Impaired conditioned emotional response and object recognition are concomitant to neuronal damage in the amygdala and perirhinal cortex in middle-aged ischemic rats

Amelioration of cognitive, motor and endogenous defense functions with silymarin, piracetam and protocatechuic acid in the cerebral global ischemic rat model

“…This injury is due to the reduction of the cell populations in the striatum, motor cortex M 1 area, and hippocampus CA 1 area during BCCAO (Araujo et al, 2012). However, it has also been documented that in middle-aged animals, CA 1 neuronal injury during cerebral global ischemia is accompanied by a 20-25% neuronal loss in the basolateral nucleus of the amygdala and perirhinal cortex ischemia compared to Sham-operated animals (Tremblaye and Plamondon, 2011). The elevated plus maze test is routinely used for screening of antianxiety drugs.…”

Review paper Neurogenesis and neuroprotection in postischemic brain neurodegeneration with Alzheimer phenotype: is there a role for curcumin?

“…The concentration of these proteins may lead to amyloid precursor protein proteolysis and β-amyloid peptide formation with final extracellular deposition as plaques [52,55]. Summing up, experimental data on postischemic brains show that Alzheimer's disease-related changes render the brain more susceptible to ischemic damage and in consequence lead to the development of Alzheimertype dementia [3,24,29].…”

“…An overarching consequence of ischemic brain injury is both short-and long-term cognitive deficits. These deficits typically occur in attention, memory, learning and higher order executive functions [3,24,29]. Cognitive deficits after ischemia can be attributed to damage to certain vulnerable brain regions including the hippocampus [47] and temporal cortex [42], as well as sub-cortical white matter tracts [44,45].…”

Discrepancy in Expression of β-Secretase and Amyloid-β Protein Precursor in Alzheimer-Related Genes in the Rat Medial Temporal Lobe Cortex Following Transient Global Brain Ischemia

“…At the synaptic level, dysfunction induced by ischemia in hippocampus and amyloid-␤ (A␤) peptide [17] cause aberrant patterns of activity in the associated neural circuits, destabilize neuronal networks, and impair oscillatory activity. This scenario, ultimately, seems responsible for the early alteration of the processes implicated in learning and memory tasks observed in AD patients [13] and post-ischemic dementia with Alzheimer phenotype [14][15][16]18].…”