I'm trying out a new neuroprotective substance on animal models of ischemic stroke, so far I could prove that this particular thing could cause caspase 3 activity to decrease at 24h of reperfusion. But my boss wants to see if it also affects other forms of cell death/damage during this time period. From the papers that I've seen so far, 24h to 72h is a pretty nice time span to see apoptosis, too early for autophage and too late for excitotoxicity. Does anyone have any suggestions on where I should look or what papers I should read?
There are various apoptotic pathways some ar as follows: extrinsic( death receptor) and intrinsic( cytochrome c mediated). intrinsic pathway is divided into two caspases dependent and caspases independent ( AIF translocation to nucleus), P53 mediated cell death is the another mechanism of cell death.
no, no, no. I meant other ways besides apoptosis, like oxidative stress, neuroinflammation, necrosis, autophage, things like that. I know all of these processes are present in the mouse brain after 1h mcao and reperfusion, but which is the more dominant between 24h and 72h of reperfusion?
I could recommend Hossmann 2006, pathophysiology and therapy of experimental stroke, cell mol neurobiol,
as well as the thesis of Sarah McCann 2012, Oxidative stress and therapeutic targets for ischemic stroke, univ. of Melbourne.
Due to my experience with neurorehabilitation of patients after long-term coma with the following outcome in the apallic syndrome or in vegetative states, we observe the minimal brain electrical activity similar to serow line activity or dominant delta-wave activity with convulsive activity. We connect this brain damage not only with brain hypoxia, but also with severe ischemia, oedema and venous stasis in the brain tissue. We had a good result of the intensive medicaments treatment combine with intensive rehabilitation - the restore of the conscience, speech, memory, active moves of limbs etc. More - http://inno-health.com/istoriji-uspihu-roman-shvorak/ and http://angio-veritas.com/technologies/nejroreabilitatsiya-psyhonevrolohichnyh-hvoryh/apalichnyj-syndrom/?lang=en
Dear Li,
During Ischemic damage, the predominant form of initial neuronal damage might be attributed to excitotoxicity, Inflammatory and Necrotic cell damage. Perhaps, there will also be oxidative stress as a result of reperfusion which worsens the damage. During the time frame, 24-72 hours, apoptosis gradually gets the upper hand as a result of all these pathophysiological mechanisms. It seems autophagic cell death also plays a significant role.
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