HOW TO PRESERVE POST SYNAPTIC NEURON DESTRUCTION
HOW TO STOP THE CYTOKINES INDUCED BY STRESS AND THE INFLAMMATORY RESPONSE?
1.HYPOTHERMIA TO COOL PRODUCTION OF STRESS AND INFLAMMATORY RESPONSES!
-ie Reducing production of IL-1 beta to decrease frequency of cellular attachment to endothelial /blood vessel to reduce tissue destruction. (Integrin Alpha-v-beta-5-target of therapy).
2. MASS EFFECT AND INTERRUPTION OF BLOOD VESSEL LEAD TO ANOXIA
-ie Activity at NMDA receptors---interaction with NOX2 leads to Super-Oxide production.
-ie NMDA needed in the production of Peroxy-nitrite (beyond the Nitric Oxyde).
-ie NADPH Oxidase derived Reactive Oxygen Species (ROS)
-HIF-1- Angiogenesis - VEGF- (EGFR cross-talking)
3.PKC inhibition reduces STRESS RESPONSE
4.AT HIPPOCAMPUS : Prodymorphin and its derivative peptides could modulate neurotransmitters by interacting with the activation of presynatic k opioid receptors.
-also Hyperactivation of NMDAR increases Calcium influx, through the CRMP2, resulting in decrease of Hyppocampal Neuronal death by reducing surface expression of Dendritic NR2B receptors.
5.EXCITATORY RESPONSES
-ie. Decrease of GABA release in inhibitory Interneuron synapses increase risk of Seizure activity. This associated potentially with increase activity at excitatatory synapses resulting from AMPA Receptor conductance.
-ie Glutamate removal (from synapses) critical in controlling excitatory stimulation
6.NOW the focus in on CAP'N COLLARS!
these factor's transcription leads to Nrf 1,2,3 (Nrf (s) activity at Blood Barrier)
ie Protein Tyrosine Phosphase inhibits the Nrf.
==========================================
Gobally, the research is haphazard.
but there is increased focus on delayed effect
and recognition of the role of post synaptic Neuron in the long term outcome and chances of Rehabilitation
and its vulnerability to inflammatory attacks. NOTE THE INCREASE MENTION OF GENES!
PLEASE NOTE THE MENTIONED GENES AS THEY WILL COME-UP AS WE DISCUSS THE SIRTUINS!
No comments:
Post a Comment