Pluta Ryszard, Kocki Janusz, Bogucki Jacek, Bogucka-Kocka Anna, Czuczwar Stanisław J
Department of Pathophysiology, Medical University of Lublin, Lublin, Poland.
Department of Clinical Genetics, Medical University of Lublin, Lublin, Poland.
J Alzheimers Dis. 2025 Jan;103(2):627-634. doi: 10.1177/13872877241303950. Epub 2024 Dec 16.
Changes in the Alzheimer's disease-related apolipoprotein genes expression, occurring parallel with brain ischemia-induced neurodegeneration in the hippocampal CA3 area, may be crucial for the development of memory loss and dementia.
The aim of the study was to investigate changes in genes expression of () () and () in CA3 area post-ischemia with survival of 2 years.
The gene expression was evaluated with the use of an RT-PCR protocol after 2, 7, and 30 days and 6, 12, 18, and 24 months post-ischemia.
The expression of the gene (encoding apolipoprotein A1) was below the control values at 2 days, 6 and 12 months while at 7 and 30 days and 18 and 24 months post-ischemia this gene expression exceeded the control values. In the case of the gene (encoding clusterin) expression, it was above the control values at all times post-ischemia. Similar expression was observed for the gene (encoding apolipoprotein E) except on day 7 after ischemia where its expression was below the control value.
The results seem to indicate that the observed changes in the gene expression may reflect the activation and inhibition of a variety of processes involved in ischemia-induced neurodegeneration. The enhanced expression of and genes may be associated with induction of neuroprotective mechanisms while increased expression of the gene may produce detrimental effects.
阿尔茨海默病相关载脂蛋白基因表达的变化与海马CA3区脑缺血诱导的神经退行性变同时发生，可能对记忆丧失和痴呆的发展至关重要。
本研究旨在调查缺血2年后CA3区（）（）和（）基因表达的变化。
在缺血后2天、7天、30天以及6个月、12个月、18个月和24个月，使用逆转录聚合酶链反应（RT-PCR）方案评估基因表达。
载脂蛋白A1编码基因在缺血后2天、6个月和12个月时的表达低于对照值，而在缺血后7天、30天以及18个月和24个月时，该基因表达超过对照值。就簇集蛋白编码基因的表达而言，在缺血后的所有时间均高于对照值。载脂蛋白E编码基因除在缺血后第7天其表达低于对照值外，观察到类似的表达情况。
结果似乎表明，观察到的基因表达变化可能反映了缺血诱导的神经退行性变中各种过程的激活和抑制。和基因的表达增强可能与神经保护机制的诱导有关，而基因表达增加可能产生有害影响。
