View clinical trials related to Nerve Degeneration.
Filter by:Neurodegeneration with brain iron accumulation (NBIA) represent a group of rare neurodevelopmental diseases, genetically as well as phenotypically heterogeneous. The diagnosis is based on brain MRI. It is also based on genetic testing. However overlaps exist between the different clinical presentations and the molecular diagnosis may be misinterpreted. Two main purposes must be addressed to get a better molecular diagnosis: on one hand reaching enough exhaustivity which may be performed with a larger gene panel and next generation sequencing; on the other hand, it is now necessary to validate or infirm the deleterious consequences of variants with the help of functional studies.
Schizophrenia is a progressive psychiatric disorder with a lifetime prevalence of 1%, its etiology is not fully understood, and it progresses with relapses. There are significant differences between patients in the age of onset, frequency of attacks, response to treatment, and clinical course of the disease. Failure to respond adequately to treatment is defined as resistance to treatment and poses a great challenge in the clinical management of the disease, but the exact cause of treatment resistance has not been clarified yet. Neurodevelopmental hypothesis, neurodegenerative hypothesis, stress-diathesis hypothesis are some of them. In the neurodegenerative hypothesis, it is thought that biochemical changes cause chronic and progressive disorders of the nervous system, and schizophrenia is considered as one of these disorders. S100B, one of the biomarkers released from the central nervous system, is a glycoprotein synthesized by astrocytes; At low concentration, it ensures neuron survival, while at high concentration it causes neuronal cell apoptosis and is associated with neurodegeneration. GFAP on the other hand, can be measured in serum in proportion to the degree of damage by passing into the bloodstream as a result of astrocyte damage. It has been shown that these markers are associated with neurodegenerative diseases, autoimmune diseases and cerebrovascular pathologies and can be measured at a significant level in the blood. As far as is known, neurodegeneration has been found in patients with schizophrenia; however, there are not enough studies in the literature regarding the relationship of this neurodegeneration with treatment response and resistance. In recent years, many biomarker studies related to schizophrenia have been conducted. These studies continue in many different areas such as the early diagnosis of schizophrenia, the treatments to be applied after diagnosis, the response to the treatment given, and the clinical course of the disease, but no biomarker indicating the desired results has yet been found. In this study, measurement of s100B and GFAP serum levels in patients with treatment-resistant schizophrenia, remission schizophrenia and healthy controls, and evaluation of their relationship with response to treatment; Thus, it is aimed to investigate these points that have not been fully elucidated in the pathogenesis of schizophrenia and their use as biomarkers in predicting the response to treatment.
This study aims to assess the impact of the choice of visual feedback solution (immersive via CAVE and VR headset; non-immersive via screen only) on driving performance and quality of experience on a physical driving simulator and its acceptability to wheelchair drivers with neurological disorders.
Using Optical Coherence Tomography and ImageJ software the investigators will analyze retinal and choroidal vascular changes and their impact on retinal layers among patients with diabetes without retinopathy and patients with diabetes and retinopathy.
Alzheimer's disease (AD) and frontotemporal dementia (FTD) are two of the most common types of age-related neurodegenerative disorders. Identifying at-risk patients and gauging disease progression in a non-invasive manner would be invaluable. Early and correct diagnosis is crucial for coordinating supportive care, patient expectations, caregiver arrangements and family planning. In addition, as treatments become available, beginning therapy early in the disease before symptoms become severe will be important. Multimodal ocular imaging (MOI) includes an ophthalmic (eye) exam and eye photographs to evaluate different layers of the retina, which is the light sensing layer of the eye. Newer technologies make it possible to visualize the disease process occurring in AD and FTD by using MOI to look at the retina, since the retina is fundamentally an outward extension of the brain itself. This study will attempt to correlate signs of disease in the retina, as determined by MOI, with plaque buildup in the brain as seen by imaging. This will demonstrate the sensitivity and specificity of MOI for diagnosing AD and FTD in a noninvasive manner.
This study is a prospective study with a mean of 5-year follow-up interval, aims to monitor the progression of α-synucleinopathy neurodegeneration by the evolution of prodromal markers and development of clinical disorders in first-degree relatives (FDRs) of idiopathic REM Sleep Behavior Disorder (RBD) patients and healthy controls.
