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Parietal Cortex Matters in Alzheimer's Disease

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Neuroscience and Biobehavioral Reviews 36 (2012) 297–309 Contents lists available at ScienceDirect Neuroscience and Biobehavioral Reviews jou rnal homepage: www.elsevier.com/locate/neubiorev Review Parietal cortex matters in Alzheimer’s disease: An overview of structural, functional and metabolic findings a,b,∗ a,b a,b,c a,b a,b,d Heidi I.L. Jacobs , Martin P.J. Van Boxtel , Jelle Jolles , Frans R.J. Verhey , Harry B.M. Uylings a School for Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands b European Graduate School of Neuroscience EURON, Maastricht University, Maastricht, The Netherlands c AZIRE Research Institute, Faculty of Psychology and Education, VU University, Amsterdam, The Netherlands d Department of Anatomy and Neuroscience, VU University Medical Centre, Amsterdam, The Netherlands a r t i c l e i n f o a b s t r a c t Article history: Atrophy of the medial temporal lobe, especially the hippocampus and the parahippocampal gyrus, is Received 15 March 2011 considered to be the most predictive structural brain biomarker for Alzheimer’s Dementia (AD). However, Received in revised form 15 June 2011 recent neuroimaging studies reported a possible mismatch between structural and metabolic findings, Accepted 21 June 2011 showing medial temporal lobe atrophy and medial parietal hypoperfusion as biomarkers for AD. The role of the parietal lobe in the development of AD is only recently beginning to attract attention. The current Keywords: review discusses parietal lobe involvement in the early stages of AD, viz. mild cognitive impairment, Posterior parietal cortex as reported from structural, functional, perfusion and metabolic neuroimaging studies. The medial and Mild cognitive impairment posterior parts of the parietal lobe seem to be preferentially affected, compared to the other parietal lobe Alzheimer’s disease Neuroimaging parts. On the basis of the reviewed literature we propose a model showing the relationship between the Disconnection various pathological events, as measured by different neuroimaging techniques, in the development of AD. In this model myelin breakdown is a beginning of the chain of pathological events leading to AD pathology and an AD diagnosis. © 2011 Elsevier Ltd. All rights reserved. Contents 1. Introduction . 298 2. Methods . 298 2.1. Search strategy and selection criteria . 298 2.2. Data analysis . 298 3. Structure of this review . 298 4. Parietal lobe structure and function . 299 4.1. Parietal lobe structure . 299 4.2. Parietal lobe functions . 299 4.3. Relevance of the parietal lobe to neuropsychological deficits in AD . 300 5. Involvement of the parietal lobe during conversion from MCI to AD in neuroimaging studies . 300 5.1. Structural neuroimaging . 300 5.1.1. Grey matter studies . 300 5.1.2. White matter studies . 300 5.2. Functional neuroimaging . 301 5.2.1. Resting state activity studies . 301 5.2.2. Task-related activity studies . 301 5.3. Metabolic neuroimaging . 301 5.4. Multimodal neuroimaging: MRI and PET . 302 ∗ Corresponding author at: School for Mental Health and Neuroscience, Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands. Tel.: +31 43 388 41 26; fax: +31 43 388 40 92. E-mail addresses: [email protected] (H.I.L. Jacobs), [email protected] (M.P.J. Van Boxtel), [email protected] (J. Jolles), [email protected] (F.R.J. Verhey), [email protected] (H.B.M. Uylings). 0149-7634/$ – see front matter © 2011 Elsevier Ltd. All rights reserved. doi:10.1016/j.neubiorev.2011.06.009 298 H.I.L. Jacobs et al. / Neuroscience and Biobehavioral Reviews 36 (2012) 297–309 6. Discussion . 302 6.1. Involvement of the parietal lobe in various neuroimaging studies in early AD . 302 6.2. Investigating the parietal lobe as a next step in early AD detection . 303 6.3. Future research directions . 304 6.4. Conclusion . 305 Funding . 305 Appendix A. Supplementary data . 305 References . 305 1. Introduction changes (Jagust et al., 2002; Villain et al., 2010b; Zhang et al., 2011). Thus, there might be a mismatch between structural and metabolic findings (Buckner et al., 2005; Caroli et al., 2010; Hunt et al., 2007; Alzheimer’s disease (AD), the most common cause of dementia, Ishii et al., 2005; Klunk et al., 2004; Matsuda, 2007; Villain et al., is characterized by an insidious decline in memory, later affecting 2010b). Understanding this mismatch requires a better compre- language, visuospatial perception, arithmetic abilities and execu- hension of the relevance of the posterior association areas and their tive functioning. Behavioral and psychiatric symptoms have also connectivity with the rest of the brain. been frequently reported (Cummings, 2004). AD is characterized by This overview summarizes the evidence of structural, functional both the accumulation.
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