Alterations of Apolipoprotein A1, E, and J Genes in the Frontal Cortex in an Ischemic Model of Alzheimer’s Disease with 2-Year Survival

Sep 30, 2026

Upload by Himbo

Genetic studies examine apolipoproteins linked to Alzheimer’s disease in ischemic frontal cortex, focusing on how post-ischemia changes contribute to neurodegeneration. Gene expression is measured with RT-PCR at multiple time points after 10-minute total cerebral ischemia (2, 7, 30 days; 6, 12, 18, 24 months). ApoA1 expression shows time-dependent decreases and later overexpression; ApoE decreases early then increases; ApoJ displays a comparable dual pattern. Results suggest ApoA1 supports neuroprotection, ApoE is detrimental, and ApoJ shifts from protective early effects to later neurodegenerative progression.

LanguageEnglish

CategoryResearch & Report

FormatPDF

Pages17

Reading Time43 min

AccessFree to download

Abstract

Introduction

Article Alterations of Apolipoprotein A1, E, and J Genes in the Frontal Cortex in an Ischemic Model of Alzheimer’s Disease with 2-Year Survival Ryszard Pluta 1, *,†, Marzena Ułamek-Kozioł 2,†, Janusz Kocki 3, Anna Bogucka-Kocka 4, Jacek Bogucki 5 and Stanisław J. Czuczwar 1 Academic Editors: José Marco-Contelles and Kiminobu Sugaya Received: 8 December 2025 Revised: 23 December 2025 Accepted: 26 December 2025 Published: 28 December 2025 Copyright: © 2025 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license. 1 Department of Pathophysiology, Medical University of Lublin, 20-090 Lublin, Poland; [czuczwarsj@yahoo.com](czuczwarsj@yahoo.com) [2](2 Department of Neurology)[ Department of Neurology](2 Department of Neurology), [Institute of Psychiatry and Neurology](Institute of Psychiatry and Neurology), [02-957 Warsaw](02-957 Warsaw), [Poland](Poland); [marzena_ulamek@wp.pl](marzena_ulamek@wp.pl) 3 Department of Clinical Genetics, Medical University of Lublin, 20-080 Lublin, Poland; [janusz.kocki@tlen.pl](janusz.kocki@tlen.pl) 4 Department of Biology and Genetics, Medical University of Lublin, 20-093 Lublin, Poland; [anna.kocka@tlen.pl](anna.kocka@tlen.pl) 5 Faculty of Medicine, John Paul II Catholic University of Lublin, 20-708 Lublin, Poland; [jacekbogucki@wp.pl](jacekbogucki@wp.pl) * Correspondence: pluta2018@wp.pl † These authors contributed equally to this work. Abstract In this article, we present genetic studies of apolipoproteins associated with Alzheimer’s disease in the frontal cortex after ischemia and discuss their involvement in the development of neurodegeneration. Gene expression was assessed using an RT-PCR protocol at 2, 7, and 30 days and at 6, 12, 18, and 24 months after an episode of 10 min total cerebral ischemia. ApoA1 expression (encoding apolipoprotein A1) in the ischemic frontal cortex was lower than control values after 2 days, 6 and 12 months, while its overexpression was observed after 7 and 30 days and 18 and 24 months. In the case of ApoE (encoding apolipoprotein E) expression, it was lower than control values after 2 and 30 days and after 6 months; in the remaining periods after ischemia, the expression was above control values. A similar expression pattern after ischemia was revealed for ApoJ (encoding apolipoprotein J) . The data indicate that the observed changes in gene expression may reflect the activation and inhibition of various pathological processes involved in the development of post-ischemia neurodegeneration. Thus, overexpression of ApoA1 may be associated with the induction of neuroprotective mechanisms, whereas increased expression of ApoE may have harmful effects. Regarding the overexpression of ApoJ, the data indicate a dual behavior: in the early stages after ischemia, it has a protective effect, whereas in the later stages, it participates in the progression of neurodegenerative processes. Keywords: brain ischemia; Alzheimer’s disease; apolipoprotein A1; apolipoprotein E; apolipoprotein J; clusterin; frontal cortex; genes 1. Introduction Rising life expectancy and an aging population worldwide are leading to a dramatic increase in the number of people suffering from dementia in late life, which is now the second leading cause of death in high-income countries [1] . The causes of the described situation are brain diseases, leading to neurodegeneration, which drastically limit brain activity and reduce the quality and length of life, posing a serious problem for modern society. These include Alzheimer’s disease and focal or complete brain ischemia, which occupy a special place among the most common causes of disability, dementia and mortality worldwide [1–7] . Recent studies have shown that Alzheimer’s disease and cerebral ischemia share common pathogenetic processes, such as overlapping genomic and proteomic alterat

FAQs

How were gene expression levels measured after cerebral ischemia in the frontal cortex?

Gene expression was assessed using an RT-PCR protocol at multiple post-ischemia time points: 2, 7, and 30 days, and 6, 12, 18, and 24 months after a 10-minute total cerebral ischemia episode.

What is the observed time-dependent pattern of ApoA1 expression after ischemia?

ApoA1 expression in the ischemic frontal cortex is lower than controls after 2 days, 6 and 12 months, but overexpression occurs after 7 and 30 days and after 18 and 24 months.

How do the findings interpret the roles of ApoE and ApoJ in neurodegeneration?

Increased ApoE expression may have harmful effects. ApoJ shows dual behavior: it appears protective in early stages after ischemia, while in later stages it participates in the progression of neurodegenerative processes.

Sep 30, 2026

Upload by Himbo