scholarly journals Altered Patterns of Amplitude of Low-Frequency Fluctuations and Fractional Amplitude of Low-Frequency Fluctuations Between Amnestic and Vascular Mild Cognitive Impairment: An ALE-Based Comparative Meta-Analysis

2021 ◽  
Vol 13 ◽  
Author(s):  
Xulian Zhang ◽  
Chen Xue ◽  
Xuan Cao ◽  
Qianqian Yuan ◽  
Wenzhang Qi ◽  
...  

Background: Changes in the amplitude of low-frequency fluctuations (ALFF) and the fractional amplitude of low-frequency fluctuations (fALFF) have provided stronger evidence for the pathophysiology of cognitive impairment. Whether the altered patterns of ALFF and fALFF differ in amnestic cognitive impairment (aMCI) and vascular mild cognitive impairment (vMCI) is largely unknown. The purpose of this study was to explore the ALFF/fALFF changes in the two diseases and to further explore whether they contribute to the diagnosis and differentiation of these diseases.Methods: We searched PubMed, Ovid, and Web of Science databases for articles on studies using the ALFF/fALFF method in patients with aMCI and vMCI. Based on the activation likelihood estimation (ALE) method, connectivity modeling based on coordinate meta-analysis and functional meta-analysis was carried out.Results: Compared with healthy controls (HCs), patients with aMCI showed increased ALFF/fALFF in the bilateral parahippocampal gyrus/hippocampus (PHG/HG), right amygdala, right cerebellum anterior lobe (CAL), left middle temporal gyrus (MTG), left cerebrum temporal lobe sub-gyral, left inferior temporal gyrus (ITG), and left cerebrum limbic lobe uncus. Meanwhile, decreased ALFF/fALFF values were also revealed in the bilateral precuneus (PCUN), bilateral cuneus (CUN), and bilateral posterior cingulate (PC) in patients with aMCI. Compared with HCs, patients with vMCI predominantly showed decreased ALFF/fALFF in the bilateral CUN, left PCUN, left PC, and right cingulate gyrus (CG).Conclusions: The present findings suggest that ALFF and fALFF displayed remarkable altered patterns between aMCI and vMCI when compared with HCs. Thus, the findings of this study may serve as a reliable tool for distinguishing aMCI from vMCI, which may help understand the pathophysiological mechanisms of these diseases.

2021 ◽  
Vol 13 ◽  
Author(s):  
Qianqian Yuan ◽  
Wenzhang Qi ◽  
Chen Xue ◽  
Honglin Ge ◽  
Guanjie Hu ◽  
...  

Background: Mild cognitive impairment (MCI) represents a transitional state between normal aging and dementia disorders, especially Alzheimer's disease (AD). The disruption of the default mode network (DMN) is often considered to be a potential biomarker for the progression from MCI to AD. The purpose of this study was to assess MRI-specific changes of DMN in MCI patients by elucidating the convergence of brain regions with abnormal DMN function.Methods: We systematically searched PubMed, Ovid, and Web of science for relevant articles. We identified neuroimaging studies by using amplitude of low frequency fluctuation /fractional amplitude of low frequency fluctuation (ALFF/fALFF), regional homogeneity (ReHo), and functional connectivity (FC) in MCI patients. Based on the activation likelihood estimation (ALE) algorithm, we carried out connectivity modeling of coordination-based meta-analysis and functional meta-analysis.Results: In total, this meta-analysis includes 39 articles on functional neuroimaging studies. Using computer software analysis, we discovered that DMN changes in patients with MCI mainly occur in bilateral inferior frontal lobe, right medial frontal lobe, left inferior parietal lobe, bilateral precuneus, bilateral temporal lobe, and parahippocampal gyrus (PHG).Conclusions: Herein, we confirmed the presence of DMN-specific damage in MCI, which is helpful in revealing pathology of MCI and further explore mechanisms of conversion from MCI to AD. Therefore, we provide a new specific target and direction for delaying conversion from MCI to AD.


2019 ◽  
Vol 1 (1) ◽  
Author(s):  
Rimona S Weil ◽  
Joey K Hsu ◽  
Ryan R Darby ◽  
Louis Soussand ◽  
Michael D Fox

