View clinical trials related to Optic Atrophy, Hereditary, Leber.
Filter by:The Leber Hereditary Optic Neuropathy is a genetic disorder caused by maternal transmission of mitochondrial DesoxiroboNucleid Acid mutations. It is manifested by a rapidly progressive blindness, profound, due to atrophic optic nerve. The visual loss is primarily unilateral bilateralisation taking place in the vast majority of cases in weeks or months. The neuro-cardio-protective properties of cyclosporine (and its analogs specifically targeting the anti-apoptotic mechanisms) are particularly promising. The investigators hypothesis is that cyclosporine may limit apoptosis during the acute phase of the disease process and would limit the loss of visual acuity and improve the visual prognosis of these patients.
Hypotheses: The primary hypothesis being tested is that there will be no toxicity resulting in loss of vision to no light perception in injected eyes.
The purpose of this study is to evaluate the safety and tolerability profile of ascending doses of GS010 in Leber Hereditary Optic Neuropathy (LHON) patients.
The objective of this survey is to establish the clinical course of vision loss and recovery in patients with a genetically confirmed diagnosis of Leber Hereditary Optic Neuropathy (LHON). Visual acuity changes over time from onset of symptoms and from visual acuity nadir will be the main endpoint analysed. The survey will collect historically documented visual acuity data for all patients at participating sites with a genetically confirmed diagnosis of LHON. No exclusion criteria apply. Patients are not required to attend the clinic for the survey. Data will be collected in a completely anonymous manner. Ethical approvals and data release agreements will be obtained as required by local regulations.
The objective of the study is to determine whether administration of idebenone can shorten the time to improvement of visual acuity in patients with chronic vision loss due to LHON.
This study aims to evaluate the current visual acuity of SNT-II-003 participants and compare this with the last visit from the SNT-II-003 study.
The overall objective of the proposed research is to test the hypothesis that Near-infrared Light-emitting Diode (NIR-LED) therapy will stimulate mitochondrial function, attenuate oxidative stress, and improve cell survival and vision in subjects with Leber's Hereditary Optic Neuropathy (LHON).
This study is meant to assess the safety and efficacy of rAAV2-ND4 treatment of Leber hereditary optic neuropathy with 11778 LHON mutation.
This study is meant to assess the effectiveness of idebenone on visual function measures in patients with Leber's Hereditary Optic Neuropathy over a 6 months period.
Background Leber's Hereditary Optic Neuropathy (LHON) is a maternally inherited ocular disorder associated with a mutation in mtDNA . The common manifestation is visual loss which caused by the respiratory chain enzymes complex dysfunction resulting in increased oxidative stress enzymes production. Purpose To determine whether curcumin which is an antioxidant agent is beneficial to the patients with 11778 LHON mutation. Material and Method Seventy patients with 11778 LHON mutation were randomly treated with oral curcumin (500 mg/day) and placebo for 1 year. The visual acuity, computerized visual field, electrophysiologic parameters and oxidative stress enzymes in plasma were compared before and after treatment at 3, 6, and 12 months interval.