Feasibility of observing rTMS on improving cognitive function of mild cognitive impairment based on resting state functional magnetic resonance imaging

2019 ◽  
Vol 1 (10) ◽  
pp. 821-831
Author(s):  
Fan Xiwang ◽  
Liu Li ◽  
Jiang Hui ◽  
Chen Yanhua ◽  
Wang Ling
Keyword(s):  
Magnetic Resonance Imaging ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cognitive Function ◽  
Magnetic Resonance ◽  
Functional Magnetic Resonance Imaging ◽  
Resting State ◽  
Functional Magnetic Resonance ◽  
Resonance Imaging

scholarly journals Functional magnetic resonance imaging changes in amnestic and nonamnestic mild cognitive impairment during encoding and recognition tasks

2009 ◽  
Vol 15 (3) ◽  
pp. 372-382 ◽  
Author(s):  
MARY M. MACHULDA ◽  
MATTHEW L. SENJEM ◽  
STEPHEN D. WEIGAND ◽  
GLENN E. SMITH ◽  
ROBERT J. IVNIK ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Magnetic Resonance ◽  
Functional Magnetic Resonance Imaging ◽  
Temporal Cortex ◽  
Functional Magnetic Resonance ◽  
Resonance Imaging ◽  
Complex Scene ◽  
Amnestic Mci

AbstractFunctional magnetic resonance imaging (fMRI) shows changes in multiple regions in amnestic mild cognitive impairment (aMCI). The concept of MCI recently evolved to include nonamnestic syndromes, so little is known about fMRI changes in these individuals. This study investigated activation during visual complex scene encoding and recognition in 29 cognitively normal (CN) elderly, 19 individuals with aMCI, and 12 individuals with nonamnestic MCI (naMCI). During encoding, CN activated an extensive network that included bilateral occipital–parietal–temporal cortex; precuneus; posterior cingulate; thalamus; insula; and medial, anterior, and lateral frontal regions. Amnestic MCI activated an anatomic subset of these regions. Non-amnestic MCI activated an even smaller anatomic subset. During recognition, CN activated the same regions observed during encoding except the precuneus. Both MCI groups again activated a subset of the regions activated by CN. During encoding, CN had greater activation than aMCI and naMCI in bilateral temporoparietal and frontal regions. During recognition, CN had greater activation than aMCI in predominantly temporoparietal regions bilaterally, while CN had greater activation than naMCI in larger areas involving bilateral temporoparietal and frontal regions. The diminished parietal and frontal activation in naMCI may reflect compromised ability to perform nonmemory (i.e., attention/executive, visuospatial function) components of the task. (JINS, 2009, 15, 372–382.)

scholarly journals Abnormal Functional Connectivity of the Amygdala in Mild Cognitive Impairment Patients With Depression Symptoms Revealed by Resting-State fMRI

2021 ◽  
Vol 12 ◽  
Author(s):  
Ting Yang ◽  
Bangli Shen ◽  
Aiqin Wu ◽  
Xinglu Tang ◽  
Wei Chen ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Cognitive Impairment ◽  
Prefrontal Cortex ◽  
Mild Cognitive Impairment ◽  
Magnetic Resonance ◽  
Functional Connectivity ◽  
Resting State ◽  
Depression Symptoms ◽  
Functional Magnetic Resonance ◽  
Resonance Imaging

Convergent evidence indicates that individuals with symptoms of depression exhibit altered functional connectivity (FC) of the amygdala, which is a key brain region in processing emotions. At present, the characteristics of amygdala functional circuits in patients with mild cognitive impairment (MCI) with and without depression are not clear. The current study examined the features of amygdala FC in patients with MCI with depression symptoms (D-MCI) using resting-state functional magnetic resonance imaging. We acquired resting-state functional magnetic resonance imaging data from 16 patients with D-MCI, 18 patients with MCI with no depression (nD-MCI), and 20 healthy controls (HCs) using a 3T scanner and compared the strength of amygdala FC between the three groups. Patients with D-MCI exhibited significant FC differences in the amygdala–medial prefrontal cortex and amygdala–sensorimotor networks. These results suggest that the dysfunction of the amygdala–medial prefrontal cortex network and the amygdala–sensorimotor network might be involved in the neural mechanism underlying depression in MCI.

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