Cellular markers of neuroinflammation and neurogenesis after ischemic brain injury in the long-term survival rat model.

MRI was employed to follow the neurodegenerative foci and the localization of inflammatory cells by magnetically labeled CD4+ or CD8+ lymphocytes in the ischemia/reperfusion long-lived rats (9 and 13 months after 10 min of cardiac arrest). MRI of ischemic rats showed: (1) blood-brain barrier (BBB) leakage in the area of the dorsal hippocampus and brainstem-hindbrain level in basal cerebellum, (2) unlike anti-CD8 magnetic antibodies anti-CD4 ultra small paramagnetic iron oxide particles (USPIO) antibodies revealed hypointense areas in the brainstem-interbrain region and caudoputamen not found in animals that were not injected with USPIO antibodies, and (3) dilation in the retrosplenial area. Immunocytochemistry revealed microglial activation in the hippocampus and striatum, with indications of activation in thalamic lateral dorsal nuclei and the subventricular zone.

Transient brain ischemia due to cardiac arrest causes irreversible long-lasting cognitive injury.

Herein, we used a clinically-relevant model of 10 min cardiac arrest (CA) in Wistar rats. Histological analyses of the ischemic brains of old rats showed significant atrophy of CA(1) sector of hippocampus (Nissl and NeuN stainings) corresponding with increase of glial fibrillary acidic protein expression. The long-term behavioral consequences of above manipulation producing global brain ischemia were assessed in young, middle-aged and old rats, i.

Consideration of the ischaemic basis and treatment of Alzheimer's disease.

Victims of Alzheimer's disease (AD) develop a progressive dementia over years, accompanied by development of neurofibrillary tangles and finally neuronal death, accumulation of amyloid plaques and deposition of amyloid in neuro-vessels. Currently AD is the major form of dementia and the fourth leading cause of death in aged population. The investigation of etiology and therapy of AD, now more than ever, needs an infusion of new concepts.

Factors in creepy delayed neuronal death in hippocampus following brain ischemia-reperfusion injury with long-term survival.

Brain ischemia is well known for its ability to compromise the function of the blood-brain barrier. We assessed blood-brain barrier integrity by examining the leakage of horseradish peroxidase (HRP) and different fragments of amyloid precursor protein from the vascular network into hippocampal parenchyma in rats exposed to brain ischemia with long-term survival. The areas of blood-brain barrier leakage were associated with increased staining of HRP and C-terminal of amyloid precursor protein/beta-amyloid peptide in perivascular space suggesting, respectively, an additional response to ischemia and neuronal death.

Alzheimer's mechanisms in ischemic brain degeneration.

There is increasing evidence for influence of Alzheimer's proteins and neuropathology on ischemic brain injury. This review investigates the relationships between beta-amyloid peptide, apolipoproteins, presenilins, tau protein, alpha-synuclein, inflammation factors, and neuronal survival/death decisions in brain following ischemic episode. The interactions of these molecules and influence on beta-amyloid peptide synthesis and contribution to ischemic brain degeneration and finally to dementia are reviewed.

Ischemic blood-brain barrier and amyloid in white matter as etiological factors in leukoaraiosis.

Background: Pathology of white matter, which is observed in ischemic brain, indicates that similar processes contribute to Alzheimer's disease development. These injuries have been seen in the subcortical and periventricular regions. Periventricular white matter changes in ischemic and Alzheimer's disease brain, referred to as leukoaraiosis, are responsible for changes in memory, cognition and behavior.