1. Neurodegenerative metabolites and neuroprotective strategies in diabetic retinopathy
نویسندگان
چکیده
Diabetic retinopathy is widely considered a neurodegenerative disease. A number of cellular and molecular studies showed that retinal neuronal cells are vulnerable to be damaged soon after diabetes. In addition, retinal function tests also confirmed functional deficit in diabetic retina early in diabetes indicating dysfunction of neuronal cells. Altered levels of diabetes induced neurodegenerative metabolites have been found to be implicated in initiating those damages. Those metabolites include increased levels of glucose, glutamate, branched chain amino acids and homocysteine and decreased levels of certain vitamins such as folic acid and vitamin-B12. These altered metabolites activate a number of metabolic pathways leading to increases in oxidative stress and decreases in neurotrophic support in the diabetic retina. In turn, they damage neurons in diabetic retina. In this chapter, we discuss those potential excitotoxic metabolites and possible therapeutic targets to protect neurons. By protecting retinal neuronal damage early in diabetic retina, retinal vessels can be regressed to ameliorate the progression of diabetic retinopathy, a leading cause of blindness worldwide. Correspondence/Reprint request: Dr. Mohammad Shamsul Ola, Department of Biochemistry, Faculty of Science, King Saud University, Riyadh 11415, Saudi Arabia E-mail: [email protected] or [email protected] Mohammad Shamsul Ola & Abdullah S. Alhomida 2
منابع مشابه
Neurodegeneration in Diabetic Retina and Its Potential Drug Targets
Diabetic retinopathy (DR) is one of the major complications of diabetes causing vision loss and blindness worldwide. DR is widely recognized as a neurodegenerative disease as evidenced from early changes at cellular and molecular levels in the neuronal component of the diabetic retina, which is further supported by various retinal functional tests indicating functional deficits in the retina so...
متن کاملAn integrated approach to diabetic retinopathy research.
This review discusses the pathophysiology of diabetic retinopathy related to direct effects of loss of insulin receptor action and metabolic dysregulation on the retina. The resulting sensory neuropathy can be diagnosed by structural and functional tests in patients with mild nonproliferative diabetic retinopathy. Research teams can collaborate to integrate ocular and systemic factors that impa...
متن کاملA specific phosphorylation regulates the protective role of αA-crystallin in diabetes.
Neurodegeneration is a central aspect of the early stages of diabetic retinopathy, the primary ocular complication associated with diabetes. While progress has been made to improve the vascular perturbations associated with diabetic retinopathy, there are still no treatment options to counteract the neuroretinal degeneration associated with diabetes. Our previous work suggested that the molecul...
متن کاملEndogenous and Synthetic Cannabinoids as Therapeutics in Retinal Disease
The functional significance of cannabinoids in ocular physiology and disease has been reported some decades ago. In the early 1970s, subjects who smoked Cannabis sativa developed lower intraocular pressure (IOP). This led to the isolation of phytocannabinoids from this plant and the study of their therapeutic effects in glaucoma. The main treatment of this disease to date involves the administr...
متن کاملDiabetic Retinal Neurodegeneration Is Associated With Mitochondrial Oxidative Stress and Is Improved by an Angiotensin Receptor Blocker in a Model Combining Hypertension and Diabetes
OBJECTIVE Diabetic retinopathy displays the features of a neurodegenerative disease. Oxidative stress is involved in the pathogenesis of diabetic retinopathy. This investigation sought to determine whether hypertension exacerbates the oxidative stress, neurodegeneration, and mitochondrial dysfunction that exists in diabetic retinopathy and whether these changes could be minimized by the angiote...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره شماره
صفحات -
تاریخ انتشار 2014