GPR37 and its neuroprotective mechanisms: bridging osteocalcin signaling and brain function DOI Creative Commons
Xiaofeng Bian,

Y. M. Wang,

Weijie Zhang

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2024, Volume and Issue: 12

Published: Nov. 20, 2024

Osteocalcin (OCN) is a hormone secreted by osteoblasts and has attracted widespread attention for its role in regulating brain function. Clinical studies indicate positive correlation between levels of circulating OCN cognitive performance. Indeed, lower been detected various neurodegenerative diseases (NDs), while supplementation under certain conditions may improve GPR37, G protein-coupled receptor, recently identified as receptor OCN. It exhibits distinct expression patterns across regions cell types, potentially influencing functional roles within the brain. Research indicates that GPR37 regulates neuronal migration, proliferation, differentiation, myelination. Furthermore, shown to mitigate inflammation apoptosis through mechanisms, exerting neuroprotective effects. However, regulatory influence on function inconsistency, highlighting duality actions. Therefore, this review thoroughly summarizes mechanisms modulating cellular physiological activities involvement immune responses, stress reactions, neuroprotection. aims enhance understanding how modulates facilitate identification novel therapeutic targets or strategies related diseases.

Language: Английский

Mechanisms of the Beneficial Effects of Exercise on Brain-Derived Neurotrophic Factor Expression in Alzheimer’s Disease DOI Creative Commons

Sama Jaberi,

Margaret Fahnestock

Biomolecules, Journal Year: 2023, Volume and Issue: 13(11), P. 1577 - 1577

Published: Oct. 26, 2023

Brain-derived neurotrophic factor (BDNF) is a key molecule in promoting neurogenesis, dendritic and synaptic health, neuronal survival, plasticity, excitability, all of which are disrupted neurological cognitive disorders such as Alzheimer's disease (AD). Extracellular aggregates amyloid-β (Aβ) the form plaques intracellular hyperphosphorylated tau protein have been identified major pathological insults AD brain, along with immune dysfunction, oxidative stress, other toxic stressors. Although aggregated Aβ lead to decreased brain BDNF expression, early losses prior plaque tangle formation may be due stress contribute dysfunction. Physical exercise, on hand, protects structure function, increased mediator exercise-induced enhancements function. Here, we review recent literature mechanisms behind upregulation its effects improving learning memory pathology. Exercise releases into circulation host hormones factors from variety peripheral tissues. Mechanisms induction discussed here osteocalcin, FNDC5/irisin, lactate. The fundamental how exercise impacts cognition not yet fully understood but prerequisite developing new biomarkers therapies delay or prevent decline.

Language: Английский

Citations

19
Research progress in Alzheimer's disease and bone-brain axis DOI Creative Commons
Fan Zhang, Wei Zhang

Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 98, P. 102341 - 102341

Published: May 15, 2024

Alzheimer's disease (AD) is the most common type of cognitive impairment. AD closely related to orthopedic diseases, such as osteoporosis and osteoarthritis, in terms epidemiology pathogenesis. Brain bone tissues can regulate each other different manners through bone-brain axis. This article reviews research progress relationship between axis mechanisms AD, therapy by targeting axis, order deepen understanding communication, promote early diagnosis explore new for patients. Keywords

Language: Английский

Citations

6
Crosstalk between bone and brain in Alzheimer's disease: Mechanisms, applications, and perspectives DOI Creative Commons

Zhuo‐Ting Liu,

Ming‐Han Liu, Yan Xiong

et al.

Alzheimer s & Dementia, Journal Year: 2024, Volume and Issue: 20(8), P. 5720 - 5739

Published: June 2, 2024

Abstract Alzheimer's disease (AD) is a neurodegenerative that involves multiple systems in the body. Numerous recent studies have revealed bidirectional crosstalk between brain and bone, but interaction bone AD remains unclear. In this review, we summarize human of association provide an overview their interactions underlying mechanisms AD. We review effects on from aspects pathogenic proteins, risk genes, neurohormones, neuropeptides, neurotransmitters, brain‐derived extracellular vesicles (EVs), autonomic nervous system. Correspondingly, elucidate involvement pathogenesis AD, including bone‐derived hormones, marrow‐derived cells, EVs, inflammation. On basis brain, propose potential strategies for management with hope offering novel perspectives its prevention treatment. Highlights The along consequent changes may involve disturbing homeostasis. Degenerative disorders influence progression through series pathophysiological mechanisms. Therefore, relevant intervention be beneficial comprehensive

Language: Английский

Citations

6
Osteoporosis and Alzheimer´s disease (or Alzheimer´s disease and Osteoporosis) DOI
Nahuel Ezequiel Wanionok,

Gustavo R Morel,

Juan Manuel Fernández

et al.

Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 99, P. 102408 - 102408

Published: July 3, 2024

Language: Английский

Citations

5
Bone-brain communication mediates the amelioration of Polgonatum cyrtonema Hua polysaccharide on fatigue in chronic sleep-deprived mice DOI

Ting Zhang,

Xueying Li,

Dan-Dan Kuang

et al.