Abstract Dementia is a common and devastating symptom of Parkinson’s disease but the anatomical substrate remains unclear. Some evidence points towards hippocampal involvement but neuroimaging abnormalities have been reported throughout the brain and are largely inconsistent across studies. Here, we test whether these disparate neuroimaging findings for Parkinson’s disease dementia localize to a common brain network. We used a literature search to identify studies reporting neuroimaging correlates of Parkinson’s dementia (11 studies, 385 patients). We restricted our search to studies of brain atrophy and hypometabolism that compared Parkinson’s patients with dementia to those without cognitive involvement. We used a standard coordinate-based activation likelihood estimation meta-analysis to assess for consistency in the neuroimaging findings. We then used a new approach, coordinate-based network mapping, to test whether neuroimaging findings localized to a common brain network. This approach uses resting-state functional connectivity from a large cohort of normative subjects (n = 1000) to identify the network of regions connected to a reported neuroimaging coordinate. Activation likelihood estimation meta-analysis failed to identify any brain regions consistently associated with Parkinson’s dementia, showing major heterogeneity across studies. In contrast, coordinate-based network mapping found that these heterogeneous neuroimaging findings localized to a specific brain network centred on the hippocampus. Next, we tested whether this network showed symptom specificity and stage specificity by performing two further analyses. We tested symptom specificity by examining studies of Parkinson’s hallucinations (9 studies, 402 patients) that are frequently co-morbid with Parkinson’s dementia. We tested for stage specificity by using studies of mild cognitive impairment in Parkinson’s disease (15 studies, 844 patients). Coordinate-based network mapping revealed that correlates of visual hallucinations fell within a network centred on bilateral lateral geniculate nucleus and correlates of mild cognitive impairment in Parkinson’s disease fell within a network centred on posterior default mode network. In both cases, the identified networks were distinct from the hippocampal network of Parkinson’s dementia. Our results link heterogeneous neuroimaging findings in Parkinson’s dementia to a common network centred on the hippocampus. This finding was symptom and stage-specific, with implications for understanding Parkinson’s dementia and heterogeneity of neuroimaging findings in general.


2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Zhilian Zhao ◽  
Jie Lu ◽  
Xiuqin Jia ◽  
Wang Chao ◽  
Ying Han ◽  
...  

Mild cognitive impairment (MCI) refers to a transitional state between normal aging and dementia and is a syndrome with cognitive decline greater than expected for an individual’s age and educational level. As a subtype of MCI, amnestic mild cognitive impairment (aMCI) most often leads to Alzheimer’s disease. This study aims to elucidate the altered brain activation in patients with aMCI using resting-state functional magnetic resonance. We observed Frequency-dependent changes in the amplitude of low-frequency fluctuations in aMCI patients (n=20), and normal subjects (n=18). At the same time, we took gray matter volume as a covariate. We found that aMCI patients had decreased amplitude of low-frequency fluctuation signal in left superior temporal gyrus, right middle temporal gyrus, right inferior parietal lobe, and right postcentral gyrus compared to the control group. Specially, aMCI patients showed increased signal in left superior and middle frontal gyrus. Our results suggested that increased activation in frontal lobe of aMCI patients may indicate effective recruitment of compensatory brain resources. This finding and interpretation may lead to the better understanding of cognitive changes of aMCI.


2021 ◽  
Vol 13 ◽  
Author(s):  
Yu Song ◽  
Wenwen Xu ◽  
Shanshan Chen ◽  
Guanjie Hu ◽  
Honglin Ge ◽  
...  

Background Mild cognitive impairment (MCI) is an intermediate stage between normal aging and dementia. Amnestic MCI (aMCI) and non-amnestic MCI are the two subtypes of MCI with the former having a higher risk for progressing to Alzheimer's disease (AD). Compared with healthy elderly adults, individuals with MCI have specific functional alterations in the salience network (SN). However, no consistent results are documenting these changes. This meta-analysis aimed to investigate the specific functional alterations in the SN in MCI and aMCI.Methods: We systematically searched PubMed, Embase, and Web of Science for scientific neuroimaging literature based on three research methods, namely, functional connectivity (FC), regional homogeneity (ReHo), and the amplitude of low-frequency fluctuation or fractional amplitude of low-frequency fluctuation (ALFF/fALFF). Then, we conducted the coordinate-based meta-analysis by using the activation likelihood estimation algorithm.Results: In total, 30 functional neuroimaging studies were included. After extracting the data and analyzing it, we obtained specific changes in some brain regions in the SN including decreased ALFF/fALFF in the left superior temporal gyrus, the insula, the precentral gyrus, and the precuneus in MCI and aMCI; increased FC in the thalamus, the caudate, the superior temporal gyrus, the insula, and the cingulate gyrus in MCI; and decreased ReHo in the anterior cingulate gyrus in aMCI. In addition, as to FC, interactions of the SN with other networks including the default mode network and the executive control network were also observed mainly in the middle frontal gyrus and superior frontal gyrus in MCI and inferior frontal gyrus in aMCI.Conclusions: Specific functional alternations in the SN and interactions of the SN with other networks in MCI could be useful as potential imaging biomarkers for MCI or aMCI. Meanwhile, it provided a new insight in predicting the progression of health to MCI or aMCI and novel targets for proper intervention to delay the progression.Systematic Review Registration: [PROSPERO], identifier [No. CRD42020216259].


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