Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) positively regulates lipopolysaccharide-induced expression of CXC chemokine ligand 10 and 11 in mouse macrophages

Bandow, Kenjiro; Smith, Avi; Garlick, Jonathan A.

doi:10.1016/j.bbrc.2022.10.048

Cited by 2 publications

(2 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Dysregulation of TREM2 function due to genetic variations may contribute to the development and progression of AD, making it a potential target for therapeutic intervention. However, further research is needed to fully understand the mechanisms underlying TREM2-mediated neurodegeneration in Alzheimer's disease [154,155].…”

Section: In Uence On Biochemical Pathways and Cellular Processesmentioning

confidence: 99%

Alzheimer's Disease Investigated via Gene-Environment Interactions, Biochemical Pathways, Cellular Processes, and Disease Phenotype Variability

Shafi,

Siddiqui

2024

Preprint

View full text Add to dashboard Cite

Background: Alzheimer's disease (AD) is a neurodegenerative disorder influenced by genetic and environmental factors. APOE, APP, PSEN1, PSEN2, CLU, SORL1, BIN1, CR1, PICALM, TREM2, ABCA7, and CD33 play key roles in AD pathogenesis, affecting biochemical pathways and cellular processes. However, the interaction between genetic predisposition and environmental factors, as well as the reasons for variability in disease phenotype, remain poorly understood. This study aims to investigate these interactions to improve our understanding of AD etiology and inform personalized interventions. Methods: A comprehensive search encompassing databases such as PubMed, MEDLINE, Google Scholar, and open access/subscription-based journals was conducted to retrieve relevant articles for the investigation of genes involved in Alzheimer's disease (AD) pathogenesis, including APOE, APP, PSEN1, PSEN2, CLU, SORL1, BIN1, CR1, PICALM, TREM2, ABCA7, and CD33. Articles were searched without any date restrictions. Utilizing the criteria delineated in the methodology section, studies were systematically reviewed to elucidate how environmental factors and genetics influence Alzheimer's disease onset, progression, symptom severity, and progression rates. This study adheres to relevant PRISMA guidelines (Preferred Reporting Items for Systematic Reviews and Meta-Analyses). Results: Our investigation revealed the complicated interactions between genetic predisposition, environmental factors, biochemical pathways, and cellular processes in Alzheimer's disease (AD) pathogenesis. APOE, APP, PSEN1, PSEN2, CLU, SORL1, BIN1, CR1, PICALM, TREM2, ABCA7, and CD33 influence amyloid-beta production, tau pathology, lipid metabolism, and inflammation in AD. These genes interact with environmental factors such as diet, pollutants, head trauma, and lifestyle, modulating disease risk and progression. Additionally, we found variability in disease phenotype among individuals carrying similar genetic mutations, influenced by genetic modifiers, environmental factors, cognitive reserve, and neurobiological differences. Conclusion: Alzheimer's disease (AD) is a multifactorial disorder influenced by genetic and environmental factors. APOE, APP, PSEN1, PSEN2, CLU, SORL1, BIN1, CR1, PICALM, TREM2, ABCA7, and CD33 play critical roles in AD pathogenesis by affecting amyloid-beta production, tau pathology, lipid metabolism, and inflammation. These genes interact with environmental factors such as diet, pollutants, head trauma, and lifestyle, further modulating disease risk and progression. Understanding these complicated interactions is essential for developing personalized interventions to delay onset, reduce severity, and slow AD progression.

show abstract

Section: In Uence On Biochemical Pathways and Cellular Processesmentioning

confidence: 99%

Alzheimer's Disease Investigated via Gene-Environment Interactions, Biochemical Pathways, Cellular Processes, and Disease Phenotype Variability

Shafi,

Siddiqui

2024

Preprint

View full text Add to dashboard Cite

show abstract

“…The release of sTREM2 from its membrane-bound precursor is influenced by various stimuli, including LPS, interleukin-1β (IL-1β), oligomeric Aβ, Vascular Endothelial Growth Factor (VEGF), viral infections like HIV, and cytokines such as IL-13 and IL-4, which promote sTREM2 secretion ( Wu et al, 2015 ; Gisslén et al, 2019 ; Zhong et al, 2019 ; Vilalta et al, 2021 ). Notably, LPS stimulation has been shown to decrease TREM2 surface expression and increase sTREM2 release in RAW264.7 cells, highlighting its role in TREM2 shedding and sTREM2 generation ( Bandow et al, 2022 ). Additionally, BRI2 modulates sTREM2 functionality by inhibiting α-secretase-mediated cleavage of TREM2, affecting microglial phagocytic capabilities under pathological conditions ( Yin T. et al, 2024 ).…”

Section: Regulatory Mechanisms Of Strem2 Shedding and Metabolic Degra...mentioning

confidence: 99%

Decoding sTREM2: its impact on Alzheimer’s disease – a comprehensive review of mechanisms and implications

Lin,

Kong,

Chen

et al. 2024

Front. Aging Neurosci.

View full text Add to dashboard Cite

Soluble Triggering Receptor Expressed on Myeloid Cells 2 (sTREM2) plays a crucial role in the pathogenesis of Alzheimer’s disease (AD). This review comprehensively examines sTREM2’s involvement in AD, focusing on its regulatory functions in microglial responses, neuroinflammation, and interactions with key pathological processes. We discuss the dynamic changes in sTREM2 levels in cerebrospinal fluid and plasma throughout AD progression, highlighting its potential as a therapeutic target. Furthermore, we explore the impact of genetic variants on sTREM2 expression and its interplay with other AD risk genes. The evidence presented in this review suggests that modulating sTREM2 activity could influence AD trajectory, making it a promising avenue for future research and drug development. By providing a holistic understanding of sTREM2’s multifaceted role in AD, this review aims to guide future studies and inspire novel therapeutic strategies.

show abstract

Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) positively regulates lipopolysaccharide-induced expression of CXC chemokine ligand 10 and 11 in mouse macrophages

Cited by 2 publications

References 44 publications

Alzheimer's Disease Investigated via Gene-Environment Interactions, Biochemical Pathways, Cellular Processes, and Disease Phenotype Variability

Alzheimer's Disease Investigated via Gene-Environment Interactions, Biochemical Pathways, Cellular Processes, and Disease Phenotype Variability

Decoding sTREM2: its impact on Alzheimer’s disease – a comprehensive review of mechanisms and implications

Contact Info

Product

Resources

About