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Age related effects on pathophysiology of chronic cerebral hypoperfusion
Author(s) -
Wappler Edina Amalia,
Nemeth Istvan B,
Bari Ferenc,
Nagy Zoltan
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1024.24
Subject(s) - synaptophysin , perfusion , pathophysiology , hippocampus , medicine , cerebral blood flow , pathology , immunohistochemistry , endocrinology
We investigated the effects of age on cerebral hypopoperfusion in 6‐, and 18 months old male Wistar rats after 3 months of bilateral common carotid artery occlusion (BCCAO). Brain pathology was investigated on coronal sections using Nissle staining (cell number and satellitosis) and immunohisotology for microtubule‐associated protein 2 (MAP‐2), synaptophysin, and growth associated protein 43 (GAP‐43). Increased satellitosis was found in the hippocampus and the frontal and parietal cortices with decreased cell number in the same regions in young animals. Decreased dendritic and synaptic density was observed in every investigated region in the young hypoperfused brain; however, some groups of neurons had higher synaptophysin expression than others. Old control animals had similar changes to young hypoperfused animals, but the, old hypoperfused rats had more serious changes that those of young BCCAO animals. In summary, cerebral hypoperfusion in young animals induces several changes in the brain that are similar to that of non‐BCCAO old rats. Additionally, hypoperfusion at a later age causes the same pattern of changes but of more serious nature than in young BCCAO rats. We conclude that cerebral hypoperfusion seems to be an important factor which accelerates the deterioration associated with brain aging.