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Mediation of episodic memory performance by the executive function network in patients with amnestic mild cognitive
Baoyu Yuan1, Jiu Chen1, Liang Gong1
1Department of Neurology, ZhongDa Hospital, Neuropsychiatric Institute, Medical School of Southeast University, Nanjing, PR China.
Abstract:
Deficits in episodic memory (EM) are a hallmark clinical symptom of patients with amnestic mild cognitive impairment (aMCI). Impairments in executive function (EF) are widely considered to exacerbate memory deficits and to increase the risk of conversion from aMCI to Alzheimer's disease (AD). However, the specific mechanisms underlying the interaction between executive dysfunction and memory deficits in aMCI patients remain unclear. Thus, the present study utilized resting-state functional magnetic resonance imaging (fMRI) scans of the EF network and the EM network to investigate this relationship in 79 aMCI patients and 119 healthy controls (HC). The seeds were obtained from the results of a regional homogeneity (ReHo) analysis. Functional connectivity (FC) within the EM network was determined using a seed in the right retrosplenial cortex (RSC), and FC within EF network was assessed using seeds in the right dorsolateral prefrontal cortex (DLPFC). There was a significant negative correlation between EM scores and EF scores in both the aMCI and HC groups. Compared to the HC group, aMCI patients had reduced right RSC connectivity but enhanced right DLPFC connectivity. The overlapping brain regions between the EM and EF networks were associated with FC in the right inferior parietal lobule (IPL) in the right RSC network, and in the bilateral middle cingulate cortex (MCC) and left IPL in the right DLPFC network. A mediation analysis revealed that the EF network had an indirect positive effect on EM performance in the aMCI patients. The present findings provide new insights into the neural mechanisms underlying the interaction between impaired EF and memory deficits in aMCI patients and suggest that the EF network may mediate EM performance in this population.
Insights
Executive function networks may mediate episodic memory performance in individuals with amnestic mild cognitive impairment (aMCI). This study found that while aMCI patients showed altered functional connectivity in both executive function and episodic memory networks, the executive function network indirectly benefited memory performance.
Area of Science:
- Neuroscience
- Cognitive Neurology
- Medical Imaging
Background:
- Episodic memory (EM) deficits are key in amnestic mild cognitive impairment (aMCI).
- Executive function (EF) impairments are thought to worsen memory loss and predict progression to Alzheimer's disease (AD).
- The precise neural mechanisms linking executive dysfunction and memory deficits in aMCI are not fully understood.
Purpose of the Study:
- To investigate the relationship between executive function (EF) and episodic memory (EM) networks in aMCI patients.
- To explore the neural mechanisms underlying the interaction between EF and EM deficits.
Main Methods:
- Resting-state functional magnetic resonance imaging (fMRI) was used to analyze functional connectivity (FC) in EF and EM networks.
- Participants included 79 aMCI patients and 119 healthy controls (HC).
- Seed regions for EM and EF networks were identified using regional homogeneity (ReHo) analysis, specifically the right retrosplenial cortex (RSC) for EM and right dorsolateral prefrontal cortex (DLPFC) for EF.
Main Results:
- A negative correlation between EM and EF scores was observed in both aMCI and HC groups.
- aMCI patients exhibited reduced right RSC connectivity (EM network) but enhanced right DLPFC connectivity (EF network) compared to HC.
- Mediation analysis indicated that the EF network had an indirect positive effect on EM performance in aMCI patients.
Conclusions:
- The findings offer novel insights into the neural underpinnings of the EF-EM interaction in aMCI.
- The executive function network appears to play a mediating role in episodic memory performance in individuals with aMCI.
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