Alistair J. Barber
Photo
Academic title Associate Professor of Ophthalmology and Cellular and Molecular Physiology
College College of Medicine
Campuses Penn State Milton S. Hershey Medical Center
Department Ophthalmology
Graduate programs Anatomy
Physiology
Cell and Molecular Biology
Neuroscience
Email Phone FAX
  abarber@psu.edu
  717 531 6506
  717 531 0065
Educational background
  Ph.D. Open University, Milton Keynes, UK, 1990
Postdoctoral: University of Saskatchewan, 1990-1993
Postdoctoral: Pennsylvania State University College of Medicine, 1993-1995
Research interests
 

Diabetic Retinopathy

Diabetic retinopathy is a complication of diabetes that leads to legal blindness in many people. It has been characterized as a disease of the retinal vasculature, which loses its blood-retinal barrier properties, leading to edema. But diabetes also induces a number of pathological changes within the neural retina, including apoptosis and glial malfunction. The increase in apoptosis becomes significant very soon after the onset of hyperglycemia and remains higher than normal throughout the duration of diabetes. The glial cells of the retina also become less able to metabolize glutamate into glutamine, and expression of glial fibrillary acidic protein increases. Together these changes suggest that diabetes causes a chronic loss of neurons in the inner retina, much like neurodegenerative diseases of the central nervous system, and that glutamate-induced excitotoxicity may be responsible for the neuronal cell loss. Projects to study the way that diabetes alters glutamate metabolism in the retina, and the potential for neuroprotective drugs to reverse diabetic retinopathy are currently underway.

Graphic
  Graphic
  Immunohistochemistry of a flat-mount retina from streptozotocin-diabetic rat, showing labeling for the pro-apoptotic enzyme caspase-3 in red and the vascular basement membrane protein agrin in green. Since caspase-3 immunoreactive cells usually do not localized to blood vessels they are likely to be neurons or glia. These data suggest that apoptosis of cells in the neural retina occurs as a consequence of experimental diabetes, and that chronic neurodegeneration is a component of diabetic retinopathy.
Areas of expertise
 
Diabetic RetinopathyNeurosciences
Blood-Retinal BarrierGlial Fibrillary Acidic Protein
NeurogliaReceptors, Glutamate
ApoptosisRetina
Retinal DegenerationRetinal Diseases
Retinal Ganglion CellsRetinal Vessels
Diabetes Mellitus, ExperimentalCaspases
Eye ProteinsGlutamic Acid
AgrinCapillary Permeability
Diabetes MellitusNeuroprotective Agents
EyeDisease Models, Animal
Amacrine CellsDendrites
Calcium SignalingCell Differentiation
Erythroid Precursor CellsErythropoietin
Receptors, ErythropoietinTRPC Cation Channels
Publication author name
  Barber AJ
Research techniques
 
ImmunohistochemistryMolecular Probe Techniques
Models, AnimalMicroscopy, Confocal

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