International Journal of Biological Macromolecules, Journal Year: 2025, Volume and Issue: unknown, P. 139706 - 139706

Published: Jan. 1, 2025

Language: Английский

Citations

0
The potential link between the development of Alzheimer’s disease and osteoporosis DOI Creative Commons

Fariha Nasme,

Jyotirmaya Behera,

Prisha Tyagi

et al.

Biogerontology, Journal Year: 2025, Volume and Issue: 26(1)

Published: Jan. 20, 2025

Language: Английский

Citations

0
Unraveling the impact of blood RANKL and OPG levels on Alzheimer's disease: Independent of bone mineral density and inflammation DOI Creative Commons
Xingzhi Guo, Wenzhi Shi, Juanjuan Lu

et al.

Alzheimer s & Dementia Translational Research & Clinical Interventions, Journal Year: 2025, Volume and Issue: 11(1)

Published: Jan. 1, 2025

Language: Английский

Citations

0
Antiageing strategy for neurodegenerative diseases: from mechanisms to clinical advances DOI Creative Commons
Qiu Jiang, Jie Liu, Shan Huang

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2025, Volume and Issue: 10(1)

Published: March 10, 2025

Abstract In the context of global ageing, prevalence neurodegenerative diseases and dementia, such as Alzheimer’s disease (AD), is increasing. However, current symptomatic disease-modifying therapies have achieved limited benefits for in clinical settings. Halting progress neurodegeneration cognitive decline or even improving impaired cognition function are clinically meaningful goals treatments diseases. Ageing primary risk factor their associated comorbidities, vascular pathologies, elderly individuals. Thus, we aim to elucidate role ageing from perspective a complex system, which brain core peripheral organs tissues form holistic network support functions. During progressive deterioration structure entire body hampers its active adaptive responses various stimuli, thereby rendering individuals more vulnerable Consequently, propose that prevention treatment should be grounded antiageing rejuvenation means complemented by interventions targeting disease-specific pathogenic events. This integrated approach promising strategy effectively prevent, pause slow down progression

Language: Английский

Citations

0
Evaluation of the Effects of Thymoquinone on RAGE/NOX4 Expressions and Brain Tissue Morphometry in Experimental Alzheimer’s Disease Induced by Amyloid Beta 1–42 Peptide DOI Creative Commons
Şükrü Ateş, Harun Ülger, Sümeyye Uçar

et al.

Biomolecules, Journal Year: 2025, Volume and Issue: 15(4), P. 543 - 543

Published: April 7, 2025

The onset of Alzheimer’s disease (AD) is attributed to widespread amyloid beta (Aβ) plaque accumulation, tau hyperphosphorylation, oxidative stress, and neuroinflammation. However, the underlying mechanism AD remains unclear, no curative treatment currently exists. aim was investigate effect thymoquinone by suppressing RAGE/NOX4 pathway in AD. Mice (n = 60) were divided into five groups, an experimental model induced Aβ1–42 peptide established two groups. We also administered 5 mg/kg (TMQ) mice for its properties slow or treat neurodegeneration Behavioral tests memory emotional states, micro-computed tomography (Micro CT) assess brain volume, ELISA measure malondialdehyde (MDA) levels, hematoxylin eosin staining (H&E) evaluate neuronal degeneration used. Immunohistochemical (IHC), Western blot (WB), real-time polymerase chain reaction (PCR) methods used inhibitory TMQ on a receptor advanced glycation end products (RAGE)/nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 4 (NOX4) signaling results showed that may have ameliorative effects memory, spatial learning, learning ability, anxiety has antioxidative decreasing MDA levels ELSIA method (p < 0.05). There marked increase compared other groups concluded could ameliorate H&E suppress IHC WB analysis. be therapeutic reducing AB expression level analysis Real-time PCR APP 0.05), RAGE, NOX4 0.05) gene expressions reduced TMQ. In conclusion, high potential effective preventive strategy can developed with more comprehensive studies

Language: Английский

Citations

0
Osteocalcin and GPR158: linking bone and brain function DOI Creative Commons
Jingjing Li, Shujie Lou, Xiaofeng Bian

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2025, Volume and Issue: 13

Published: April 23, 2025

Osteocalcin (OCN), a small protein secreted by osteoblasts, has attracted significant attention for its role as an endocrine factor in regulating the central nervous system (CNS) via bone-brain axis. As critical receptor OCN, G protein-coupled 158 (GPR158) facilitates proliferation, differentiation, and survival of neural cells while directly influencing neurons' structural functional plasticity, thereby modulating cognitive function. Additionally, GPR158 is involved cellular energy metabolism interacts with proteins such regulators signaling 7 (RGS7), broadening understanding OCN’s impact on activity. Notably, displays region- cell type-specific bidirectional effects under certain pathological conditions, tumor development mood regulation, adding complexity to mechanisms action. Although precise biological underlying OCN/GPR158 pathway remain incompletely understood, association neurodegenerative diseases (NDs), including Alzheimer’s disease (AD) Parkinson’s (PD), becoming increasingly evident. Thus, systematic summary CNS regulation NDs will deepen brain function support new therapeutic targets strategies.

Language: Английский

Citations

0