Postmortem Brain, Cerebrospinal Fluid, and Blood Neurotrophic Factor Levels in Alzheimer's Disease: A Systematic Review and Meta-Analysis.
Level 3 - non-randomized controlled study
Systematic review and meta-analysis of observational case-control studies
PubMed 29956088 · doi:10.1007/s12031-018-1100-8
What was done
The authors conducted a systematic review and random-effects meta-analysis searching PubMed and Web of Science for studies comparing blood, cerebrospinal fluid (CSF), and post-mortem brain neurotrophic factor levels (BDNF, NGF, IGF, VEGF) between patients with Alzheimer's disease (AD) and controls. A total of 98 articles encompassing over 9,000 samples were included, with quantitative meta-analyses performed on blood and CSF biomarkers alongside a qualitative review of 23 post-mortem brain studies.
What was found
The abstract reports directional findings without specific numerical effect sizes, confidence intervals, or p-values: - Peripheral blood: BDNF levels were significantly decreased in AD patients compared with controls. Blood NGF, IGF, and VEGF showed no significant differences between groups. - CSF: BDNF levels were significantly decreased and NGF levels were significantly increased in AD patients relative to controls. CSF IGF and VEGF showed no significant differences. - Post-mortem brain: Across 23 studies, findings were not fully consistent, but the majority reported decreased BDNF and increased (pro)NGF in the hippocampus and neocortex of AD patients.
Why it matters
This meta-analysis clarifies conflicting clinical literature by demonstrating a distinct neurotrophic profile in AD characterized specifically by BDNF depletion across central and peripheral compartments and central (pro)NGF elevation, helping prioritize BDNF and NGF over IGF and VEGF for biomarker and therapeutic development.
Limits
The abstract provides no exact quantitative metrics (standardized mean differences, p-values, or 95% confidence intervals) or measures of between-study heterogeneity. Post-mortem brain findings were derived from inconsistent qualitative reports rather than quantitative pooling, and the observational case-control design cannot determine whether neurotrophic alterations are causative or secondary to neurodegeneration.
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