F4‐02‐02: Assessment of Regional Cortical Thickness on Mri in Dementia With Lewy Bodies and Alzheimer's Disease

O’Brien, John; Blamire, AM; Watson, Rosie; Colloby, Sean J.

doi:10.1016/j.jalz.2014.04.369

Cited by 2 publications

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“…9 ). One fact that may explain the discrepancies between our results and those reported in literature ( Blanc et al, 2015 , Clerx et al, 2013 , Dickerson et al, 2009 , Lerch, 2004 , O'Brien et al, 2014 ) are the number of images acquired and processing method used. Dickerson et al (2009) acquired multiple images (n = 4) of the same patient to improve the contrast–to-noise ratio and the quality of segmentation ( Dickerson et al, 2009 ).…”

Section: Discussioncontrasting

confidence: 97%

“…Several studies based on MRI have shown that volumetric reductions of hippocampus, entorhinal cortex, posterior cingulate gyrus, amygdala and parahippocampal gyrus are indicators of early AD ( Basso et al, 2006 , Bottino et al, 2002 , Csernansky et al, 2005 , Devanand et al, 2007 , Du et al, 2001 , Pennanen et al, 2004 , Spulber et al, 2013 , Stoub et al, 2005 , Uotani et al, 2006 , Wolf et al, 2004 , Xu et al, 2000 ). The measurement of cortical thickness by MRI also may reveal reduction of these and other regions, such as medial temporal, parietal and frontal lobes ( Blanc et al, 2015 , Dickerson et al, 2009 , Lerch, 2004 , O'Brien et al, 2014 ). Therefore, MRI shows initial reduction at the parahippocampal gyrus, followed by a widespread pattern of volume reduction involving the temporal medial lobe and posterior parietal region ( Busatto et al, 2008 , Jacobs et al, 2012 , Karas et al, 2004 , Tondelli et al, 2012 ).…”

Section: Introductionmentioning

confidence: 99%

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Neuro-degeneration profile of Alzheimer's patients: A brain morphometry study

Filho

Barbosa

Rondinoni

et al. 2017

NeuroImage: Clinical

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IntroductionAlzheimer's disease (AD) is a primary and progressive neurodegenerative disorder, which is marked by cognitive deterioration and memory impairment. Atrophy of hippocampus and other basal brain regions is one of the most predominant structural imaging findings related to AD. Most studies have evaluated the pre-clinical and initial stages of AD through clinical trials using Magnetic Resonance Imaging. Structural biomarkers for advanced AD stages have not been evaluated yet, being considered only hypothetically.ObjectiveTo evaluate the brain morphometry of AD patients at all disease stages, identifying the structural neuro-degeneration profile associated with AD severity.Material and methodsAD patients aged 60 years or over at different AD stages were recruited and grouped into three groups following the Clinical Dementia Rating (CDR) score: CDR1 (n = 16), CDR2 (n = 15), CDR3 (n = 13). Age paired healthy volunteers (n = 16) were also recruited (control group). Brain images were acquired on a 3T magnetic resonance scanner using a conventional Gradient eco 3D T1-w sequence without contrast injection. Volumetric quantitative data and cortical thickness were obtained by automatic segmentation using the Freesurfer software. Volume of each brain region was normalized by the whole brain volume in order to minimize age and body size effects. Volume and cortical thickness variations among groups were compared.ResultsAtrophy was observed in the hippocampus, amygdala, entorhinal cortex, parahippocampal region, temporal pole and temporal lobe of patients suffering from AD at any stage. Cortical thickness was reduced only in the parahippocampal gyrus at all disease stages. Volume and cortical thickness were correlated with the Mini Mental State Examination (MMSE) score in all studied regions, as well as with CDR and disease duration.Discussion and conclusionAs previously reported, brain regions affected by AD during its initial stages, such as hippocampus, amygdala, entorhinal cortex, and parahippocampal region, were found to be altered even in individuals with severe AD. In addition, individuals, specifically, with CDR 3, have multiple regions with lower volumes than individuals with a CDR 2. These results indicate that rates of atrophy have not plateaued out at CDR 2–3, and in severe patients there are yet neuronal loss and gliosis. These findings can add important information to the more accepted model in the literature that focuses mainly on early stages. Our findings allow a better understanding on the AD pathophysiologic process and follow-up process of drug treatment even at advanced disease stages.

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