title: Mechanisms of Neuronal Cell Death in AGE-exposed Retinas - Research and Literature Review.
abstract: BACKGROUND
  Accelerated formation of AGE due to increasing rise in blood glucose levels leads to developments of metabolic changes, further leading to such complications as diabetic retinopathy which is a major reason of leading to blindness and affecting working population worldwide.
  
  
  BACKGROUND
  The results of recent investigations have demonstrated that the death of retinal ganglion cells (RGCs) and their axons is the common pathological changes in AGE-exposed retina and the possible mechanisms that are responsible for the onset and progression of RGC death and axonal degeneration in patients with diseases associated with AGEs accumulation are represented in this review. Identifying the mechanisms of the onset and the progression of RGC neuropathy can help in discovering the pathogenetic orientated treatment.
  
  
  OBJECTIVE
  This review describes recently discovered possible mechanisms of diabetic retinopathy obtained by laboratory studies with the suggestion that AGEs play an important role in the pathogenesis of diabetic retinal neuropathy triggering different mechanisms that result in neuronal dysfunction. For searching therapeutic approach the regenerative effect of different neurotrophic factors has been studied such as neurotrophin-4, hepatocyte growth factor, glial cell line-derived neurotrophic factor, and Tauroursodeoxycholic acid.
  
  
  CONCLUSIONS
  The findings for the establishment of neuroprotective and regenerative therapies for AGE-related diseases including diabetic retinopathy are represented in this review.
authors.affiliation: Department of Ophthalmology and Visual Science Chiba University Graduate School of Medicine, Inohana 1-8-1, Chuo-ku, Chiba 260-8670, Chiba. Japan.
authors.forename: Guzel
authors.initials: G
authors.lastname: Bikbova
authors.affiliation: Department of Ophthalmology and Visual Science, Chiba University Graduate School of Medicine, Inohana 1-8-1, Chuo-ku, Chiba 260-8670, Chiba. Japan.
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Oshitari
authors.affiliation: Department of Ophthalmology and Visual Science Chiba University Graduate School of Medicine, Inohana 1-8-1, Chuo-ku, Chiba 260-8670, Chiba. Japan.
authors.forename: Takayuki
authors.initials: T
authors.lastname: Baba
authors.affiliation: Department of Ophthalmology and Visual Science Chiba University Graduate School of Medicine, Inohana 1-8-1, Chuo-ku, Chiba 260-8670, Chiba. Japan.
authors.forename: Shuichi
authors.initials: S
authors.lastname: Yamamoto
mesh_terms: D000818:Animals; D016923:Cell Death; D017127:Glycation End Products, Advanced / Q000502:physiology*; D006801:Humans; D009414:Nerve Growth Factors / Q000627:therapeutic use; D012164:Retinal Diseases / Q000517:prevention & control; D012165:Retinal Ganglion Cells / Q000502:physiology*
chemical_list: D017127:Glycation End Products, Advanced; D009414:Nerve Growth Factors
keywords: AGEs; JNK; neurotrophic factors; p38; regeneration