Alzheimer's disease (AD) is a major cause of dementia. Growing evidence suggests that dysregulation of autophagy, a cellular mechanism essential for self-digestion of damaged proteins and organelles, is involved in neurological degenerative diseases including AD. Previously, we reported that autophagosomes are increased in the brains of AD mouse model. However, the plasma levels of autophagic markers have not yet been investigated in patients with AD. In this study, we investigated the expression of autophagy-related genes 5 and 12 (ATG5 and ATG12, respectively) in cells in vitro upon amyloid-beta (Aβ) treatment and in the plasma of AD patients. ATG5-ATG12 complex levels were increased in primary rat cortical neurons and human umbilical vein endothelial cells after Aβ treatment. Furthermore, we compared plasma from 69 patients with dementia, 82 patients with mild cognitive impairment (MCI), and 127 cognitively normal control participants. Plasma levels of ATG5 were significantly elevated in patients with dementia (149.3 ± 7.5 ng/mL) or MCI (152.9 ± 6.9 ng/mL) compared with the control subjects (129.0 ± 4.1 ng/mL) (p = 0.034, p = 0.016, respectively). Our results indicate that alterations in the plasma ATG5 levels might be a potential biomarker in patients at risk for AD.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6427023 | PMC |
| http://dx.doi.org/10.1038/s41598-019-41347-2 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Noncanonical roles of ATG5 and membrane atg8ylation in retromer assembly and function.
Elife
January 2025
Autophagy, Inflammation and Metabolism Center of Biochemical Research Excellence, University of New Mexico School of Medicine, Albuquerque, United States.
ATG5 is one of the core autophagy proteins with additional functions such as noncanonical membrane atg8ylation, which among a growing number of biological outputs includes control of tuberculosis in animal models. Here, we show that ATG5 associates with retromer's core components VPS26, VPS29, and VPS35 and modulates retromer function. Knockout of ATG5 blocked trafficking of a key glucose transporter sorted by the retromer, GLUT1, to the plasma membrane.
View Article and Find Full Text PDFPlatelet-rich plasma combined with isometric quadriceps contraction regulates autophagy in chondrocytes via the PI3K/AKT/mTOR pathway to promote cartilage repair in knee osteoarthritis.
Regen Ther
March 2025
Sichuan Academy of Chinese Medicine Sciences, Chengdu, China.
Background: This study investigated the molecular mechanism by which the combination of platelet-rich plasma (PRP) and isometric contraction of the quadriceps (ICQ) intervention regulates autophagy in chondrocytes to prevent and treat knee osteoarthritis (KOA).
Methods: Thirty Sprague-Dawley rats were divided into a control group (CG, n = 6) and a model group (n = 24). After one week, the model group was randomly divided into a joint intervention group (JIG), a rapamycin group (RAG), an MHY1485 group (MYG), and a model blank group (MBG), with JIG, RAG, and MYG receiving the same combined intervention.
Macrophage autophagy protects against acute kidney injury by inhibiting renal inflammation through the degradation of TARM1.
Autophagy
January 2025
Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Macroautophagy/autophagy activation in renal tubular epithelial cells protects against acute kidney injury (AKI). However, the role of immune cell autophagy, such as that involving macrophages, in AKI remains unclear. In this study, we discovered that macrophage autophagy was an adaptive response during AKI as mice with macrophage-specific autophagy deficiency () exhibited higher serum creatinine, more severe renal tubule injury, increased infiltration of ADGRE1/F4/80 macrophages, and elevated expression of inflammatory factors compared to WT mice during AKI induced by either LPS or unilateral ischemia-reperfusion.
View Article and Find Full Text PDFATG5 is one of the core autophagy proteins with additional functions such as noncanonical membrane atg8ylation, which among a growing number of biological outputs includes control of tuberculosis in animal models. Here we show that ATG5 associates with retromer's core components VPS26, VPS29 and VPS35 and modulates retromer function. Knockout of ATG5 blocked trafficking of a key glucose transporter sorted by the retromer, GLUT1, to the plasma membrane.
View Article and Find Full Text PDFLassa virus Z protein hijacks the autophagy machinery for efficient transportation by interrupting CCT2-mediated cytoskeleton network formation.
Autophagy
November 2024
State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China.
The Lassa virus (LASV) is a widely recognized virulent pathogen that frequently results in lethal viral hemorrhagic fever (VHF). Earlier research has indicated that macroautophagy/autophagy plays a role in LASV replication, but, the precise mechanism is unknown. In this present study, we show that LASV matrix protein (LASV-Z) is essential for blocking intracellular autophagic flux.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!