Late-life depression has been frequently associated with cognitive impairment. Several meta-analyses consistently suggested that a history of depression approximately doubles an individual's risk for developing dementia later in life. Neurodegeneration may play an important component in late-life depression. The pathophysiology behind the link between late-life depression and the subsequent development of dementia largely remains unclear, and should be heterogeneous. This highlights the need to identify specific neurodegenerative pathways involved in late-life depression, which will facilitate research on mechanisms and new treatments in the future. The recently published the National Institute on Aging and the Alzheimer Association (NIA-AA) criteria might provide new insights and frameworks to explore the patterns of neurodegenerative process in elderly depressed patients and to categorize them into different biomarker-based groups. In the present project, the investigators will recruit 40 patients with lifetime major depressive disorder, and 20 non-depressed cognitively normal comparison subjects. Alzheimer's disease pathology (A) was determined by measuring Aβ deposition by F-18 AV-45 PET, and neurodegeneration (N) was established by measuring hippocampal volume using MRI. Individuals were categorised as A-N-, A+N-, A+N+, or suspected non-Alzheimer's disease pathophysiology (A-N+, SNAP). All subjects will further undergo F-18-THK-5351 image study to detect underlying tau pathology. By doing this, the investigators will elucidate the neurodegenerative pathophysiology behind the link between depressive disorder and the subsequent development of dementia.
OBJECTIVE To investigate neurodegeneration and demyelination in the central and peripheral nervous system in multiple sclerosis linked to disease progression and mechanisms that can explain different responses to Fampridine treatment in MS patients with walking disability. METHOD The study is a prospective cohort follow-up study with 98 participants with MS and walking disability. Participants are identified as responders or non-responders to Fampridine treatment prior to the study. Participants will undergo MRI of the cerebrum with lesion load quantification, neurophysiological tests comprised of motor evoked potentials and electroneurographic examination, blood samples examining KIR4.1 antibodies, brain derived neurotrophic factor (BDNF), myelin protein zero (MPZ), peripheral myelin protein 22 (PMP22), p75-nerve growth factor receptor (p75NGFR) and anti-myelin associated glycoprotein (anti-MAG). The presence of SORCS-3 gene mutation will also be examined, as will cerebrospinal fluid levels of myelin basic protein, neurofilament heavy and light chains. Functional test of Timed 25-foot walk test (T25FW) will identify response to Fampridine treatment. A functional test battery will further detail function of upper extremities and cognition. CONCLUSION This study will add to the understanding of neurodegeneration and demyelination in CNS and PNS in patients with MS having walking disability. This will impact clinical decision-making by improving organization of immunomodulatory treatment, identifying biomarkers thus facilitating earlier treatment and improving patient control, information and education.
Background: Previous studies have confirmed that most patients with idiopathic REM sleep behaviour disorder (iRBD) eventually develop neurodegenerative diseases. In addition, REM sleep without atonia (RSWA), a hallmark of RBD feature, is a significant predictor of development of neurodegenerative diseases in patients with iRBD. Some preliminary studies have implied that isolated RSWA in the absence of RBD symptoms may also indicate neurodegeneration. However, this speculation needs to be confirmed by more refined study with sophisticated measures in both RSWA and markers of neurodegeneration Objectives: 1) to determine the differences in striatal dopamine transmission and other markers of neurodegeneration among individuals with isolated RSWA and healthy controls; 2) to examine the correlation of severity of RSWA with striatal dopamine transmission. Design: Case-control study Setting: Community-based sample Participants: 1) iRBD first degree relatives with isolated RSWA (n=18) 2) iRBD first degree relatives without isolated RSWA (n=18) 3) Community-based health controls without isolated RSWA (n=18) Main outcome measures: 1. The dopamine transmission as measured by triple-tracer PET/ CT imaging protocol including 18F-DOPA, 11C-Raclopride and 18F-FDG images; 2. Brain glucose metabolism and neurocognitive measures; 3. Severity of EMG activity during REM sleep
This project aims to determine the effects of the HiBalance program on neuroplastic changes in people with mild to moderate Parkinson´s disease. The main hypothesis is that highly challenging exercise will lead to greater gait and balance ability, increased levels of physical activity and an improved health related quality of life. The investigators further hypothesize that neuroplasticity changes will be seen in corresponding areas of the brain, neuropsychological changes on cognitive test measures, and that exercise will inhibit the degeneration of dopaminergic neurons in the brain through the mediation of neurotrophic factors.