ArticleAlzheimer's research & therapy2025
Cerebrospinal fluid NPTX2 and [
Article in Alzheimer's research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Article
- Correspondence of Basal Forebrain Resting-State Functional Connectivity and Cerebral Glucose Metabolism Alterations With Neurotransmitter Maps in Alzheimer's Disease.CNS neuroscience & therapeutics · 2026Article
- Metabolic Dysfunction in Alzheimer's Disease: Brain Glucose Hypometabolism as an Early Precursor to Amyloid and Tau Pathology.Journal of clinical medicine · 2026Review
Corrections and comments
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Authors and funding
26 authors.
Funding
Abstract
backgroundIn Alzheimer’s disease (AD) the progressive accumulation of misfolded proteins, notably amyloid-β and hyperphosphorylated tau, initiates a cascade of metabolic and synaptic dysfunction, and ultimately neurodegeneration. These early molecular alterations interact with diffuse neurotrasmitter projection systems, contributing to cognitive and behavioural manifestations.
methodsThis study assessed baseline [18F]FDG-PET metabolism and its relationship with neurotransmitter receptor/transporter maps and cerebrospinal fluid (CSF) markers of AD neuropathology (Aβ42/Aβ40, pTau181, t-Tau), neuroaxonal (NFL), and synaptic damage (NPTX2, neurogranin) in 49 Mild Cognitive Impairment (MCI)-AD patients. Relative hypometabolism was derived by comparing [¹⁸F]FDG-PET scans of patients and 40 healthy controls. Spatial correlation coefficients between hypometabolism maps and normative cortical maps of neurotransmitter receptor/transporter density were computed and included in linear models with CSF biomarkers, adjusting for demographic and cognitive variables.
resultsPatients exhibited significant hypometabolism in bilateral temporo-parietal regions. Negative correlations emerged between hypometabolism and receptor distributions for 5-HT1A (r = − 0.36, p < 0.001), D1 (r = − 0.15, p = 0.03), and mGluR5 (r = − 0.14, p = 0.02), which indicates that reduced glucose uptake in MCI-AD was mostly found in areas with normally high receptor densities. Noteworthy, CSF NPTX2 levels correlated with the co-localization of hypometabolism and 5-HT1A receptor distribution (β = 0.003, p = 0.038) with no significant associations for other CSF markers.
conclusionsAccording to our findings, correlations between reduced glucose metabolism and specific neurotransmitter receptor densities suggest early involvement and vulnerability of these systems in MCI-AD. Moreover, the association between CSF NPTX2 and 5-HT1A receptor vulnerability indicates that synaptic dysfunction in AD may parallel serotonergic involvement, and supports CSF NPTX2 as a potential biomarker for disease staging.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.