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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Tissue macrophages play important roles in maintaining homeostasis in most organs of the body including the brain where microglia represent the resident phagocytic cells of this compartment.
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The mitogen-activated protein kinases (MAPKs) in mammals include c-Jun NH2-terminal kinase (JNK), p38 MAPK, and extracellular signal-regulated kinase (ERK).
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Alzheimer's disease (AD) is a neurodegenerative disorder, marked by senile plaques composed of amyloid-β (Aβ) peptide, neurofibrillary tangles, neuronal loss and neuroinflammation.
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Whole brain irradiation remains important in the management of brain tumors.
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Neuroinflammation and the accompanying activation of glial cells is an important feature of many neurodegenerative conditions.
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Comparison of inflammatory markers between mice infected with scrapie strains 22L and RML indicated that the inflammatory responses and gene expression profiles in the brains were strikingly similar, even though these scrapie strains infect different brain regions.
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Astrocyte reactivity is a hallmark of neurodegenerative diseases (ND), but its effects on disease outcomes remain highly debated.
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Intriguingly, the process is dependent on the presence of B cells and significantly contributes to the development of AAA and the occurrence of aortic rupture.
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LSKL peptide administration was associated with greater aortic elastin fragmentation and lower expression and activity of the TGF-β1-target gene lysyl oxidase like 1 ( LOXL1 ).
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The detection of nucleic acids by the innate immune system is an essential host response during viral infection.
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One of the most striking hallmarks shared by various neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease (AD), and amyotrophic lateral sclerosis, is microglia-mediated neuroinflammation.
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Physiologically, the retinal pigment epithelium (RPE) expresses immunosuppressive signals such as FAS ligand (FASL), which prevents the accumulation of leukocytes in the subretinal space.
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Infection of microglia with the HIV-1 SF162 macrophage-tropic strain resulted in increased Beclin1 expression, accompanied by an increase of LC3 protein levels and accumulation of LC3 reporter RFP + GFP + (yellow) puncta, suggesting that HIV-1 infection triggers autophagosome formation without promoting protein degradation by the lysosome.
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Aging is the predominant risk factor for neurodegenerative diseases.
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Atherosclerotic phenotypes were significantly accelerated in RGS 5 −/− ApoE −/− mice, as indicated by increased inflammatory mediator expression and apoptosis of endothelial cells and macrophages.
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There has been a growing need for in vitro models of neurodegenerative diseases such as Alzheimer's disease that would enable a better understanding of etiology and faster development of treatment strategies.
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Atherosclerosis is essentially a vascular inflammatory process in the presence of an excess amount of lipid.
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Abnormal NFκB activation has been implicated in Alzheimer's disease (AD).
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Epidemiological studies have shown a clear association between maternal infection and schizophrenia or autism in the progeny.
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Astrocyte activation and reactive gliosis accompany most of the pathologies in the brain, spinal cord, and retina.
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Loss of neurons after brain injury and in neurodegenerative disease is often accompanied by reactive gliosis and scarring, which are difficult to reverse with existing treatment approaches.
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In Alzheimer's disease (AD), amyloid plaques are surrounded by reactive astrocytes with an increased expression of intermediate filaments including glial fibrillary acidic protein (GFAP).
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The choroid plexus epithelium is a cuboidal cell monolayer, which produces the majority of the cerebrospinal fluid.
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Inflammatory processes play both regenerative and destructive roles in multiple sclerosis, stroke, CNS trauma, amyotrophic lateral sclerosis and aging-related neurodegenerative diseases such as Alzheimer's, Parkinson's and Huntington's. Endogenous defence mechanisms against these pathologies include those that are directly neuroprotective, and those that modulate the expression of inflammatory mediators in microglia, astrocytes, and invading inflammatory cells.
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Microglia in the central nervous system are usually maintained in a quiescent state.
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.
- Patients With Ankylosing Spondylitis Have Increased Cardiovascular and Cerebrovascular Mortality: A Population-Based Study
- Spatial Transcriptomics and In Situ Sequencing to Study Alzheimer's Disease
- Reducing Neutrophil Sialic Acid Residues Alleviates Cerebral Hypoperfusion in Alzheimer’s Models
- TREM2 Overexpression Attenuates Cognitive Deficits in Experimental Models of Vascular Dementia
- Blood-brain barrier permeability and physical exercise
- The Vagal Autonomic Pathway of COVID-19 at the Crossroad of Alzheimer's Disease and Aging: A Review of Knowledge
- Alzheimer disease and neuroinflammation
- [Inflammatory cerebral amyloid angiopathy]
- Alzheimer risk-increasing TREM2 variant causes aberrant cortical synapse density and promotes network hyperexcitability in mouse models
- The Alzheimer's disease risk genes MS4A4A and MS4A6A cooperate to negatively regulate TREM2 and microglia states