ArticleNPJ aging and mechanisms of disease2021
Adropin correlates with aging-related neuropathology in humans and improves cognitive function in aging mice.
Article in NPJ aging and mechanisms of disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Beneficial Hepatokines in MASLD/MASH: Therapeutic Potentials and Drug Delivery Challenges.International journal of molecular sciences · 2026Review
- Low circulating adropin concentrations identify vulnerability in learning-dependent cognitive performance in aged rhesus macaques.npj aging · 2026Article
- Review
- The Emerging Role of Adropin in Neurological Health: A Systematic Review.Iranian journal of public health · 2025Review
- Changes in adropin levels in brain and peripheral tissues with aging.Neuroscience letters · 2025Article
- Single-Cell Analysis Dissects the Effects of Vitamin D on Genetic Senescence Signatures Across Murine Tissues.Nutrients · 2025Article
- Role of the Unique Secreted Peptide Adropin in Various Physiological and Disease States.Biomolecules · 2024Review
- Metabolic Crosstalk between Liver and Brain: From Diseases to Mechanisms.International journal of molecular sciences · 2024Review
- Low circulating adropin concentrations predict increased risk of cognitive decline in community-dwelling older adults.GeroScience · 2024Article
- Prognostic value of nomogram model based on clinical risk factors and CT radiohistological features in hypertensive intracerebral hemorrhage.Frontiers in neurology · 2024Article
- Low circulating adropin levels in late-middle aged African Americans with poor cognitive performance.npj aging · 2023Article
- Expression of G protein-coupled receptor GPR19 in normal and neoplastic human tissues.Scientific reports · 2023Article
- Friend or foe for obesity: How hepatokines remodel adipose tissues and translational perspective.Genes & diseases · 2023Review
- Protective roles of adropin in neurological disease.American journal of physiology. Cell physiology · 2023Review
- Article
- Intersection of the Orphan G Protein-Coupled Receptor, GPR19, with the Aging Process.International journal of molecular sciences · 2022Review
- Potentials of Neuropeptides as Therapeutic Agents for Neurological Diseases.Biomedicines · 2022Review
- Adropin transgenesis improves recognition memory in diet-induced obese LDLR-deficient C57BL/6J mice.Peptides · 2021Article
- Role of Adropin in Cardiometabolic Disorders: From Pathophysiological Mechanisms to Therapeutic Target.Biomedicines · 2021Review
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
Abstract
The neural functions of adropin, a secreted peptide highly expressed in the brain, have not been investigated. In humans, adropin is highly expressed in astrocytes and peaks during critical postnatal periods of brain development. Gene enrichment analysis of transcripts correlating with adropin expression suggests processes relevant to aging-related neurodegenerative diseases that vary with age and dementia state, possibly indicating survivor bias. In people aged <40 y and 'old-old' (>75 y) diagnosed with dementia, adropin correlates positively with genes involved in mitochondrial processes. In the 'old-old' without dementia adropin expression correlates positively with morphogenesis and synapse function. Potent neurotrophic responses in primary cultured neurons are consistent with adropin supporting the development and function of neural networks. Adropin expression in the 'old-old' also correlates positively with protein markers of tau-related neuropathologies and inflammation, particularly in those without dementia. How variation in brain adropin expression affects neurological aging was investigated using old (18-month) C57BL/6J mice. In mice adropin is expressed in neurons, oligodendrocyte progenitor cells, oligodendrocytes, and microglia and shows correlative relationships with groups of genes involved in neurodegeneration and cellular metabolism. Increasing adropin expression using transgenesis improved spatial learning and memory, novel object recognition, resilience to exposure to new environments, and reduced mRNA markers of inflammation in old mice. Treatment with synthetic adropin peptide also reversed age-related declines in cognitive functions and affected expression of genes involved in morphogenesis and cellular metabolism. Collectively, these results establish a link between adropin expression and neural energy metabolism and indicate a potential therapy against neurological aging.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.