Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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Monoclonal antibodies (mAbs) have made significant progress in the treatment of Alzheimer's disease (AD).
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The ApoE-ε4 gene is a well-established genetic risk factor for neurodegenerative diseases, such as Alzheimer's disease and multiple sclerosis, which are characterized by axonal demyelination in the central nervous system.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, memory impairment, and neuroinflammation, with no definitive cure currently available.
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Alzheimer's disease (AD) is a predominant form of dementia in elderly.
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TREM2, a microglia-specific receptor, is strongly associated with Alzheimer's disease (AD) risk, mediating microglial responses to amyloid pathology critical to AD development.
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Neuroinflammation plays an important role in the pathogenesis of various central nervous system (CNS) diseases.
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43/100
Microglia impact brain development, homeostasis, and pathology.
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Ischemic stroke and vascular cognitive impairment, caused by a sudden arterial occlusion or more subtle but protracted vascular insufficiency, respectively, are leading causes of morbidity and mortality worldwide with limited therapeutic options.
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Cerebral small vessel disease (SVD) is a vascular disorder that increases the risk of stroke and dementia and is diagnosed through brain MRI.
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Chronic neuroinflammation is a principal cause of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease.
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43/100
Autophagy plays a pivotal role in the pathogenesis and progression of Alzheimer's disease (AD).
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The major genetic risk factor for Alzheimer's disease (AD), APOE4, accelerates beta-amyloid (Aβ) plaque formation, but whether this is caused by APOE expressed in microglia or astrocytes is debated.
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Parkinson's disease (PD) is a prevalent neurodegenerative disorder, and recent evidence suggests that pathogenesis may be in part mediated by inflammatory processes, the molecular and cellular architectures of which are largely unknown.
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Neurovascular unit (NVU) inflammation via activation of glial cells and neuronal damage plays a critical role in neurodegenerative diseases.
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Isogenic BMEC-like cells with different APOE genotypes had similar trans-endothelial electrical resistance, tight junction integrity and efflux transporter gene expression.
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The 64Cu-labeled antibodies were obtained in high radiochemical purity (RCP), radiochemical yield (RCY), and specific activity.
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In the central nervous system, triggering receptor expressed on myeloid cells 2 (TREM2) is exclusively expressed by microglia and is critical for microglial proliferation, migration, and phagocytosis.
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Apolipoprotein E4 (ApoE4) plays an important role responding to monomeric C-reactive protein (mCRP) via binding to CD31 leading to cerebrovascular damage and Alzheimer's disease (AD).
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The pathological role of interferon signaling is emerging in neuroinflammatory disorders, yet, the specific role of Interferon Regulatory Factor 3 (IRF3) in neuroinflammation remains poorly understood.
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There is an urgent need for effective disease-modifying therapeutic interventions for Alzheimer's disease (AD)-the most prevalent cause of dementia with a profound socioeconomic burden.
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Alzheimer's disease (AD) is a neurodegenerative disease with a projected significant increase in incidence.
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Cerebral small vessel disease (CSVD) is a group of pathologies that affect the cerebral blood vessels.
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As shown previously, there was a robust association between Lin bodies and GFAP-positive astrocyte processes.
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43/100
Microglia, as resident macrophages in the central nervous system, play a multifunctional role in the pathogenesis of Alzheimer's disease (AD).
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Reactive oxygen species (ROS) are metabolic by-products that constitute an indispensable component of physiological processes, albeit their heightened presence may proffer substantial perils to biological entities.