SynthesisBMC neurology2025
Glutamatergic and GABAergic metabolite levels in Alzheimer's disease: a systematic review and meta-analysis.
Synthesis in BMC neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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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Who cites it
5 citing papers in PubMed.
- Association of serum biomarkers for lipid and amino acid metabolism with cognition in adolescents.Pediatric research · 2026Article
- The interactions of copper, glutamate, and cuproptosis: insights into brain health and Alzheimer's disease pathology.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- Astrocytes at the crossroads of obstructive sleep apnea and Alzheimer's disease: from oxygen sensing to neurodegeneration.Sleep & breathing = Schlaf & Atmung · 2026Review
- AI-enabled multimodal neuroimaging for neurotransmitter mapping in normal aging and age-related disease.Frontiers in aging neuroscience · 2026Review
- Sleep and stress as modifiable drivers of Alzheimer's disease.NPJ dementia · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesThis systematic review and meta-analysis compares glutamate, glutamine, and GABA levels in cerebrospinal fluid (CSF), blood, and brain tissue between individuals with Alzheimer's disease (AD) and cognitively unimpaired (CU) controls.
methodsWe systematically searched PubMed and Web of Science up to February 20, 2025, for studies reporting GABA, glutamate, or glutamine levels in AD and CU controls. Effect sizes were calculated using Hedges' g, with heterogeneity assessed via I² statistics and publication bias evaluated using funnel plots and Egger's and Begg's tests.
resultsFrom 14,857 records, 53 studies were included. Glutamate levels were significantly lower in AD brains, including the cortex (SMD = - 0.42; 95% CI [-0.79, - 0.05]; I² = 67.26%; p = 0.03), hippocampus (SMD = - 0.56; 95% CI [-0.91, - 0.20]; I² = 37.29%; p < 0.05), and temporal cortex (SMD = - 0.87; 95% CI [-1.52, - 0.23]; I² = 77.60%; p = 0.01), but not in CSF or blood. Glutamine showed no significant differences in brain regions, CSF, or blood. GABA levels were significantly lower in AD patients across the cortex (SMD = - 0.53; 95% CI [-0.81, - 0.25]; I² = 58.60%; p < 0.05), CSF (SMD = - 0.38; 95% CI [-0.65, - 0.11]; I² = 0.00%; p = 0.01), and blood (SMD = - 0.72; 95% CI [-1.08, - 0.37]; I² = 43.18%; p < 0.05).
conclusionOur findings underscore the potential of targeting glutamatergic and GABAergic systems in AD clinical research. We recommend prioritizing future investigations in earlier disease stages, such as preclinical AD and mild cognitive impairment.
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