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      The subcortical default mode network and Alzheimer’s disease: a systematic review and meta-analysis

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          Abstract

          The default mode network is a central cortical brain network suggested to play a major role in several disorders and to be particularly vulnerable to the neuropathological hallmarks of Alzheimer’s disease. Subcortical involvement in the default mode network and its alteration in Alzheimer’s disease remains largely unknown. We performed a systematic review, meta-analysis and empirical validation of the subcortical default mode network in healthy adults, combined with a systematic review, meta-analysis and network analysis of the involvement of subcortical default mode areas in Alzheimer’s disease. Our results show that, besides the well-known cortical default mode network brain regions, the default mode network consistently includes subcortical regions, namely the thalamus, lobule and vermis IX and right Crus I/II of the cerebellum and the amygdala. Network analysis also suggests the involvement of the caudate nucleus. In Alzheimer’s disease, we observed a left-lateralized cluster of decrease in functional connectivity which covered the medial temporal lobe and amygdala and showed overlap with the default mode network in a portion covering parts of the left anterior hippocampus and left amygdala. We also found an increase in functional connectivity in the right anterior insula. These results confirm the consistency of subcortical contributions to the default mode network in healthy adults and highlight the relevance of the subcortical default mode network alteration in Alzheimer’s disease.

          Abstract

          Seoane et al. find the most consistently identified subcortical default mode network in healthy adults and its disruption in Alzheimer’s disease. Through systematic review, meta-analysis and network analysis, they identify a left-lateralized functional connectivity decrease, particularly in the medial temporal lobe and amygdala, in Alzheimer’s disease.

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          Most cited references144

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          The diagnosis of dementia due to Alzheimer's disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease

          Guy M McKhann, David S. Knopman, Howard Chertkow … (2011)
          The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of revising the 1984 criteria for Alzheimer's disease (AD) dementia. The workgroup sought to ensure that the revised criteria would be flexible enough to be used by both general healthcare providers without access to neuropsychological testing, advanced imaging, and cerebrospinal fluid measures, and specialized investigators involved in research or in clinical trial studies who would have these tools available. We present criteria for all-cause dementia and for AD dementia. We retained the general framework of probable AD dementia from the 1984 criteria. On the basis of the past 27 years of experience, we made several changes in the clinical criteria for the diagnosis. We also retained the term possible AD dementia, but redefined it in a manner more focused than before. Biomarker evidence was also integrated into the diagnostic formulations for probable and possible AD dementia for use in research settings. The core clinical criteria for AD dementia will continue to be the cornerstone of the diagnosis in clinical practice, but biomarker evidence is expected to enhance the pathophysiological specificity of the diagnosis of AD dementia. Much work lies ahead for validating the biomarker diagnosis of AD dementia. Copyright © 2011. Published by Elsevier Inc.
          Article 0 comments Cited 2933 times – based on 0 reviews     Review now
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            The organization of the human cerebral cortex estimated by intrinsic functional connectivity.

            B. Yeo, Fenna M. Krienen, Jorge Sepulcre … (2011)
            Information processing in the cerebral cortex involves interactions among distributed areas. Anatomical connectivity suggests that certain areas form local hierarchical relations such as within the visual system. Other connectivity patterns, particularly among association areas, suggest the presence of large-scale circuits without clear hierarchical relations. In this study the organization of networks in the human cerebrum was explored using resting-state functional connectivity MRI. Data from 1,000 subjects were registered using surface-based alignment. A clustering approach was employed to identify and replicate networks of functionally coupled regions across the cerebral cortex. The results revealed local networks confined to sensory and motor cortices as well as distributed networks of association regions. Within the sensory and motor cortices, functional connectivity followed topographic representations across adjacent areas. In association cortex, the connectivity patterns often showed abrupt transitions between network boundaries. Focused analyses were performed to better understand properties of network connectivity. A canonical sensory-motor pathway involving primary visual area, putative middle temporal area complex (MT+), lateral intraparietal area, and frontal eye field was analyzed to explore how interactions might arise within and between networks. Results showed that adjacent regions of the MT+ complex demonstrate differential connectivity consistent with a hierarchical pathway that spans networks. The functional connectivity of parietal and prefrontal association cortices was next explored. Distinct connectivity profiles of neighboring regions suggest they participate in distributed networks that, while showing evidence for interactions, are embedded within largely parallel, interdigitated circuits. We conclude by discussing the organization of these large-scale cerebral networks in relation to monkey anatomy and their potential evolutionary expansion in humans to support cognition.
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              Neuropathological stageing of Alzheimer-related changes

