Abstract
Recent evidence suggests that amyloid and tau protein are of vital importance in post-ischemic death of CA1 pyramidal neurons of the hippocampus. In this review, we summarize protein alterations associated with Alzheimer’s disease and their gene expression (amyloid protein precursor and tau protein) after cerebral ischemia, as well as their roles in post-ischemic hippocampus neurodegeneration. In recent years, multiple studies aimed to elucidate the post-ischemic processes in the development of hippocampus neurodegeneration. Their findings have revealed the dysregulation of genes for amyloid protein precursor, β-secretase, presenilin 1 and 2, tau protein, autophagy, mitophagy, and apoptosis identical in nature to Alzheimer’s disease. Herein, we present the latest data showing that amyloid and tau protein associated with Alzheimer’s disease and their genes play a key role in post-ischemic neurodegeneration of the hippocampus with subsequent development of dementia. Therefore, understanding the underlying process for the development of post-ischemic CA1 area neurodegeneration in the hippocampus in conjunction with Alzheimer’s disease-related proteins and genes will provide the most important therapeutic development goals to date.
Highlights
Hippocampus in animals and humans is one of the brain’s most sensitive areas to ischemia, especially for pyramidal neurons in the CA1 area [1,2,3,4]
The paper presents the genotypic and phenotypic neurodegeneration of Alzheimer’s disease type in the hippocampal CA1 region after cerebral ischemia, such as neuropathology, neuropathophysiology, amyloid, tau protein, and its genes, which play a key role in the occurrence and development of dementia (Figure 1)
2, and tau protein in rats following ischemia in the CA1 region of the hippocampus, as well as genes involved in the death of neurons after ischemia in the hippocampus, i.e., autophagy, mitophagy, and apoptosis
Summary
Hippocampus in animals and humans is one of the brain’s most sensitive areas to ischemia, especially for pyramidal neurons in the CA1 area [1,2,3,4]. In the CA1 area of the hippocampus, the expression of amyloid protein precursor gene is lower than that of the control 2 days after ischemia (Table 1) [32]. At 7–30 days following ischemia, the expression of tau protein gene decreases obviously compared with the control values (Table 1) [34]. Alterations in the mean expression level of amyloid protein precursor gene are statistically significant between 2 and 7, between 2 and 30, and between 7 and 30 days after hippocampal ischemia [32]. The statistical significance of changes in the expression of tau protein gene after the CA1 area ischemia is between 2 and 7 and between 2 and 30 days [34]
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