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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Ageing is a major risk factor for many neurological pathologies, but its mechanisms remain unclear.
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Innate immune memory is a vital mechanism of myeloid cell plasticity that occurs in response to environmental stimuli and alters subsequent immune responses.
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Genome-wide association studies have identified a number of risk variants for Alzheimer’s disease implicated in inflammatory responses (Bettens et al., 2013); exome sequencing has revealed polymorphisms in the microglial receptor TREM2 gene as a rare but significant risk for Alzheimer’s disease (Guerreiro et al., 2013; Jonsson et al., 2013); and recently, the CD33 risk allele has been shown to inhibit microglial clearance of amyloid-β (Bradshaw et al., 2013; Griciuc et al., 2013).
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There have been 87 cases of superficial siderosis of the CNS reported in the world literature and 63 cases had developed the clinical syndrome with sufficient details to be reviewed.
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In order to define the histopathological substrate of the dementia that frequently complicates the acquired immune deficiency syndrome (AIDS), we analyzed the neuropathological findings in 70 autopsied adult AIDS patients, 46 of whom had suffered clinically overt dementia.
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Alzheimer's disease (AD) is widely recognized as a multifactorial disorder involving neurovascular and glial dysfunction beyond amyloid-β and tau pathology.
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ACAT1 inhibition increased LRP1 levels and soluble TREM2 (sTREM2) release via enhanced TREM2 cleavage by ADAM metallopeptidase domain 10/17 (ADAM10/17).
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Protective PLCG2P522R microglia showed significant transcriptomic similarity to isogenic controls.
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The amyloid/tau/neurodegeneration (ATN) biomarker framework has greatly progressed the diagnosis and staging of Alzheimer's disease (AD).
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Ms4a4a deficiency reduced steady-state Aβ levels and shortened its half-life in brain interstitial fluid.
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Diabetic retinopathy (DR) and Alzheimer's disease (AD) are progressive neurodegenerative disorders affecting the eye and the brain, respectively.
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Genome-wide association studies have identified many gene polymorphisms associated with an increased risk of developing late-onset Alzheimer's disease (LOAD).
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In 5xFAD mice, the absence of PLCG2 resulted in reduced TREM2 expression and impaired microglial associations with amyloid beta plaques.
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Frontotemporal dementia and amyotrophic lateral sclerosis are neurodegenerative diseases with considerable clinical, genetic and pathological overlap.
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We report CSF soluble TREM2 (sTREM2) and CSF chitinase-3-like protein 1 (CHI3L1/YKL-40) as PD biomarkers for the TREM2 agonist hPara.09.
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46/100
High levels of proinflammatory cytokines induce neurotoxicity and catalyze inflammation-driven neurodegeneration, but the specific release mechanisms from microglia remain elusive.
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Cerebral amyloid angiopathy-related inflammation (CAA-RI) is an encephalopathy caused by inflammation of β-amyloid peptide deposition in cerebrovascular vessels.
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CSF levels of apoE2, apoE3, and apoE4 were significantly higher (all nominal P < 10 × 10-5 , false discovery rate < 0.001) and those of tumor necrosis factor-α (TNF-α) were significantly lower (nominal P = 1.39 × 10-6 , false discovery rate < 0.001) in APOE-ε4 carriers than in noncarriers.
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We address translation bottlenecks-including blood-brain barrier (BBB) shuttles, human trial scarcity and soluble TREM2 (sTREM2) biomarker harmonisation-outlining a biomarker-guided, context-tailored precision therapeutic framework for targeting the TREM2 axis.
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Cerebrovascular disease is a major but poorly understood feature of Alzheimer's disease (AD).
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Lysosomal dysfunction in myeloid cells is increasingly implicated in neurodegenerative diseases.
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Alzheimer's disease (AD) and related Tauopathies are neurodegenerative disorders characterized by the accumulation of hyperphosphorylated Tau protein in neurofibrillary tangles and frequently accompanied by amyloid-β (Aβ) pathology.1 While Tau aggregation has long been considered a primary driver of neurodegeneration, growing evidence highlights neuroinflammation as a central and early contributor to disease onset and progression.
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The brain endothelial Gαq/11 signalling pathway preserves normal vascular reactivity, and its loss resembles mild endothelial dysfunction in the brain.
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The prevailing view frames microglia and macrophages as guardians against amyloid beta (Aβ) accumulation in Alzheimer's disease (AD).
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Mild traumatic brain injury (mTBI) from a closed-head injury (CHI) can lead to prevalent neuropsychiatric disorders, including mood disorders and an increased risk for neurodegenerative diseases and dementia.
From across this topic
9 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 9. The same 9 appear here every time.
- Aducanumab anti-amyloid immunotherapy induces sustained microglial and immune alterations
- Transcriptional signature in microglia associated with Aβ plaque phagocytosis
- The dual role of astrocyte activation and reactive gliosis
- A Therapeutic Strategy for Alzheimer's Disease Focused on Immune-inflammatory Modulation
- Single cell RNA sequencing of human microglia uncovers a subset associated with Alzheimer's disease
- Neuroprotectin D1-mediated anti-inflammatory and survival signaling in stroke, retinal degenerations, and Alzheimer's disease
- As48, a first-in-class dual-function TREM2 modulator: Receptor activation and shedding inhibition
- Inhibiting the NLRP3 inflammasome with MCC950 promotes non-phlogistic clearance of amyloid-β and cognitive function in APP/PS1 mice
- APOE4 impairs autophagy and Aβ clearance by microglial cells