              H Braak, E Braak (1991)
              Eighty-three brains obtained at autopsy from nondemented and demented individuals were examined for extracellular amyloid deposits and intraneuronal neurofibrillary changes. The distribution pattern and packing density of amyloid deposits turned out to be of limited significance for differentiation of neuropathological stages. Neurofibrillary changes occurred in the form of neuritic plaques, neurofibrillary tangles and neuropil threads. The distribution of neuritic plaques varied widely not only within architectonic units but also from one individual to another. Neurofibrillary tangles and neuropil threads, in contrast, exhibited a characteristic distribution pattern permitting the differentiation of six stages. The first two stages were characterized by an either mild or severe alteration of the transentorhinal layer Pre-alpha (transentorhinal stages I-II). The two forms of limbic stages (stages III-IV) were marked by a conspicuous affection of layer Pre-alpha in both transentorhinal region and proper entorhinal cortex. In addition, there was mild involvement of the first Ammon's horn sector. The hallmark of the two isocortical stages (stages V-VI) was the destruction of virtually all isocortical association areas. The investigation showed that recognition of the six stages required qualitative evaluation of only a few key preparations.
              Article 0 comments Cited 1942 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Sara Seoane:
                ORCID: https://orcid.org/0000-0002-8321-018X
                Martijn van den Heuvel
                Ángel Acebes
                Niels Janssen
                Journal
                Journal ID (nlm-ta): Brain Commun
                Journal ID (iso-abbrev): Brain Commun
                Journal ID (publisher-id): braincomms
                Title: Brain Communications
                Publisher: Oxford University Press (UK )
                ISSN (Electronic): 2632-1297
                Publication date Collection: 2024
                Publication date (Electronic): 10 April 2024
                Publication date PMC-release: 10 April 2024
                Volume: 6
                Issue: 2
                Electronic Location Identifier: fcae128
                Affiliations
                Department of Complex Traits Genetics, Center for Neurogenomics and Cognitive Research (CNCR), Amsterdam Neuroscience, Vrije Universiteit Amsterdam , Amsterdam 1081 HV, The Netherlands
                Institute of Biomedical Technologies (ITB), University of La Laguna , Tenerife 38200, Spain
                Instituto Universitario de Neurociencia (IUNE), University of La Laguna , Tenerife 38200, Spain
                Department of Complex Traits Genetics, Center for Neurogenomics and Cognitive Research (CNCR), Amsterdam Neuroscience, Vrije Universiteit Amsterdam , Amsterdam 1081 HV, The Netherlands
                Department of Child and Adolescent Psychiatry and Psychology, Section Complex Trait Genetics, Amsterdam Neuroscience, Vrije Universiteit Medical Center, Amsterdam UMC , Amsterdam 1081 HV, The Netherlands
                Institute of Biomedical Technologies (ITB), University of La Laguna , Tenerife 38200, Spain
                Department of Basic Medical Sciences, University of La Laguna , Tenerife 38200, Spain
                Institute of Biomedical Technologies (ITB), University of La Laguna , Tenerife 38200, Spain
                Instituto Universitario de Neurociencia (IUNE), University of La Laguna , Tenerife 38200, Spain
                Department of Cognitive, Social and Organizational Psychology, University of La Laguna , Tenerife 38200, Spain
                Author notes
                Correspondence to: Sara L. Seoane Department of Complex Trait Genetics Center for Neurogenomics and Cognitive Research (CNCR) Vrije Universiteit Amsterdam, De Boelelaan 1085, Amsterdam 1081 HV, The Netherlands E-mail: saralseoane@ 123456gmail.com
                Author information
                https://orcid.org/0000-0002-8321-018X
                Article
                Publisher ID: fcae128
                DOI: 10.1093/braincomms/fcae128
                PMC ID: 11043657
                PubMed ID: 38665961
                SO-VID: 771303b4-ab0e-4638-af19-c382ba571138
                Copyright © © The Author(s) 2024. Published by Oxford University Press on behalf of the Guarantors of Brain.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 09 October 2023
                Date revision received : 28 February 2024
                Date accepted : 09 April 2024
                Date: 25 April 2024
                Page count
                Pages: 17
                Funding
                Funded by: European Research Council, DOI 10.13039/501100000781;
                Funded by: Spanish Agencia Estatal de Investigación, DOI 10.13039/501100011033;
                Award ID: AEI/10.13039/501100011033
                Categories
                Subject: Original Article
                Subject: AcademicSubjects/MED00310
                Subject: AcademicSubjects/SCI01870

                Keywords: default mode network,subcortical,functional connectivity,alzheimer’s disease
                Data availability:
                Keywords: default mode network, subcortical, functional connectivity, alzheimer’s disease

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