ReviewInflammopharmacology2023
The orchestrating role of deteriorating neurons and TREM-1 in crosstalk with SYK in Alzheimer's disease progression and neuroinflammation.
Review in Inflammopharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- The lung-brain axis in neurodegeneration: inflammatory, immune, and vascular mechanisms with therapeutic implications.Inflammopharmacology · 2026Review
- Infralimbic Cortex Microglial TREM-1 Mediates Neuroinflammation and Exacerbates Depressive-Like Behaviors in Parkinson's Disease Model Mice.Inflammation · 2025Article
- Signs of Alzheimer's Disease: Tied to Aging.International journal of molecular sciences · 2025Review
- Pilot Screening of TREM1 Inhibitors in Cell-Based Reporter Assays Reflecting TREM1/DAP12 Receptor Assembly and Functionality.ACS chemical neuroscience · 2025Article
- TREM-1 as a potential gatekeeper of neuroinflammatory responses: therapeutic validation and mechanistic insights in experimental traumatic brain injury.Frontiers in immunology · 2025Article
- Development of a novel diagnostic model for Alzheimer's disease based on glymphatic system and metabolism-related genes.Frontiers in molecular biosciences · 2025Article
- The deficient CLEC5A ameliorates the behavioral and pathological deficits via the microglial Aβ clearance in Alzheimer's disease mouse model.Journal of neuroinflammation · 2024Article
- Impact of Lyophilized Milk Kefir-Based Self-Nanoemulsifying System on Cognitive Enhancement via the Microbiota-Gut-Brain Axis.Antioxidants (Basel, Switzerland) · 2024Article
- Analysis of macrophage polarization and regulation characteristics in ovarian tissues of polycystic ovary syndrome.Frontiers in medicine · 2024Article
- The orchestrating role of deteriorating neurons and TREM-1 in crosstalk with SYK in Alzheimer's disease progression and neuroinflammation.Inflammopharmacology · 2023Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a progressive type of neurodegenerative disease characterized by successive loss of the conventional structure and functions of neurons. In addition to dead neurons type detected within AD brain tissues, there are a predominantly varying number of deteriorating neurons (DTNs). As the number of deteriorating neurons increases, they exaggerate the release of inflammatory factors and oxidative stress that trigger the cascade of neuroinflammation. Triggering receptor expressed on myeloid cells 1 (TREM-1) which is a transmembrane immune receptor type regularly expressed by phagocytic cells, may act as a stimulating factor for neuroinflammation. Once TREM-1 is activated, it directly activates spleen tyrosine kinase (SYK) downstream signaling cascades, which can be considered an initiating phase for AD pathology and AD progression. Sequentially, SYK activates the pro-inflammatory microglia M1 phenotype which executes several inflammatory actions, leading to neurotoxicity. These released neurotoxins promote neuronal cell death, synaptic dysfunctions, and memory impairments. Thus, the current review outlines the direct etiological and pathologic features of Alzheimer's disease linked with deteriorating neurons, TREM-1, and SYK.
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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 OpenQuestion graph.