Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Download bibliography of all 730 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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The fibrillar peptide amyloid-beta (A beta) has a chief function in the pathogenesis of Alzheimer's disease.
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The aim of this study is to clarify the relationship of microglia to phosphorylated tau accumulation and the characteristics of microglial activation in brain lesions of human tauopathies in comparison to mutant tau transgenic (TG) mice.
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Elimination of interstitial fluid and solutes plays a role in homeostasis in the brain, but the pathways are unclear.
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The blood-brain barrier (BBB) is a highly specialized brain endothelial structure of the fully differentiated neurovascular system.
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Basic and clinical research accomplished during the last few years on embryonic, fetal, amniotic, umbilical cord blood, and adult stem cells has constituted a revolution in regenerative medicine and cancer therapies by providing the possibility of generating multiple therapeutically useful cell types.
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The results of the present study confirm in vivo anti-inflammatory actions of CBD, emphasizing the importance of this compound as a novel promising pharmacological tool capable of attenuating Abeta evoked neuroinflammatory responses.
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Susac's syndrome (SS) consists of the clinical triad of encephalopathy, branch retinal artery occlusions (BRAO) and hearing loss.
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36/100
Photoreceptor apoptosis is a major cause of visual loss in retinal detachment (RD) and several other visual disorders, but the underlying mechanisms remain elusive.
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Microglial activation similar to that which occurs in peripheral macrophages during inflammatory attack was first demonstrated in the Alzheimer's disease (AD) brain two decades ago.
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The discovery of the COX isoforms led to establishing their importance in many non-arthritic or non-pain states where there is an inflammatory component to pathogenesis, including cancer, Alzheimer's and other neurodegenerative diseases.
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The term neurodegenerative disease refers to the principal pathology associated with disorders such as amyotrophic lateral sclerosis, Alzheimer's disease, Huntington's disease and Parkinson's disease, and it is presumed that neurodegeneration results in the clinical findings seen in patients with these diseases.
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The molecular mechanism underlying the pathogenesis of the majority of cases of sporadic Alzheimer's disease (AD) is unknown.
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Central nervous system (CNS) immune privilege is an experimentally defined phenomenon.
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Deciphering what governs inflammation and its effects on tissues is vital for understanding many pathologies.
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36/100
The blood-brain barrier (BBB) is the specialized system of brain microvascular endothelial cells (BMVEC) that shields the brain from toxic substances in the blood, supplies brain tissues with nutrients, and filters harmful compounds from the brain back to the bloodstream.
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Here we review evidence of roles for NF-kappaB in the regulation of developmental and synaptic plasticity, and cell survival in physiological and pathological settings.
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Brain perfusion is tightly coupled to neuronal activity, is commonly used to monitor normal or pathological brain function, and is a direct reflection of the interactions that occur between neuronal signals and blood vessels.
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36/100
The brain is critically dependent on a continuous supply of blood to function.
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For many years, the central nervous system (CNS) was considered to be 'immune privileged', neither susceptible to nor contributing to inflammation.
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In Alzheimer's disease (AD) there is increasing evidence that neurotoxicity is mediated by CNS inflammatory processes.
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Inflammation is a critical component of the pathogenesis of Alzheimer's disease (AD).
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Extracellular adenosine 5'-triphosphate (ATP) has been recognized as a ubiquitous, unstable signalling molecule, acting as a fast neurotransmitter and modulator of transmitter release and neuronal excitability.
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A time-dependent release of endogenous free DHA followed by NPD1 formation occurs, suggesting that a phospholipase A2 releases the mediator's precursor.
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In contrast to traditional neuroncentric views of Alzheimer's disease (AD), recent findings indicate that neurovascular dysfunction contributes to cognitive decline and neurodegeneration in AD.
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Although abundant reactive microglia are found associated with beta-amyloid (Abeta) plaques in Alzheimer's disease (AD) brains, their contribution to cell loss remains speculative.
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.
- Cross-Dataset Reanalysis of Mouse Alzheimer Disease Single-Cell RNA-Sequencing Data Reveals a Reproducible Innate Immune Activation Signature
- The NLRP3 inflammasome in pathogenic particle and fibre-associated lung inflammation and diseases
- High frame rate in vivo two-photon microscopy to quantify murine cerebrospinal fluid flow heterogeneity
- Chronic colitis exacerbates NLRP3-dependent neuroinflammation and cognitive impairment in middle-aged brain
- Excitotoxicity, synaptic repair, and functional recovery in the mammalian cochlea: a review of recent findings
- Microglia emerge as central players in brain disease
- Inflammasome activation in neurodegenerative diseases
- Focused ultrasound-mediated APOE4 knockdown in mouse brain
- Negative regulation of TREM2-mediated C9orf72 poly-GA clearance by the NLRP3 inflammasome
- Chronic inflammation - inflammaging - in the ageing cochlea: A novel target for future presbycusis therapy