Integrating VBM into the General Linear Model with voxelwise anatomical covariates

Oakes, Terrence R.; Fox, Andrew S.; Johnstone, Tom; Chung, Moo K.; Kalin, Ned H.; Davidson, Richard J.

doi:10.1016/j.neuroimage.2006.10.007

Cited by 234 publications

(197 citation statements)

References 34 publications

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“…Visual examination of the fMRI and VBM results showed that the differences between the MCI and HC groups were in different regions for the two modalities. A more detailed analysis integrating the two modalities is necessary, such as performed by Oakes and colleagues [71], to make statements about the possible interaction between brain activation and GM density.…”

Section: Discussionmentioning

confidence: 99%

Altered Brain Activation During a Verbal Working Memory Task in Subjects with Amnestic Mild Cognitive Impairment

Bokde

Karmann

Born

et al. 2010

JAD

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In subjects with Mild Cognitive Impairment (MCI) memory disorders indicate a high risk for conversion to Alzheimer's disease (AD). The objective of this study was to delineate the differences in brain activation between amnestic MCI and age-matched healthy controls (HC) during a verbal working memory task. The verbal working memory task was a delay match to sample design. Brain activation was measured using functional magnetic resonance imaging. There were 8 subjects in each group and were matched for performance. The task was analyzed as an event-related design. Group differences were calculated using Analysis of Covariance (ANCOVA) with statistical significance at p < 0.05 corrected. Both groups activated a wide network in the posterior and frontal areas of the brain. There was higher activation in the parietal and frontal lobes in the MCI compared to the HC during the maintenance phase. There were no areas in the HC that activated higher than the MCI subjects. Response time in the task in the HC group was correlated to the left hippocampus during encoding phase and to the parietal and frontal areas during the recall phase. In the MCI group there was strong correlation to the inferior and middle temporal gyrii during encoding, the middle frontal gyrus during the maintenance phase, and hippocampus during recall phase. The activation differences between groups may be compensatory mechanisms within the MCI group for the effects of the putative AD neuropathology. This has been the first study that has examined verbal working memory in MCI.

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Section: Discussionmentioning

confidence: 99%

Altered Brain Activation During a Verbal Working Memory Task in Subjects with Amnestic Mild Cognitive Impairment

Bokde

Karmann

Born

et al. 2010

JAD

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“…To correct for atrophy, partial volume information of grey matter was estimated and maps for all participants were created based on the T1-weighted images using the FSL script feat gm prepare. These maps were added as voxelwise explanatory variable in the GLM design [73]. Demeaned age and depression scores were entered as covariates of no interest.…”

Section: Data Preprocessing On Group Levelmentioning

confidence: 99%

Functional Disintegration of the Default Mode Network in Prodromal Alzheimer’s Disease

Dillen¹,

Jacobs

Kukolja

et al. 2017

JAD

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Abstract. Neurodegenerative brain changes can affect the functional connectivity strength between nodes of the default-mode network (DMN), which may underlie changes in cognitive performance. It remains unclear how the functional connectivity strength of DMN nodes differs from healthy to pathological aging and whether these changes are cognitively relevant. We used resting-state functional magnetic resonance imaging to investigate the functional connectivity strength across five DMN nodes in 25 healthy controls (HC), 28 subjective cognitive decline (SCD) participants, and 25 prodromal Alzheimer's disease (AD) patients. After identifying the ventral medial prefrontal cortex (vmPFC), posterior cingulate cortex (PCC), retrosplenial cortex (RSC), inferior parietal lobule, and the hippocampus we investigated the functional strength between DMN nodes using temporal network modeling. Functional coupling of the vmPFC and PCC in prodromal AD patients was disrupted. This vmPFC-PCC coupling correlated positively with memory performance in prodromal AD. Furthermore, the hippocampus decoupled from posterior DMN nodes in SCD and prodromal AD patients. There was no coupling between the hippocampus and the anterior DMN. Additional mediation analyses indicated that the RSC enables communication between the hippocampus and DMN regions in HC but none of the other two groups. These results suggest an anterior-posterior disconnection and a hippocampal de-coupling from posterior DMN nodes with disease progression. Hippocampal de-coupling already occurring in SCD may provide valuable information for the development of a functional biomarker.

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“…Also, the integration of complementary information through a multimodal approach will be very useful to overcome the shortcomings of each single protocol, requiring advanced analysis tools which are able to integrate information from different protocols into the same processing pipeline. Similar approaches are likely to aid in better discrimination and staging of AD [8,[246][247][248]. In this context, information from different modalities may be simultaneously combined using the support of machine learning algorithms enabling the classification of a single subject into a predefined group while dealing with any type of input features (e.g.…”

Section: Functional Mri Markersmentioning

confidence: 99%

Perspective on future role of biological markers in clinical therapy trials of Alzheimer's disease: A long-range point of view beyond 2020

Hampel

Lista

Teipel

et al. 2014

Biochemical Pharmacology

102

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Recent advances in understanding the molecular mechanisms underlying various paths toward the pathogenesis of Alzheimer's disease (AD) has begun to provide new insight for interventions to modify disease progression. The evolving knowledge gained from multidisciplinary basic research has begun to identify new concepts for treatments and distinct classes of therapeutic targets; as well as putative disease-modifying compounds that are now being tested in clinical trials. There is a mounting consensus that such disease modifying compounds and/or interventions are more likely to be effectively administered as early as possible in the cascade of pathogenic processes preceding and underlying the clinical expression of AD. The budding sentiment is that "treatments" need to be applied before various molecular mechanisms converge into an irreversible pathway leading to morphological, metabolic and functional alterations that characterize the pathophysiology of AD. In light of this, biological indicators of pathophysiological mechanisms are desired to chart and detect AD throughout the asymptomatic early molecular stages into the prodromal and early dementia phase. A major conceptual development in the clinical AD research field was the recent proposal of new diagnostic criteria, which specifically incorporate the use of biomarkers as defining criteria for preclinical stages of AD. This paradigm shift in AD definition, conceptualization, operationalization, detection and diagnosis represents novel fundamental opportunities for the modification of interventional trial designs. This perspective summarizes not only present knowledge regarding biological markers but also unresolved questions on the status of surrogate indicators for detection of the disease in asymptomatic people and diagnosis of AD

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Integrating VBM into the General Linear Model with voxelwise anatomical covariates

Cited by 234 publications

References 34 publications

Altered Brain Activation During a Verbal Working Memory Task in Subjects with Amnestic Mild Cognitive Impairment

Altered Brain Activation During a Verbal Working Memory Task in Subjects with Amnestic Mild Cognitive Impairment

Functional Disintegration of the Default Mode Network in Prodromal Alzheimer’s Disease

Perspective on future role of biological markers in clinical therapy trials of Alzheimer's disease: A long-range point of view beyond 2020

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