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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Transcription factors provide the link between early membrane-proximal signalling events and changes in gene expression.
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A significant fraction of the beta-amyloid precursor protein is proteolytically processed to yield large secreted forms (sAPP).
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Phospholipase A2 (PLA2) is the key enzyme that initiates the arachidonic acid cascade, which leads to the generation of multiple eicosanoid products.
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Interleukin-1 beta (IL-1 beta), interleukin-2 (IL-2), and interleukin-6 (IL-6) were measured in the cerebrospinal fluid (CSF) and plasma of 12 control subjects, 11 sporadic Alzheimer's disease (AD) and 22 de novo Parkinson's disease (PD) patients using high sensitivity enzyme-linked immunosorbent assays (ELISA).
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36/100
One of the most remarkable characteristics of astrocytes is their vigorous response to diverse neurologic insults, a feature that is well conserved across a variety of different species.
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36/100
The origin of ramified microglia has been a longstanding controversial issue, with 4 major schools of thought, which state that they are derived (1) from invasion of mesodermal pial elements, (2) from neuroectodermal matrix cells together with the macroglia, (3) from pericytes, and (4) from invasion of monocytes in early development.
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Recent studies indicated that the formation of a major constituent of Alzheimer's disease (AD) senile plaques, called beta A4-peptide, does not result from normal processing of its precursor, amyloid precursor protein (APP).
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Frozen brain specimens from eight multiple sclerosis (MS) patients were examined for the presence of leukocytes and their cell products by using a panel of monoclonal antibodies.
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SAR228810 is a humanized monoclonal antibody (mAb) binding specifically to soluble protofibrillar and fibrillar forms of Aβ peptide.
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Microglial activation and FR expression in APP/PS1 and P301S transgenic mouse models of AD was measured using flow cytometry.
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16/100
Approximately 90% of Parkinson's disease (PD) patients exhibit olfactory deficits, which often precedes motor symptoms by years, and are a robust predictor for PD and subsequent cognitive decline.
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The Triggering Receptors Expressed on Myeloid cells (TREMs) are a family of cell-surface receptors instrumental in the activation of different myeloid cells.
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Neuronal activity must be tightly controlled to maintain brain function.
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16/100
Microglial activation and subsequent neuroinflammation involves THIK-1 (KCNK13), a Two-Pore Domain (K2P) K+ channel.
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These findings identify microglia as the immune population most strongly remodeled by Ms4a4a loss in the setting of amyloid pathology.
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16/100
Single-nucleus RNA-seq (snRNA-seq) studies of Alzheimer’s disease (AD) routinely filter nuclei by mitochondrial percentage (%MT) or remove mitochondrial genes, yet whether these reads carry information about cognition is rarely examined.
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This method establishes a platform for high-throughput longitudinal drug screening in immunocompetent human COs that will enable the identification of new therapeutic candidates to modulate Aβ aggregation, glial reactivity, and neurodegeneration.
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Vascular pathology is an important contributor to dementia, and astrocyte dysfunction is increasingly recognized as a key mediator of cerebrovascular injury.
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16/100
Alzheimer’s disease (AD) is characterized by progressive memory decline, with the medial entorhinal cortex (MEC) representing an early vulnerable hub for spatial cognition.
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Alzheimer’s disease (AD) staging based on amyloid-β, tau, and neurodegeneration does not capture heterogeneous microglial functions.
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Endolysosomal dysfunction is a central feature of many neurodegenerative disorders.
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We define an astrocyte–microglia axis in which astrocytic sEH limits EET availability and thereby sustains microglial STING signaling.
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Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β (Aβ) accumulation, pathological tau aggregation, and neuronal loss.
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Truncated tau is increasingly recognized as a pivotal pathogenic event in Alzheimer’s disease (AD).
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These findings identify conserved regulatory networks that may contribute to female-biased microglial responses to AD pathology across mice and humans.
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.
- Apolipoprotein E-specific innate immune response in astrocytes from targeted replacement mice
- Pericytes in Alzheimer's Disease: Novel Clues to Cerebral Amyloid Angiopathy Pathogenesis
- Boosting angiotensin-converting enzyme (ACE) in microglia protects against Alzheimer's disease in 5xFAD mice
- ScFv-h3D6 Prevents Bapineuzumab-Induced Hemorrhagic Events in the APP23 Mouse Model of Alzheimer’s Disease
- Therapeutic Inhibition of the Complement System in Diseases of the Central Nervous System
- APOE from astrocytes restores Alzheimer's Aβ-pathology and DAM-like responses in APOE deficient microglia
- Locus Coeruleus Modulates Neuroinflammation in Parkinsonism and Dementia
- Impaired microglial phagocytosis promotes seizure development
- Activation of Glucagon-Like Peptide-1 Receptor Promotes Neuroprotection in Experimental Autoimmune Encephalomyelitis by Reducing Neuroinflammatory Responses
- Apelin-13 Suppresses Neuroinflammation Against Cognitive Deficit in a Streptozotocin-Induced Rat Model of Alzheimer's Disease Through Activation of BDNF-TrkB Signaling Pathway