The Cortical Signature of Alzheimer's Disease: Regionally Specific Cortical Thinning Relates to Symptom Severity in Very Mild to Mild AD Dementia and is Detectable in Asymptomatic Amyloid-Positive…

By Bradford C. Dickerson, A. Bakkour, David H. Salat, Eric Feczko, J. Pacheco, Douglas N. Greve, F. Grodstein, Christopher I. Wright, Deborah Blacker, H. Rosas and 7 more. 2008

1,137 citations recorded by the source corpus.

Alzheimer's disease (AD) is associated with neurodegeneration in vulnerable limbic and heteromodal regions of the cerebral cortex, detectable in vivo using magnetic resonance imaging. It is not clear whether abnormalities of cortical anatomy in AD can be reliably measured across different subject samples, how closely they track symptoms, and whether they are detectable prior to symptoms. An exploratory map of cortical thinning in mild AD was used to define regions of interest that were applied in a hypothesis-driven fashion to other subject samples. Results demonstrate a reliably quantifiable in vivo signature of abnormal cortical anatomy in AD, which parallels known regional vulnerability to AD neuropathology. Thinning in vulnerable cortical regions relates to symptom severity even in the earliest stages of clinical symptoms. Furthermore, subtle thinning is present in asymptomatic older controls with brain amyloid binding as detected with amyloid imaging. The reliability and clinical validity of AD-related cortical thinning suggests potential utility as an imaging biomarker. This “disease signature” approach to cortical morphometry, in which disease effects are mapped across the cortical mantle and then used to define ROIs for hypothesis-driven analyses, may provide a powerful methodological framework for studies of neuropsychiatric diseases.

Subfields: Cognitive Neuroscience, Physiology, Radiology, Nuclear Medicine and Imaging

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Citations in the corpus

Visual Feature Attribution Using Wasserstein GANs (2017, methodology): “As is known from the literature [8, 11] the method indicates atrophy in the hippocampi, and general brain atrophy around the ventricles.”
Toward defining the preclinical stages of Alzheimer's disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease (2011, result): “Multiple groups have now reported that cognitively normal older individuals with low CSF Aβ1–42 or high PET amyloid binding demonstrate disruption of functional networks [42–44] and decreased brain volume [45–49], consistent with the patterns seen in AD.”
An Operational Approach to NIA-AA Criteria for Preclinical Alzheimer’s Disease (2012, neutral): “[%] 94 [49] 35 [50] 19 [34] 6 [46] 41 [40] 10 [67]”
Automated MRI measures identify individuals with mild cognitive impairment and Alzheimer's disease (2009, neutral): “, 2007) or automated whole-brain approaches (Scahill et al., 2002; Buckner et al., 2005; Dickerson et al., 2009) to identify MCI and Alzheimer’s disease individuals.”
A review on neuroimaging‐based classification studies and associated feature extraction methods for Alzheimer's disease and its prodromal stages (2017, neutral): “AD patients generally show changes in temporal and parietal regions of the cortical surface (Bakkour et al., 2009; Dickerson et al., 2009, 2011).”
Constructing Subject- and Disease-Specific Effect Maps: Application to Neurodegenerative Diseases (2016, result): “Not surprisingly, the pattern resembles previous group-analysis results for AD [25].”
Amyloid deposition is associated with impaired default network function in older persons without dementia (2009, neutral): “Amyloid and Default Network fMRI Activity thinning (Dickerson et al., 2009), relative to their amyloid-free peers.”
The Lifespan Human Connectome Project in Aging: An overview (2018, neutral): “Medial temporal structural changes are the hallmark of memory disorders in aging and early stages of AD (Dickerson et al., 2009; Jack et al., 1997; Scheltens et al., 1992; Singh et al., 2006).”
DTI measures in crossing-fibre areas: Increased diffusion anisotropy reveals early white matter alteration in MCI and mild Alzheimer's disease (2011, result): “, 2009), is likely reflected by the clinical preservation of the motor functions until later stages of the disease (95% of the AD patients included in this study had mild AD) and is consistent with the preservation of the sensorimotor cortex (Karas et al., 2004; Chetelat et al., 2008; Dickerson et a”
The Episodic Memory System: Neurocircuitry and Disorders (2009, neutral): “…the involvement of these non-MTL cortical regions has been long known from studies of postmortem tissue (Arnold et al, 1991; Tomlinson et al, 1970), their early involvement has been clarified with modern in vivo neuroimaging studies (Buckner et al, 2005; Dickerson et al, 2009; Klunk et al, 2004).”
Comparison of multiple tau-PET measures as biomarkers in aging and Alzheimer's disease (2017, background): “, 2016), and to related functional and structural decline (Dickerson et al., 2009; Saint-Aubert et al., 2016; Sepulcre et al., 2016; Wang et al., 2016).”
Open Access Series of Imaging Studies (OASIS): Longitudinal MRI Data in Nondemented and Demented Older Adults (2010, methodology): “Portions of the clinical, demographic, and longitudinal image data obtained from subjects in this release have been used in previous publications (Dickerson et al., 2008; Fotenos, Mintun, Snyder, Morris, & Buckner, 2008; He, Chen, & Evans, 2008; Salat et al., 2009; Dickerson et al., 2009; Buckner…”
FreeSurfer (2012, background): “It has been used to improve our understanding of an array of neurological disorders (Becker et al., 2008; Desikan et al., 2010a,b; Dickerson et al., 2009; Gold et al., 2005; Kuperberg et al., 2003; Manoach et al., 2007; Milad et al., 2005; Oliveira et al., 2010; Rauch et al., 2005; Rosas et al.,…”
The Effects of FreeSurfer Version, Workstation Type, and Macintosh Operating System Version on Anatomical Volume and Cortical Thickness Measurements (2012, neutral): “[33] reported cortical thinning between 2.”
Longitudinal Changes in Cortical Thickness Associated with Normal Aging (2010, background): “Furthermore, decreases in cortical thickness appear to correlate well with severity of clinical impairment even in the earliest stages of AD (Dickerson et al., 2008).”