Participation of Amyloid and Tau Protein in Post-Ischemic Neurodegeneration of the Hippocampus of a Nature Identical to Alzheimer's Disease

• Main Authors: Ryszard Pluta, Liang Ouyang, Sławomir Januszewski, Yang Li, Stanisław J. Czuczwar
• Format: Article
• Language: English
• Published: MDPI AG 2021-02-01
• Series: International Journal of Molecular Sciences
• Subjects: brain ischemia; hippocampus; amyloid; tau protein; α-synuclein; secretases
• Online Access: https://www.mdpi.com/1422-0067/22/5/2460

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 (<i>amyloid protein precursor</i> and <i>tau protein</i>) 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 <i>amyloid protein precursor</i>, <i>β-secretase</i>, <i>presenilin 1</i> and <i>2</i>, <i>tau protein</i>, <i>autophagy</i>, <i>mitophagy,</i> and <i>apoptosis</i> 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.