Macrophage Polarization and Its Impact on Osteoporosis DOI

Junwei Yan,

Chenyu Huang, Dongdong Jiang

et al.

Results and problems in cell differentiation, Journal Year: 2024, Volume and Issue: unknown, P. 291 - 296

Published: Jan. 1, 2024

Language: Английский

Preclinical and first-in-human evaluation of AL002, a novel TREM2 agonistic antibody for Alzheimer’s disease DOI Creative Commons
Hua Long, Adam Simmons,

Arthur J. Mayorga

et al.

Alzheimer s Research & Therapy, Journal Year: 2024, Volume and Issue: 16(1)

Published: Oct. 23, 2024

Variants of the gene triggering receptor expressed on myeloid cells-2 (TREM2) increase risk Alzheimer's disease (AD) and other neurodegenerative disorders. Signaling by TREM2, an innate immune microglia, is thought to enhance phagocytosis amyloid beta (Aβ) damaged proteins, promote microglial proliferation, migration, survival, regulate inflammatory signaling. Thus, TREM2 activation has potential alter progression AD. AL002 investigational, engineered, humanized monoclonal immunoglobulin G1 (IgG1) antibody designed target TREM2. In AD mouse models, murine variant been previously shown induce proliferation reduce filamentous Aβ plaques neurite dystrophy.

Language: Английский

Citations

11
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

7
Spatiotemporal Dysregulation of Neuron–Glia Related Genes and Pro-/Anti-Inflammatory miRNAs in the 5xFAD Mouse Model of Alzheimer’s Disease DOI Open Access
M. Di Ianni, Miriam Corraliza-Gómez, Tiago Costa-Coelho

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(17), P. 9475 - 9475

Published: Aug. 31, 2024

Alzheimer's disease (AD), the leading cause of dementia, is a multifactorial influenced by aging, genetics, and environmental factors. miRNAs are crucial regulators gene expression play significant roles in AD onset progression. This exploratory study analyzed levels 28 genes 5 (miR-124-3p, miR-125b-5p, miR-21-5p, miR-146a-5p, miR-155-5p) related to pathology neuroimmune responses using RT-qPCR. Analyses were conducted prefrontal cortex (PFC) hippocampus (HPC)

Language: Английский

Citations

4
Sex-specific transcriptomic profiling reveals key players in bone loss associated with Alzheimer’s disease DOI

Mohini Gharpure,

Sagar Vyavahare,

Diana M. Asante

et al.

GeroScience, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 29, 2025

Language: Английский

Citations

0
Osteopontin in Alzheimer's Disease: A Double‐Edged Sword in Neurodegeneration and Neuroprotection—A Systematic Review DOI Creative Commons
Zahra Azizan, Maryam Bazrgar, Narges Bazgir

et al.

CNS Neuroscience & Therapeutics, Journal Year: 2025, Volume and Issue: 31(2)

Published: Feb. 1, 2025

ABSTRACT Background Osteopontin (OPN) has emerged as a pivotal molecule in Alzheimer's disease (AD), with studies indicating its potential to act both neuroprotective agent and contributor neurodegeneration. This systematic review aims elucidate the roles of OPN AD pathogenesis through inflammatory pathways. Methods We conducted comprehensive analysis current literature on OPN's involvement AD, focusing signaling pathways, cellular interactions, regulatory mechanisms. searched PubMed, EMBASE, Scopus databases by keyword Disease Osteopontin. Our date search was 1990 until July 1, 2024 no language limitation. Results In 758 studies, total 15 reports met eligibility criteria were included. Among findings, four provided evidence supporting protective mechanism within context AD. Eleven explain role OPN. been shown play synaptic pruning, microglial activation, processes associated Additionally, is implicated facilitating communication serves chemotactic molecule. It suggested that effects are predominantly mediated c fragment protein most prominent early stages progression. Conclusion dual effects—protecting neurons contributing their degeneration. Future research should enhance mechanisms, target specific develop therapies slow

Language: Английский

Citations

0
Special issue on “A focus on brain–body communication in understanding the neurobiology of diseases” DOI Creative Commons
Kenji Hashimoto, Wei Yan, Chun Yang

et al.

Neurobiology of Disease, Journal Year: 2024, Volume and Issue: unknown, P. 106666 - 106666

Published: Sept. 1, 2024

Language: Английский

Citations

2
Introduction to Alzheimer's Disease, Biomarkers, and the AI Revolution DOI
Bancha Yingngam

Advances in medical technologies and clinical practice book series, Journal Year: 2024, Volume and Issue: unknown, P. 1 - 23

Published: June 28, 2024

Alzheimer's disease (AD) is a progressive neurodegenerative that results in steady decline cognitive ability and memory function. As society ages, the need for an optimum AD management strategy becomes more important. This chapter analyzes stage-construction etiology escalating symptoms of discovered throughout this review, as well identification barrier to precise diagnosis. The artificial intelligence achieve quicker detection through machine learning, data analytics, predictive modeling also being considered. Therefore, employing AI AD-related studies novel approach enhancing patient outcomes. Proper diagnosis parallel increased probability many parameters one most difficult moments identify. However, use evaluation sensor network technologies big analysis has advanced, preventive instruments can be used. Thus, technology gives humanity hope stop or, at very least, slow down tragedy.

Language: Английский

Citations

1
Gut microbiome and bone health: update on mechanisms, clinical correlations, and possible treatment strategies DOI
Andrea Ticinesi, Carmine Siniscalchi, Tiziana Meschi

et al.

Osteoporosis International, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 7, 2024

Language: Английский

Citations

1
FUBP3 mediates the amyloid-β-induced neuronal NLRP3 expression DOI Creative Commons
Jing Yao, Yuan Li,

Xi Liu

et al.

Neural Regeneration Research, Journal Year: 2024, Volume and Issue: 20(7), P. 2068 - 2083

Published: May 10, 2024

JOURNAL/nrgr/04.03/01300535-202507000-00028/figure1/v/2024-09-09T124005Z/r/image-tiff Alzheimer’s disease is characterized by deposition of amyloid-β, which forms extracellular neuritic plaques, and accumulation hyperphosphorylated tau, aggregates to form intraneuronal neurofibrillary tangles, in the brain. The NLRP3 inflammasome may play a role transition from amyloid-β tau phosphorylation aggregation. Because primarily found brain microglia, predominantly located neurons, it has been suggested that expressed microglia indirectly triggers upregulating expression pro-inflammatory cytokines. Here, we neurons also express vitro vivo , neuronal regulates phosphorylation. Using biochemical methods, mapped minimal promoter identified FUBP3 as transcription factor regulating neurons. In primary neuroblastoma cell line Neuro2A, required for endogenous only when present. brains aged wild-type mice mouse model disease, was markedly increased cortical Transcriptome analysis plays neuron-mediated immune responses. We trimmed 5′ end DNA fragments bound, implying functions stress-induced These findings suggest be more directly involved amyloid-β-to–phospho-tau than microglial NLRP3, fundamentally alters regulatory mechanism Given at low levels young strongly upregulated mice, could safe therapeutic target preventing progression.

Language: Английский

Citations

0
Macrophage Polarization and Its Impact on Osteoporosis DOI

Junwei Yan,

Chenyu Huang, Dongdong Jiang

et al.

Results and problems in cell differentiation, Journal Year: 2024, Volume and Issue: unknown, P. 291 - 296

Published: Jan. 1, 2024

Language: Английский

Citations

0