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Apolipoprotein J (ApoJ), or clusterin, is one of the main apolipoproteins in the brain. It is synthesized and released from astrocytes in a healthy brain, and its expression increases in neurodegenerative disorders. Genetic evidence has suggested an association between ApoJ polymorphism and the risk of Alzheimer's disease (AD)-it is now considered the third main genetic risk factor for late-onset AD. However, the role of ApoJ overexpression in the state of disorder, toxicity, or protection is not yet clear. Since ApoJ plays different roles in AD, we review the function of ApoJ using different cell signaling pathways in AD and outline its paradoxical roles in AD. ApoJ helps in amyloid-beta (Aβ) clearance. Vice versa, ApoJ gene knock-out causes fibrillary Aβ reduction and prevents Aβ-induced neuron cell death. Understanding ApoJ, through various cellular signaling pathways, creates a new perspective on AD's cellular principles. The overall message is that ApoJ can be a valuable tool in controlling AD.
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http://dx.doi.org/10.1021/acschemneuro.0c00637 | DOI Listing |
Biogerontology
July 2025
Advanced Technology Center for Aging Research and Geriatric Mouse Clinic, IRCCS INRCA, Ancona, Italy.
Cytomegalovirus (CMV) drives immunosenescence, while its reactivation is associated with inflammation and oxidative stress. This study investigates the interplay between CMV, oxidative stress and inflammation in a cohort of 2065 age-stratified individuals randomly recruited from the general population (RASIG), as part of the MARK-AGE study, to better understand the role of CMV in immunosenescence and its potential impact on age-related diseases. CMV IgG titers were associated with oxidative stress, antioxidant, and inflammatory biomarkers.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
July 2025
Division of Endocrinology and Metabolism, Department of Internal Medicine, Korea University College of Medicine, Seoul, Republic of Korea.
Introduction: Type 2 diabetes mellitus (DM) is a known risk factor for sarcopenia. Apolipoprotein J (ApoJ) and myostatin (MSTN) have been implicated in muscle glucose metabolism. We aimed to examine the association between serum ApoJ and MSTN levels and sarcopenia in older adults, with and without DM.
View Article and Find Full Text PDFmedRxiv
June 2025
Flow and Imaging Cytometry Core Facility, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD, 20892, USA.
Introduction: The ApoE receptor 2-Disabled homolog-1 (ApoER2-Dab1) pathway suppresses Tau phosphorylation as part of a multi-arm pathway that regulates cytoskeletal and synaptic integrity. We previously showed that multiple ApoER2-Dab1 pathway components accumulate in regions affected in early Alzheimer's disease (AD). Since the amygdala is a hub for emotional regulation and fear memory, we hypothesized that accumulation of ApoER2-Dab1 components in amygdala may correlate with cognitive or neuropsychiatric manifestations of AD.
View Article and Find Full Text PDFCell Mol Gastroenterol Hepatol
June 2025
Division of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, China; Key Laboratory of Early Prevention and Treatment for Regional High Frequency Tumor (Guangxi Medical University), Ministry of Education, Nanning, China. Electronic address: shuangdi-go@foxm
Background & Aims: Dysregulation of the signal transducer and activator of transcription 3 (STAT3) signaling pathway is closely linked to redox homeostasis and exacerbates liver injury. Apolipoprotein J (ApoJ), a chaperone sensitive to redox changes. We aim to investigate how hepatocyte ApoJ regulates the STAT3 pathway to mediate paracrine signaling that activates hepatic stellate cells (HSCs).
View Article and Find Full Text PDFMol Neurodegener
May 2025
Department of Rehabilitation, The Second Affiliated Hospital of Chongqing Medical University, No. 74 Linjiang Road, Yuzhong District, Chongqing, 400010, China.
Alzheimer's disease (AD) is increasingly recognized as a systemic disorder with a substantial metabolic disorder component, where the liver significantly impacts the brain via the liver-brain axis. Key mechanisms include the liver's role in clearing peripheral β-amyloid (Aβ), the influence of hepatic enzymes and metabolites on cognitive decline, and the systemic effects of metabolic disorders on AD progression. Hepatokines, liver-secreted proteins including fibroblast growth factor (FGF)-21, selenoprotein P (SELENOP), Fetuin-A, Midbrain astrocyte-derived neurotrophic factor (MANF), apolipoprotein J (ApoJ), sex hormone-binding globulin (SHBG), Adropin and Angiopoietin-like protein 3 (ANGPTL3), could regulate insulin sensitivity, lipid metabolism, oxidative stress, immune responses, and neurotrophic support.
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