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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Cerebrospinal fluid (CSF) flows through perivascular spaces (PVSs) surrounding brain vasculature, and impaired flow has been linked to neurodegenerative diseases such as Alzheimer’s. However, the mechanisms driving CSF flow and its oscillatory dynamics remain poorly understood.
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Anti-amyloid-β (Aβ) immunotherapy improves cognitive outcomes in Alzheimer’s disease (AD) but is associated with amyloid-related imaging abnormalities (ARIA), through poorly understood mechanisms.
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These findings identify TTR as a contributor of adaptive neurovascular homeostasis during gut-derived neuroinflammation.
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16/100
Among 9,386 propensity score-matched pairs of ND patients and controls, covariates were well balanced.
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MS4A4A was higher in M2 (IL-4) than in M1 (IFN-γ + LPS) macrophages in all three donors (log2 fold change +2.68, adjusted P = 0.0013).
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Alzheimer’s disease disrupts large-scale brain networks before cognitive symptoms emerge, yet the mechanisms underlying this progression remain unclear.
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Rhabdomyolysis is a common syndrome involving the breakdown of muscle tissue.
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These results suggest that the cognitive-enhancing effects of Sob-AM2 are not the result of reduced overall plaque burden.
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Dementia with Lewy bodies (DLB) is characterized by marked biological heterogeneity, only partly explained by the frequent presence of Alzheimer’s disease (AD) copathology.
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Traumatic brain injuries (TBIs) are associated with increased risk of neurodegenerative disease, including Alzheimer’s disease (AD); however, the mechanisms by which TBI promotes AD pathogenesis remain poorly understood.
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The Alzheimer’s disease (AD) brain is characterized by dysregulated expression of multiple microRNAs (miRNA), positioning them as promising diagnostic and therapeutic targets.
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16/100
Immunoproteasome induction is prominent in Alzheimer’s disease (AD), but whether it protects proteostasis or amplifies neuroinflammation remains unresolved.
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16/100
Alzheimer's disease (AD) disproportionately affects women, who exhibit greater vulnerability to Tau pathology and neuroinflammation.
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IKZF1 is prioritised as a candidate late-disease microglial TF, supported by six convergent evidence dimensions including independent bulk replication.
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We validated results in CSF from 397 participants in the Accelerated Medicine Partnership-Alzheimer’s Disease cohort.
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Protein misfolding and aggregation, including amyloid fibril formation, underlie a large class of human diseases including prominent neurological disorders such as Alzheimer’s and Parkinson’s disease.
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Long non-coding RNAs (lncRNAs) are increasingly recognized as regulators of brain cell function, but their roles in astrocyte biology and neurodegeneration remain poorly understood.
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Anti-amyloid antibodies represent the first disease modifying therapeutics for Alzheimers disease (AD).
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Anti-Aβ immunotherapies for Alzheimer’s Disease (AD) have high rates of amyloid-related imaging abnormalities (ARIA), an adverse side effect with markedly higher rates in APOE4 carriers.
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An age-related decline in vasodilation mediated by neurovascular nitric oxide (NO) and vasoconstriction driven by the Piezo1 receptor precede the aggregation of soluble brain proteins such as amyloid-β (Aβ), which then causes further disruption of brain solute homeostasis, ultimately leading to neurodegeneration in Alzheimer’s disease.
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Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have shown promise in preclinical models of neurodegeneration, with emerging evidence suggesting these effects may be driven by modulation of neuroinflammation.
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16/100
Trem2*R47H mice had alternative splicing leading to reduced Trem2 expression; Trem2*R47HHSS mice expressed Trem2 at wild-type transcript and protein levels.
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The choroid plexus (CP) regulates barrier integrity, cerebrospinal-fluid (CSF) dynamics, and immune surveillance, yet its role in Alzheimer's disease (AD) remains poorly defined.
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The occurrence of amyloid-related imaging abnormalities (ARIA), found in clinical trials for Aβ-immunotherapy, has been related to the antibody’s effector function on glial activation by the Fc portion of the antibody.
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16/100
Cerebral small vessel disease (CSVD) is strongly linked to metabolic risk factors and represents a major cause of vascular cognitive impairment 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.
- The Meningeal Lymphatic System: A New Player in Neurophysiology
- Involvement of P2 receptors in the growth and survival of neurons in the CNS
- A map of transcriptional heterogeneity and regulatory variation in human microglia
- Amyloid-β activates NLRP3 inflammasomes by affecting microglial immunometabolism through the Syk-AMPK pathway
- Superficial siderosis of the central nervous system
- TREM2/PLCγ2 signalling in immune cells: function, structural insight, and potential therapeutic modulation
- A reporter cell system for the triggering receptor expressed on myeloid cells 2 reveals differential effects of disease-associated variants on receptor signaling and activation by antibodies against the stalk region
- Amyloid Beta Oligomers Activate Death Receptors and Mitochondria-Mediated Apoptotic Pathways in Cerebral Vascular Smooth Muscle Cells; Protective Effects of Carbonic Anhydrase Inhibitors
- NFκB-activated astroglial release of complement C3 compromises neuronal morphology and function associated with Alzheimer's disease