Evidence map›Paper›PMID 35988117›Full record

ArticleAging clinical and experimental research2022

Cerebrospinal fluid growth-associated protein 43 levels in patients with progressive and stable mild cognitive impairment.

Yuanyuan Lu, Alzheimer’s Disease Neuroimaging Initiative

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Article in Aging clinical and experimental research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.5field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Sex-specific brain reserve and progression from mild cognitive impairment to Alzheimer's disease dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  3. Hippocampal volume moderates the association between cerebrospinal fluid growth-associated protein 43 and episodic memory performance in older adults.Neuropsychology, development, and cognition. Section B, Aging, neuropsychology and cognition · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Yuanyuan LuDepartment of Neurology and Innovation Center for Neurological Disorders, Xuanwu Hospital, Capital Medical University, 45 Changchun Street, Beijing, 100053, China. luyuanyuanpku@163.com.
Alzheimer’s Disease Neuroimaging Initiative
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCerebrospinal fluid (CSF) growth-associated protein 43 (GAP-43) is prominently elevated in Alzheimer's disease (AD) dementia patients in comparison to normal controls. CSF GAP-43 levels in mild cognitive impairment (MCI) individuals who have different clinical trajectories need to be studied.

methodsWe examined 137 cognitively normal (CN) controls, 218 stable MCI patients (sMCI), 99 progressive MCI (pMCI) patients, and 120 AD dementia patients. Associations between the CSF GAP-43 levels and the four diagnosis groups were evaluated with multiple-variable linear regression. The relationships between CSF GAP-43 and core CSF biomarkers were assessed by Spearman correlations. Cox regression analysis was performed to assess the values of GAP-43 in predicting MCI conversion. We examined associations between baseline CSF GAP-43 levels and longitudinal cognitive function, hippocampal volumes, and brain glucose metabolism using linear mixed-effects models.

resultsCSF GAP-43 was elevated in the pMCI and AD groups in comparison to the CN group and in the pMCI and AD groups in comparison to the sMCI group. CSF GAP-43 significantly predicted conversion from MCI to AD. CSF GAP-43 was a significant predictor of cognitive decline, hippocampal atrophy, and brain hypometabolism over time. Furthermore, elevated CSF GAP-43 levels were associated with accelerated deterioration in cognition and neurodegeneration.

conclusionsCSF GAP-43 is increased in the predementia stage of AD, and it may enhance the neurodegenerative process. Future efforts on pharmacological interventions targeting synaptic dysfunction could be promising in AD treatment.

Indexed as

Alzheimer DiseaseCognitive DysfunctionGAP-43 ProteinAmyloid beta-PeptidesBiomarkersBrainDisease ProgressionHumansNeuropsychological TestsPeptide Fragmentstau ProteinsAmyloid beta-PeptidesBiomarkersGAP-43 ProteinPeptide Fragmentstau ProteinsAlzheimer’s diseaseBiomarkerCerebrospinal fluidGrowth-associated protein 43Mild cognitive impairment

Identifiers

PMID35988117
OpenAlexW4292503992

What OpenQuestion holds

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Registered trials

None linked

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 OpenQuestion graph.