Comparing regional brain atrophy in mild cognitive impairment and Alzheimer’s disease

2013 ◽  
Vol 3 (5) ◽  
pp. 417-426
Author(s):  
Marina Weiler ◽  
Fernando Cendes ◽  
Marcio LF Balthazar
PLoS ONE ◽  
2013 ◽  
Vol 8 (12) ◽  
pp. e85443 ◽  
Author(s):  
Niklas Mattsson ◽  
Philip Insel ◽  
Duygu Tosun ◽  
Jing Zhang ◽  
Clifford R. Jack Jr ◽  
...  

NeuroImage ◽  
2007 ◽  
Vol 38 (1) ◽  
pp. 13-24 ◽  
Author(s):  
Stefan J. Teipel ◽  
Christine Born ◽  
Michael Ewers ◽  
Arun L.W. Bokde ◽  
Maximilian F. Reiser ◽  
...  

2016 ◽  
Vol 55 (4) ◽  
pp. 1595-1603 ◽  
Author(s):  
Andrea Slachevsky ◽  
Leonardo Guzmán-Martínez ◽  
Carolina Delgado ◽  
Pablo Reyes ◽  
Gonzalo A. Farías ◽  
...  

2013 ◽  
Vol 9 ◽  
pp. P593-P593
Author(s):  
Ranjan Duara ◽  
Warren Barker ◽  
David Loewenstein ◽  
Qian Shen ◽  
Maria Greig-Custo ◽  
...  

2018 ◽  
Author(s):  
Stefano Delli Pizzi ◽  
Miriam Punzi ◽  
Stefano L Sensi ◽  

AbstractThe entorhinal-hippocampal circuit is a strategic hub for memory but also the first site to be affected in the Alzheimer’s Disease (AD)-related pathology. We investigated MRI patterns of brain atrophy and functional connectivity in a study cohort obtained from the Alzheimer’s Disease Neuroimaging Initiative database including healthy control (HC), Mild Cognitive Impairment (MCI), and AD subjects. MCI individuals were clinically evaluated 24 months after the MRI scan, and the group further divided into a subset of subjects who either did (c-MCI) or did not (nc-MCI) convert to AD. Compared to HC subjects, AD patients exhibited a collapse of long-range connectivity from the hippocampus and entorhinal cortex, pronounced cortical/sub-cortical atrophy, and a dramatic decline in cognitive performances. c-MCI patients showed entorhinal and hippocampal hypo-connectivity, no signs of cortical thinning but evidence of right hippocampus atrophy. On the contrary, nc-MCI patients showed lack of brain atrophy, largely preserved cognitive functions, hippocampal and entorhinal hyper-connectivity with selected neocortical/sub-cortical regions mainly involved in memory processing and brain meta-stability. This hyper-connectivity can represent an early compensatory strategy to overcome the progression of cognitive impairment. This functional signature can also be employed for the diagnosis of c-MCI subjects.


2020 ◽  
Vol 16 (S4) ◽  
Author(s):  
Miguel Ángel Rivas Fernández ◽  
Cristina Lojo‐Seoane ◽  
Santiago Galdo‐Álvarez ◽  
Jose M. Aldrey‐Vázquez ◽  
Ana Nieto Vieites ◽  
...  

2002 ◽  
Vol 14 (4) ◽  
pp. 365-378 ◽  
Author(s):  
Cristina Geroldi ◽  
Lorena Bresciani ◽  
Orazio Zanetti ◽  
Giovanni B. Frisoni

Background and Objective: The pathophysiology and the neurobiology of the behavioral disturbances in Alzheimer's disease (AD) are far from understood. The aim of the study was to assess whether delusional AD patients have a specific pattern of regional brain atrophy. Methods: The setting of the study was the outpatients facility of a memory clinic. Subjects were 41 AD patients with mild dementia severity (Mini-Mental State Exam score of 22 ± 3, range 18 to 27). Delusions were assessed with the pertinent subscale of the UCLA Neuropsychiatric Inventory (NPI). Nondelusional (n = 22) AD and delusional (n = 19) AD were defined on the basis of absence (NPI delusions subscale = 0) or presence (NPI delusions subscale = 1 or higher) of delusions. Thirteen (68%) of the delusional patients had isolated theft delusions, and 6 (32%) had theft associated with another paranoid delusion (of jealousy or persecution). None of the patients had misidentifications or other delusions of nonparanoid content. Temporal lobe and frontal lobe atrophy were assessed with linear measures (radial width of the temporal horn, rWTH, and frontal index, FI) taken from computed tomographic films. Temporal and frontal asymmetries were computed as right/left ratio of the rWTH and FI. Results: AD patients without delusions had symmetrical enlargement of both temporal (8.1 ± 3.9 vs. 8.5 ± 4.5) and frontal horns (35.8 ± 4.8 vs. 35.9 ± 4.6). On the contrary, AD with delusions showed temporal horns larger to the right (9.1 ± 3.3 vs. 7.7 ± 3.1, p = .06) and the frontal horn to the left (35.7 ± 4.3 vs. 37.5 ± 4.2, p = .02). This different pattern was confirmed with a gender-adjusted repeated measures analysis of variance model (interaction term between asymmetry and group: F1,38 = 5.5, p = .03). Discussion: AD patients with delusions are characterized by a specific pattern of frontal and temporal asymmetry of brain atrophy, whereas nondelusional patients are symmetric. Because the asymmetry pattern of the delusional patients is similar to the physiological pattern of asymmetry of individuals without dementia, the data indicate that the absence of theft delusions in the mild stage of AD rather than their presence is associated with an abnormal asymmetry pattern.


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