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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Among the changes that typify Alzheimer's disease (AD) are neuroinflammation and microglial activation, amyloid deposition perhaps resulting from compromised microglial function and iron accumulation.
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The blood-brain barrier (BBB) prevents neurotoxic plasma components, blood cells, and pathogens from entering the brain.
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Epigenetic influence of brain and neuronal function plays key regulatory roles in health and diseases.
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Microglial activation is a distinguished attribute in many neurodegenerative diseases of aging.
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S100B is a Ca 2+ -binding protein mainly concentrated in astrocytes.
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Strong evidence implicates the complement pathway as an important contributor to amyloid pathology in Alzheimer's disease (AD); however, the role of complement in tau modulation remains unclear.
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The nature of fluid dynamics within the brain parenchyma is a focus of intensive research.
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Neurodegenerative diseases, the leading cause of morbidity and disability, are gaining increased attention as they impose a considerable socioeconomic impact, due in part to the ageing community.
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We here provide the first evidence that the TNFα-miR-501-3p-ZO-1 axis plays an important role in the pathogenesis of cerebral hypoperfusion-induced working memory deficits and white matter lesions, as a result of blood-brain barrier breakdown via tight junction disruption.
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38/100
Neuronal cell death occurs extensively during development and pathology, where it is especially important because of the limited capacity of adult neurons to proliferate or be replaced.
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Microglia are emerging as key players in neurodegenerative diseases, such as Alzheimer's disease (AD).
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Individual reports suggest that the central nervous system (CNS) contains multiple immune cell types with diverse roles in tissue homeostasis, immune defense, and neurological diseases.
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Microglia, the CNS-resident immune cells, play important roles in disease, but the spectrum of their possible activation states is not well understood.
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Cerebral blood flow (CBF) regulation is essential for normal brain function.
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The complement cascade not only is an innate immune response that enables removal of pathogens but also plays an important role in microglia-mediated synaptic refinement during brain development.
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Here, we studied whether multiple sclerosis (MS) could be a complement to the CNS disorders that are associated with the GLP-1/GLP-1R signaling axis.
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Microglia play critical roles in brain development, homeostasis, and neurological disorders.
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Mounting evidence suggests neuroinflammation is a key process in glaucoma, yet the precise roles are not known.
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Activation of the inflammasome is implicated in the pathogenesis of an increasing number of inflammatory diseases, including Alzheimer's disease (AD).
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We show that the glymphatic fluid transporting system contributes to the delivery of choroid plexus/CSF-derived human apoE to neurons.
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Utilizing β-amyloid precursor protein (βAPP) as a substrate, α-, β-, and γ-secretases are responsible for sequential cleavage events leading to the formation of β-amyloid, the classic pathologic hallmark of Alzheimer’s Disease.
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The blood-brain barrier (BBB) plays a key role in maintaining the specialized microenvironment of the central nervous system (CNS), and enabling communication with the systemic compartment.
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mRNA for inflammasome components (NLRP1, NLRP3, PYCARD, caspase 1, 5 and 8) and downstream effectors (IL-1β, IL-18) was up-regulated in severe and MILD AD.
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We show that inhibition of γ-secretase-dependent cleavage of the TREM2 C-terminal fragment in cellular membranes interferes with TREM2-dependent signaling and cellular function.
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Although cerebral small vessel disease has been linked to stroke and dementia, due to limitations of current neuroimaging technology, direct in vivo visualization of changes in the cerebral small vessels (e.g., cerebral arteriolar narrowing, tortuous microvessels, blood-brain barrier damage, capillary microaneurysms) is difficult to achieve.
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.
- Glial fibrillary acidic protein-apolipoprotein E (apoE) transgenic mice: astrocyte-specific expression and differing biological effects of astrocyte-secreted apoE3 and apoE4 lipoproteins
- Janus-faced microglia: beneficial and detrimental consequences of microglial phagocytosis
- Microglial NF-κB drives tau spreading and toxicity in a mouse model of tauopathy
- Inflammatory proteins associated with Alzheimer's disease reduced by a GLP1 receptor agonist: a post hoc analysis of the EXSCEL randomized placebo controlled trial
- A meta-analysis of cytokines in Alzheimer's disease
- Dll4 signalling through Notch1 regulates formation of tip cells during angiogenesis
- Activation of microglial cells by beta-amyloid protein and interferon-gamma
- A transcriptomic atlas of aged human microglia
- Ocular manifestations of central insulin resistance
- Human Monocyte Subsets and Phenotypes in Major Chronic Inflammatory Diseases