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

## TL;DR

This study examines how genes for apolipoproteins A1, E, and J change in the brain after ischemia, which may contribute to Alzheimer's disease.

## Contribution

The study reveals time-dependent gene expression patterns of ApoA1, ApoE, and ApoJ in a post-ischemic Alzheimer's model.

## Key findings

- ApoA1 expression was lower than control values at 2 days, 6 months, and 12 months, but higher at 7 days, 30 days, 18 months, and 24 months.
- ApoE expression was lower at 2 days, 30 days, and 6 months, but higher in other post-ischemia periods.
- ApoJ showed a similar expression pattern to ApoE, with a dual role in early protection and later neurodegeneration.

## 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.