Cortical Thickness in Dementia with Lewy Bodies and Alzheimer's Disease: A Comparison of Prodromal and Dementia Stages

Blanc‬, ‪Frederic; Colloby, Sean J.; Philippi, Nathalie; Petigny, Xavier de; Jung, Barbara; Demuynck, Catherine; Phillipps, Clélie; Anthony, Pierre; Thomas, Alan; Fan, Bing; Lamy, Julien; Milch, Catherine; O’Brien, John T.; Crétin, Benjamin; McKeith, Ian G.; Armspach, Jean‐Paul; Taylor, John‐Paul

doi:10.1371/journal.pone.0127396

Cited by 102 publications

(109 citation statements)

References 42 publications

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“…7) stages, in accordance with previous reports (Blanc et al, 2015, Lerch, 2004). Other regions, including the temporal, parietal and frontal lobes (Dickerson et al, 2009) showed cortical thickness reduction only at moderate and advanced stages of AD (Fig.…”

Section: Discussionsupporting

confidence: 93%

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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Section: Discussionsupporting

confidence: 93%

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

Filho

Barbosa

Rondinoni

et al. 2017

NeuroImage: Clinical

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“…It may be that higher glucose levels lead to grey matter atrophy via cerebral glucose hypometabolism, which leads to neuronal injury, which has been shown to be independent of Aβ accumulation [48]. Although research has shown that cortical thinning occurs in the prodromal stages of several types of dementia (i.e., dementia with Lewy bodies, AD, and vascular dementia) [4,13,14, 35], few studies have investigated cortical thickness in a cognitively normal, healthy sample [17,34,42]. …”

Section: Discussionmentioning

confidence: 99%

Blood glucose levels and cortical thinning in cognitively normal, middle-aged adults

Wennberg

Spira²,

Pettigrew³

et al. 2016

Journal of the Neurological Sciences

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Type II diabetes mellitus (DM) increases risk for cognitive decline and is associated with brain atrophy in older demented and non-demented individuals. We investigated (1) the cross-sectional association between fasting blood glucose level and cortical thickness in a sample of largely middle-aged, cognitively normal adults, and (2) whether these associations were modified by genes associated with both lipid processing and dementia. To explore possible modifications by genetic status, we investigated the interaction between blood glucose levels and the apolipoprotein E (APOE) ε4 allele and the translocase of the outer mitochondrial membrane (TOMM) 40 ′523 genotype on cortical thickness. Cortical thickness measures were based on mean thickness in a subset of a priori-selected brain regions hypothesized to be vulnerable to atrophy in Alzheimer's disease (AD) (i.e., ‘AD vulnerable regions’). Participants included 233 cognitively normal subjects in the BIOCARD study who had a measure of fasting blood glucose and cortical thickness measures, quantified by magnetic resonance imaging (MRI) scans. After adjustment for age, sex, race, education, depression, and medical conditions, higher blood glucose was associated with thinner parahippocampal gyri (B = −0.002; 95% CI −0.004, −0.0004) and temporal pole (B = −0.002; 95% CI −0.004, −0.0001), as well as reduced average thickness over AD vulnerable regions (B = −0.001; 95% CI −0.002, −0.0001). There was no evidence for greater cortical thinning in ε4 carriers of the APOE gene or in APOE ε3/3 individuals carrying the TOMM40 VL/VL genotypes. When individuals with glucose levels in the diabetic range (≥126 mg/dL), were excluded from the analysis, the associations between glucose levels and cortical thickness were no longer significant. These findings suggest that glucose levels in the diabetic range are associated with reduced cortical thickness in AD vulnerable regions as early as middle age.

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“…In this sense, several recent studies have analyzed and compared the local thickness between healthy controls and patients suffering MCI and AD [Blanc et al, 2015;Delli Pizzi et al, 2014;Julkunen et al, 2009;Li et al, 2011;Mak et al, 2015;Wang et al, 2016;Zhao et al, 2015] (in Wang et al, 2016, LGI is also analyzed). In general, they reported significant differences between HC and AD in similar regions as our findings, including the bilateral temporal cortex, and distributed regions in the parietal and frontal lobe [Blanc et al, 2015;Delli Pizzi et al, 2014;Li et al, 2011;Zhao et al, 2015]. The study presented in Mak et al [2015] is a longitudinal analysis involving the percent change of thickness over 12 months (longitudinal cortical thinning).…”

Section: Figurementioning

confidence: 99%

Complexity analysis of cortical surface detects changes in future Alzheimer's disease converters

Miras

Costumero

Belloch

et al. 2017

Human Brain Mapping

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Alzheimer's disease (AD) is a neurological disorder that creates neurodegenerative changes at several structural and functional levels in human brain tissue. The fractal dimension (FD) is a quantitative parameter that characterizes the morphometric variability of the human brain. In this study we investigate spherical harmonic-based FD (SHFD), thickness and local gyrification index (LGI) to assess whether they identify cortical surface abnormalities toward the conversion to AD. We study 33 AD patients, 122 mild cognitive impairment (MCI) patients (50 MCI-converters and 29 MCI-non converters) and 32 healthy controls (HC). SHFD, thickness and LGI methodology allowed us to perform not only global but also local level assessments in each cortical surface vertex. First, we found that global SHFD decreased in AD and future MCI-converters compared to HC, and in MCI-converters compared to MCI-non-converters. Second, we found that local white matter SHFD was reduced in AD compared to HC and MCI mainly in medial temporal lobe. Third, local white matter SHFD was significantly reduced in MCI-converters compared to MCI-non-converters in distributed areas, including the medial frontal lobe. Thickness and LGI metrics presented a reduction in AD compared to HC. Thickness was significantly reduced in MCI-converters compared to healthy controls in entorhinal cortex and lateral temporal. In summary, SHFD was the only surface measure showing differences between MCI individuals that will convert or remain stable in the next four years. We suggest that SHFD may be an optimal complement to thickness loss analysis in monitoring longitudinal changes in preclinical and clinical stages of AD.

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Cortical Thickness in Dementia with Lewy Bodies and Alzheimer's Disease: A Comparison of Prodromal and Dementia Stages

Cited by 102 publications

References 42 publications

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

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

Blood glucose levels and cortical thinning in cognitively normal, middle-aged adults

Complexity analysis of cortical surface detects changes in future Alzheimer's disease converters

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