By Linda on Oct 12, 2010 in F.I.G.H.T. | comments(0)
Cerebral Microvascular Occlusion is very common and yet is very frequently overlooked when dealing with dementia and stroke recovery.
This new research reminds us that we should often consider “small strokes” when we are dealing with age-related cognitive decline. I suggest adding either Endokinase or Boluoke for at least a month or so to Beyond Chelation-Improved etc. along with using all of the powerful brain enhancing nutrients available today. Brain TISSUE PERFUSION is vital and is frequently compromised, and small strokes are very commonly not diagnosed.
Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
Full article: http://www.ncbi.nlm.nih.gov/sites/entrez/20505729?dopt=Abstract&holding=f1000,f1000m,isrctn
“Alterations in the efficiency of the protective mechanism that we have identified may have important implications in microvascular pathology, stroke recovery and age-related cognitive decline”
Cerebral microvascular occlusion is a common phenomenon throughout life that might require greater recognition as a mechanism of brain pathology. Failure to recanalize microvessels promptly may lead to the disruption of brain circuits and significant functional deficits. Haemodynamic forces and the fibrinolytic system are considered to be the principal mechanisms responsible for recanalization of occluded cerebral capillaries and terminal arterioles. Here we identify a previously unrecognized cellular mechanism that may also be critical for this recanalization. By using high-resolution fixed-tissue microscopy and two-photon imaging in living mice we observed that a large fraction of microemboli infused through the internal carotid artery failed to be lysed or washed out within 48 h. Instead, emboli were found to translocate outside the vessel lumen within 2-7 days, leading to complete re-establishment of blood flow and sparing of the vessel. Recanalization occurred by a previously unknown mechanism of microvascular plasticity involving the rapid envelopment of emboli by endothelial membrane projections that subsequently form a new vessel wall. This was followed by the formation of an endothelial opening through which emboli translocated into the perivascular parenchyma. The rate of embolus extravasation was significantly decreased by pharmacological inhibition of matrix metalloproteinase 2/9 activity. In aged mice, extravasation was markedly delayed, resulting in persistent tissue hypoxia, synaptic damage and cell death. Alterations in the efficiency of the protective mechanism that we have identified may have important implications in microvascular pathology, stroke recovery and age-related cognitive decline.