Marfan Syndrome | NYU Langone Health
Doctors at NYU Langone are experts in treating Marfan syndrome, which can affect the heart, bones, eyes, lungs, and nervous system.
Master protocol of two independent randomized double-blind Phase 3 studies comparing efficacy and safety of frexalimab (SAR441344) to teriflunomide in adult participants with relapsing forms of multiple sclerosis.
This clinical trial aims to assess the effectiveness and safety of an investigational drug, frexalimab, for treating relapsing multiple sclerosis (RMS). Frexalimab works by targeting and blocking the CD40 ligand (CD40L) protein, which plays a key role in the immune system's response to infection. In MS, the immune system mistakenly attacks the brain, leading to lesions and disability. The study will compare the efficacy and safety of frexalimab to the FDA-approved drug teriflunomide (Aubagio). Participants will be randomly assigned to receive either frexalimab (with placebo) or teriflunomide (with placebo) for up to 40 months. Frexalimab will be administered intravenously every 4 weeks, while teriflunomide is taken orally once a day. The study will evaluate relapse rates, disease progression, brain lesions through MRI, and overall safety of the treatments.
Maternal–Fetal Medicine at NYU Langone Obstetrics & Gynecology Associates | NYU Langone Health
Doctors at Maternal–Fetal Medicine at NYU Langone Obstetrics and Gynecology Associates care for women experiencing high-risk pregnancies.
Maternal–Fetal Medicine at NYU Langone Obstetrics & Gynecology Associates Doctors | NYU Langone Health
Find a doctor at Maternal–Fetal Medicine at NYU Langone Obstetrics & Gynecology Associates.
Maternal-Fetal Medicine Doctors | NYU Langone Health
View all NYU Langone doctors who specialize in maternal-fetal medicine.
Maternal–Fetal Medicine Services | NYU Langone Health
Maternal–fetal medicine specialists at NYU Langone provide screening, diagnostic testing, and treatment during high-risk pregnancies.
Mechanisms and Enhancement of Learning During Sleep
Memory dysfunction represents one of the most common cognitive complaints in patients with epilepsy and significantly impairs quality of life. Our work aims to (1) better characterize memory function in the context of everyday life, and (2) remediate memory impairment, through rigorous exploration of the mechanisms of memory and its dysfunction. In this study, we are seeking to enroll patients with temporal lobe epilepsy and control participants to complete various questionnaires and memory tasks during a 2-hour session.
Mechanisms of Paired Vagus Nerve Stimulation in Chronic Stroke: A Randomized Blinded Sham-Controlled Single-Center Mechanistic Trial
This study is investigating how an experimental treatment, paired vagus nerve stimulation (VNS), may improve motor function after a stroke. Enrolled participants be asked to have a VNS device surgically placed on their vagus nerve in their neck. They will then take part in two 6-week blocks of rehabilitation therapy: Block 1: Participants will receive active VNS with rehabilitation therapy Block 2: Participants will receive placebo VNS with rehabilitation therapyNote: Participants will not know which block they will receive first. The study will then assess how the brain responds though tests such as transcranial magnetic stimulation (TMS), MRI scans, and clinical tests to measure movement, thinking, and emotional health. Participants will be expected to complete 42 visits over 4 months (36 visits are for rehabilitation therapy and 6 visits are for assessments). There is no cost for participating in the study. Participants will receive up to $1,720 for their participation. Transportation to visits will be covered.
Mechanisms of Peripheral Vascular Disease
The proposed study will enable the use of human tissue samples and outcome data by basic and clinical investigators for research into the biology, causes, prevention and therapy of patients with documented peripheral arterial vascular disease secondary to atherosclerosis. The collection of paired information will provide important clinically relevant findings that will add to the growing understanding of the natural history of plaque formation in the arteries of the periphery and will enable to decipher the molecular mechanisms in this pathology. We will prospectively collect both tissue to study the mechanism of the natural history of PAD. We will also collect relevant clinical and medical information on these subjects and continue to collect follow-up information on the surgical patients using their medical records in order to follow their outcome.
Mechanisms of rAcial dIfferences in the relatioNship between Obstructive Sleep Apnea and in vivo Tau deposition in the context of AmYloid burden
African-Americans (blacks) have two times the risk of developing Alzheimer’s disease (AD) compared to non-Hispanic whites.1-6 Neuropathological studies show blacks with more mixed pathology1-6. Recent evidence demonstrate differences in AD biomarkers with blacks having decreased cortical thickness, and lower cerebrospinal fluid (CSF) P-tau, and T-tau.7-10. Notably, area-based socio-economic status (SES) partly explain racial differences in cortical thickness.11 This suggests the possible existence of additional physiologic differences on AD-risk by race, mediated by SES and resulting to greater neuronal loss, similar or less CSF-tau for similar levels of amyloid. Recent studies suggest that obstructive sleep apnea (OSA) increases AD-risk,12-14 is associated with higher brain amyloid and tau in cognitive normal (CN) participants.15-22. Notably, blacks have a higher burden of symptomatic OSA, particularly with excessive daytime sleepiness (EDS),23 which is associated with longitudinal amyloid-PET uptake.24. Potential intermediate mechanisms linking OSA and AD, such as decreased non rapid eye movement (NREM) slow wave activity (SWA) and increased inflammation affect amyloid and tau pathology,25,26 are associated with changes in cognition in late-life,27 and are more burdensome in blacks.28 OSA effects changes in circulating levels of CRP, TNFa, IL-6, and IL-17A.29,30 . More importantly, inflammation arising from cumulative stress exposure placed blacks at a greater risk for developing vascular risk factors,31-33 that increase AD-risk. In addition, SES and psychosocial factors11,34-36 may contribute to increase OSA and AD-risk in blacks. This highlights the need to utilize OSA as a unique disease model to explore racial differences in AD biomarkers.