitory Neurotransmission in the Human Epileptic Brain.","Functional Study of Inhibitory and Excitatory Neurotransmission in the Nervous Tissue Resected From Human Brain: Understanding New Molecular Mechanisms and Discovering New Therapeutic Targets to Cure Drug-resistant Epilepsy.","Inclusion Criteria:\n\nPatients with drug-resistant temporal lobe epilepsy.\n\nExclusion Criteria:\n\n* Patients suffering from Temporal lobe epilepsy caused by stroke, ischemia, cavernous angiomas, or meningiomas growth.",{"count":254,"type":21},60,"Epilepsy is a neurological condition that afflicts 1% of the world population. 30% of patients become drug-resistant to classic antiepileptic treatment and only a small percentage, 5%, can undergo a neurosurgical resection of epileptic focus and recover almost completely from symptoms. To date, an imbalance between inhibitory and excitatory neurotransmission has been well accepted as the main root cause of epilepsy. A better understanding of the molecular mechanisms of this can lead to developing new therapeutic strategies. The investigators of the project want to describe the functional alteration of GABA- A receptor, the main actor of inhibitory neurotransmission in the central nervous system and characterize its subunit composition in the epileptic foci of patients with temporal lobe epilepsy. The authors, also, want to modulate, by means of selective neuroactive molecules, the function of this receptor to increase the inhibitory tone in the epileptic brain.",[257],"Drug Resistant Epilepsy","2022-07-29",{"date":260,"type":51},"2022-08-02",{"date":258,"type":51},{"date":263,"type":21},"2027-07-31",{"name":57,"class":58},""]