I must confess that I had little knowledge of Ischemic Conditioning and its therapeutic potential before accessing this publication by my friend +Laura A. Pasquini and her team at University of Buenos Aires (users of Neuromics' Neuronal-Glial Markers and Neurotrophins Antibodies.
In the conditioning or pre-conditioning process, blood supply to an organ or a tissue is impaired for a short time (usually less than five minutes) then restored so that blood flow is resumed, and the process repeated two or more times, the cells downstream of the tissue or organ are robustly protected from a final ischemic insult when the blood supply is cut off entirely and permanently.
Here the authors used pressure pulses to induce retinal ischemia. Their results suggest that early vision loss in diabetes could be abated by ischemic conditioning which preserved axonal function and structure: Diego C. Fernandez, Laura A. Pasquini, Damián Dorfman, Hernán J. Aldana Marcos, Ruth E. Rosenstein. Ischemic Conditioning Protects from Axoglial Alterations of the Optic Pathway Induced by Experimental Diabetes in Rats. Research Article | published 20 Dec 2012 | PLOS ONE.
They used our PDGFR-α and an O1 marker to compare conditioned, diabetic with unconditioned, diabetic and controls rats to determine protection on ONs of the eye.
Immature OL (O1+ cells) and OL precursor (PDGFR-α+ cells) were evaluated by immunostaining in transverse ON sections. In the diabetic ON from eyes that received a sham treatment, a significant increase in O1(+) and PDGFR-α (+) area was observed, with the presence of disorganized and hypertrophic cells. In the right panel, the area occupied by glial cells (measured as total optical density (OD)) is shown. Ischemic conditioning significantly prevented these alterations and a clear decrease in O1- and PDGFR-α-immunoreactivity, with cells aligned parallel to axon bundles were found. Data are mean ± SEM (n = 6 nerves/group).
Results suggest that early vision loss in diabetes could be abated by ischemic conditioning which preserved distal axonal function and structure before the neuronal soma loss. Moreover, the present results add new potentialities to the therapeutic effects of ischemic tolerance, which is axon protection. Thus, ischemic tolerance could have promise for application in other neurodegenerative axonal diseases. I will keep you updated on progress.