Role of Lipocalin-2 in Amyloid-Beta Oligomer-Induced Mouse Model of Alzheimer’s Disease
| Autor: | Hae Ryong Lee, Hyeong Seok An, Soo Kyoung Kim, Kun Ho Lee, Jong Youl Lee, Kyu Yeong Choi, Zhen Jin, Kyung Eun Kim, Catriona McLean, Gu Seob Roh, Eun Ae Jeong, Heeyoung Kang, Jaewoong Lee, Hyun Joo Shin |
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| Rok vydání: | 2021 |
| Předmět: |
medicine.medical_specialty
Amyloid Physiology Amyloid beta Clinical Biochemistry RM1-950 medicine.disease_cause Biochemistry Article neuroinflammation White matter Internal medicine medicine oxidative stress Molecular Biology Neuroinflammation biology Microglia business.industry lipocalin-2 Cell Biology Human brain amyloid-beta medicine.anatomical_structure Endocrinology Frontal lobe iron accumulation biology.protein Therapeutics. Pharmacology business Alzheimer’s disease blood–brain barrier leakage Oxidative stress |
| Zdroj: | Antioxidants, Vol 10, Iss 1657, p 1657 (2021) Antioxidants Volume 10 Issue 11 |
| ISSN: | 2076-3921 |
| Popis: | Lipocalin-2 (LCN2) is an inflammatory protein with diverse functions in the brain. Although many studies have investigated the mechanism of LCN2 in brain injuries, the effect of LCN2 on amyloid-toxicity-related memory deficits in a mouse model of Alzheimer’s disease (AD) has been less studied. We investigated the role of LCN2 in human AD patients using a mouse model of AD. We created an AD mouse model by injecting amyloid-beta oligomer (AβO) into the hippocampus. In this model, animals exhibited impaired learning and memory. We found LCN2 upregulation in the human brain frontal lobe, as well as a positive correlation between white matter ischemic changes and serum LCN2. We also found increased astrocytic LCN2, microglia activation, iron accumulation, and blood–brain barrier disruption in AβO-treated hippocampi. These findings suggest that LCN2 is involved in a variety of amyloid toxicity mechanisms, especially neuroinflammation and oxidative stress. |
| Databáze: | OpenAIRE |
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