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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Our comprehensive atlas revealed pronounced heterogeneity among microglial states, with disease-associated microglia (DAM) significantly enriched in AD brains compared to controls.
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We demonstrate that the small-molecule TREM2 ligand SULF A functions as an immunomodulator that reprograms microglia toward a reparative phenotype.
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Neuroinflammation driven by microglial activation is a hallmark of Alzheimer's disease (AD).
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43/100
Triggering receptor expressed on myeloid cells 2 (TREM2) dysfunction contributes to Alzheimer's disease pathogenesis, yet current therapeutics cannot prevent ADAM-mediated receptor shedding that diminishes signaling efficacy.
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43/100
Neuroinflammation plays a vital role in determining the trajectory of Alzheimer's disease (AD) progression.
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43/100
The cerebellum, essential for motor coordination and increasingly recognized for its role in cognition, is typically considered more resilient to aging and largely spared from hallmark Alzheimer's disease (AD) pathology.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is an innate immune receptor abundantly expressed in microglia in the brain.
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Evidence indicates that chronic proteotoxic stress, arising from aging, oxidative damage, and environmental influences, disrupts the proteostasis network (PN).
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Apolipoprotein E (APOE) is the major lipid transport protein in the brain.
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Variants in the triggering receptor expressed on myeloid cells 2 (TREM2) gene have been demonstrated to increase the risk of late-onset Alzheimer's disease (AD) and Nasu-Hakola disease.
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The blood-brain barrier (BBB) is a critical structure for maintaining homeostasis in the central nervous system, and its dysfunction is widely implicated in the pathogenesis and progression of various neurological disorders.
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In the MWM, syringin reduced escape latency.
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Inflammation is a key factor in neurodegenerative diseases (NDs) development, such as Alzheimer's disease (AD) and Parkinson's disease (PD).
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Chronic neuroinflammation and impaired protein clearance are hallmarks of neurodegenerative diseases such as Alzheimer's disease (AD) and HIV-associated neurocognitive disorders (HAND).
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Microglia play a significant role in the development and progression of Alzheimer's disease (AD).
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Neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS), represent significant global health challenges, affecting millions and straining healthcare systems.
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We identified a significant upregulation of COX-1 in 5 × FAD mice, with expression specifically localized to microglia in an age-dependent manner.
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Cerebral small vessel disease (cSVD) is the most common cause of vascular cognitive impairment and dementia (VCID) and highly associated with Alzheimer's disease pathogenesis.
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Temporal lobe epilepsy (TLE) is the most common and drug-resistant type of epilepsy with an unknown mechanism.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by β-amyloid (βA) accumulation, neuroinflammation, excessive synaptic pruning, and cognitive decline.
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Our results demonstrate CA effectively inhibits NLRP3 inflammasome activation, reduces microglial pyroptosis, and mitigates oxidative stress-induced mitochondrial impairment in BV-2 cells.
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Alzheimer's disease (AD) is a typical neurodegenerative disease, with the most highlighted pathologic changes identified in the β-amyloid peptide (Aβ) and neurofibrillary tangles (NFTs).
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43/100
Alzheimer's disease (AD) and age-related macular degeneration (AMD) represent the leading causes of dementia and vision impairment in the elderly, respectively.
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Neurodegenerative diseases, including Alzheimer's and Parkinson's disease, affect an increasing number of people in aging societies, dramatically reducing the quality of life of those affected.
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Growing genetic and pathological evidence has identified microglial dysfunction as a key contributor to the pathogenesis and progression of various neurological disorders, positioning microglia replacement as a promising therapeutic strategy.
From across this topic
10 of the 730 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Stavudine Reduces NLRP3 Inflammasome Activation and Modulates Amyloid-β Autophagy
- Amyloid-β (Aβ) immunotherapy induced microhemorrhages are associated with activated perivascular macrophages and peripheral monocyte recruitment in Alzheimer's disease mice
- Neurovascular Inflammaging in Health and Disease
- Interleukin 1 in the brain: biology, pathology and therapeutic target
- A pericyte-to-myofibroblast transition links APOE4 to cerebrovascular degeneration
- An NF-kappaB-sensitive micro RNA-146a-mediated inflammatory circuit in Alzheimer disease and in stressed human brain cells
- A shared disease-associated oligodendrocyte signature among multiple CNS pathologies
- Induction of monocyte chemoattractant protein-1 in HIV-1 Tat-stimulated astrocytes and elevation in AIDS dementia
- Microglia-derived ASC specks cross-seed amyloid-β in Alzheimer's disease
- Innate Immune Cell Death in Neuroinflammation and Alzheimer's Disease