Alzheimer-associated presenilin 2 gene is dysregulated in rat medial temporal lobe cortex after complete brain ischemia due to cardiac arrest

Abstract

Thus, presented changes suggest that the significant dysregulation of presenilin 2 gene may be connected with a response of neuronal cells to transient global brain ischemia due to cardiac arrest. Finally, the ischemia-induced gene dysregulation may play a key role in the late onset of Alzheimer's-type dementia.

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

“…These data corroborate earlier immunohistochemical observations from animal models of global brain ischemia and from brains after global brain ischemia in humans, which all suggest a direct relationship between ischemia and increased level of A␤ peptide accumulation in the brain tissue [19][20][21]. The findings presented above highlight a different and/or delayed regulatory mode in ischemia-induced cell death in temporal cortex as compared to hippocampus through an A␤ peptide-dependent manner [35,36]. These observations will help to understand the gradual postischemic damage in the brain, delayed A␤ peptide deposition and slow and long-term ischemic spreading neuropathology of AD from hippocampus into medial temporal lobe cortex and other parts of the brain [25,35,36,60,61].…”

“…The findings presented above highlight a different and/or delayed regulatory mode in ischemia-induced cell death in temporal cortex as compared to hippocampus through an A␤ peptide-dependent manner [35,36]. These observations will help to understand the gradual postischemic damage in the brain, delayed A␤ peptide deposition and slow and long-term ischemic spreading neuropathology of AD from hippocampus into medial temporal lobe cortex and other parts of the brain [25,35,36,60,61]. The present data may partly help to define the molecular mechanism of higher occurrence of neuronal death in ischemic layers 3, 5, and 6 of medial temporal lobe cortex.…”

“…Unfortunately, the relationship between hippocampus neuronal injury and medial temporal lobe injury in brain ischemia and AD has received little attention. On the basis of the known anatomical connectivity between the hippocampus and medial temporal lobe, we hypothesized that in ischemic brain injury of hippocampus there would be an association with neuronal pathology in temporal cortex as measured by regional related metabolism of amyloid-␤ protein precursor genes [35,36]. What is more, we intended to understand how A␤ peptide deposition induces ischemic remodeling in medial temporal lobe cortex.…”

Hypoxia/ischemia activate processing of Amyloid Precursor Protein: impact of vascular dysfunction in the pathogenesis of Alzheimer's disease

“…The mechanism of increased amyloidogenic APP processing by PS2V needs to be clarified, especially since brain ischemia was able to increase the expression of PS2 in rat cortex (Pluta et al . ).…”

“…It is known that the induction of HMGA1a is a common response to hypoxia/ oxidative stress (Moussavi Nik et al 2011). The mechanism of increased amyloidogenic APP processing by PS2V needs to be clarified, especially since brain ischemia was able to increase the expression of PS2 in rat cortex (Pluta et al 2016a).…”