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      Thalamic nuclei changes in early and late onset Alzheimer's disease

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          Abstract

          Alzheimer's disease (AD) is the most common cause of dementia worldwide. Increasing evidence points to the thalamus as an important hub in the clinical symptomatology of the disease, with the ‘limbic thalamus’ been described as especially vulnerable. In this work, we examined thalamic atrophy in early-onset AD (EOAD) and late-onset AD (LOAD) compared to young and old healthy controls (YHC and OHC, respectively) using a recently developed cutting-edge thalamic nuclei segmentation method. A deep learning variant of Thalamus Optimized Multi Atlas Segmentation (THOMAS) was used to parcellate 11 thalamic nuclei per hemisphere from T1-weighted MRI in 88 biomarker-confirmed AD patients (49 EOAD and 39 LOAD) and 58 healthy controls (41 YHC and 17 OHC) with normal AD biomarkers. Nuclei volumes were compared among groups using MANCOVA. Further, Pearson's correlation coefficient was computed between thalamic nuclear volume and cortical—subcortical regions, CSF tau levels, and neuropsychological scores. The results showed widespread thalamic nuclei atrophy in EOAD and LOAD compared to their respective healthy control groups, with EOAD showing additional atrophy in the centromedian and ventral lateral posterior nuclei compared to YHC. In EOAD, increased thalamic nuclei atrophy was associated with posterior parietal atrophy and worse visuospatial abilities, while LOAD thalamic nuclei atrophy was preferentially associated with medial temporal atrophy and worse episodic memory and executive function. Our findings suggest that thalamic nuclei may be differentially affected in AD according to the age at symptoms onset, associated with specific cortical—subcortical regions, CSF total tau and cognition.

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          Highlights

          • •

            EOAD showed wider thalamic nuclei atrophy compared to LOAD.

          • •

            Anteroventral nucleus has different cognitive implication in EOAD and LOAD.

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            Only EOAD anteroventral nucleus is associated with total tau levels.

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          "Mini-mental state". A practical method for grading the cognitive state of patients for the clinician.

          M F Folstein, S Folstein, P R McHugh (1975)
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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.
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              NIA-AA Research Framework: Toward a biological definition of Alzheimer’s disease

              Clifford R. Jack, David Bennett, Kaj Blennow … (2018)
              In 2011, the National Institute on Aging and Alzheimer’s Association created separate diagnostic recommendations for the preclinical, mild cognitive impairment, and dementia stages of Alzheimer’s disease. Scientific progress in the interim led to an initiative by the National Institute on Aging and Alzheimer’s Association to update and unify the 2011 guidelines. This unifying update is labeled a “research framework” because its intended use is for observational and interventional research, not routine clinical care. In the National Institute on Aging and Alzheimer’s Association Research Framework, Alzheimer’s disease (AD) is defined by its underlying pathologic processes that can be documented by postmortem examination or in vivo by biomarkers. The diagnosis is not based on the clinical consequences of the disease (i.e., symptoms/signs) in this research framework, which shifts the definition of AD in living people from a syndromal to a biological construct. The research framework focuses on the diagnosis of AD with biomarkers in living persons. Biomarkers are grouped into those of β amyloid deposition, pathologic tau, and neurodegeneration [AT(N)]. This ATN classification system groups different biomarkers (imaging and biofluids) by the pathologic process each measures. The AT(N) system is flexible in that new biomarkers can be added to the three existing AT(N) groups, and new biomarker groups beyond AT(N) can be added when they become available. We focus on AD as a continuum, and cognitive staging may be accomplished using continuous measures. However, we also outline two different categorical cognitive schemes for staging the severity of cognitive impairment: a scheme using three traditional syndromal categories and a six-stage numeric scheme. It is important to stress that this framework seeks to create a common language with which investigators can generate and test hypotheses about the interactions among different pathologic processes (denoted by biomarkers) and cognitive symptoms. We appreciate the concern that this biomarker-based research framework has the potential to be misused. Therefore, we emphasize, first, it is premature and inappropriate to use this research framework in general medical practice. Second, this research framework should not be used to restrict alternative approaches to hypothesis testing that do not use biomarkers. There will be situations where biomarkers are not available or requiring them would be counterproductive to the specific research goals (discussed in more detail later in the document). Thus, biomarker-based research should not be considered a template for all research into age-related cognitive impairment and dementia; rather, it should be applied when it is fit for the purpose of the specific research goals of a study. Importantly, this framework should be examined in diverse populations. Although it is possible that β-amyloid plaques and neurofibrillary tau deposits are not causal in AD pathogenesis, it is these abnormal protein deposits that define AD as a unique neurodegenerative disease among different disorders that can lead to dementia. We envision that defining AD as a biological construct will enable a more accurate characterization and understanding of the sequence of events that lead to cognitive impairment that is associated with AD, as well as the multifactorial etiology of dementia. This approach also will enable a more precise approach to interventional trials where specific pathways can be targeted in the disease process and in the appropriate people.
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                Author and article information

                Contributors
                Albert Lladó
                Journal
                Journal ID (nlm-ta): Curr Res Neurobiol
                Journal ID (iso-abbrev): Curr Res Neurobiol
                Title: Current Research in Neurobiology
                Publisher: Elsevier
                ISSN (Electronic): 2665-945X
                Publication date PMC-release: 24 March 2023
                Publication date Collection: 2023
                Publication date (Electronic): 24 March 2023
                Volume: 4
                Electronic Location Identifier: 100084
                Affiliations
                [a ]Alzheimer's Disease and Other Cognitive Disorders Unit, Neurology Service, Hospital Clínic of Barcelona, Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain
                [b ]Laboratorio de Neuropsicología y Neurociencias Clínicas (LANNEC), Facultad de Medicina, Universidad de Chile, Chile
                [c ]School of Psychology, Universidad de los Andes, Santiago, Chile
                [d ]Radiology, University of Massachusetts Chan Medical School, Worcester, MA, United States
                [e ]Atlantic Fellow for Equity in Brain Health, Global Brain Heath Institute, University of California San Francisco, Trinity College Dublin, Ireland
                [f ]Institute of Neurosciences, Department of Medicine, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain
                [g ]Norwich Medical School, University of East Anglia, Norwich, UK
                Author notes
                [∗ ]Corresponding author. Alzheimer's disease and other cognitive disorders unit, Neurology Service, Hospital Clínic, IDIBAPS, Universitat de Barcelona, C/Villarroel, 170, Barcelona, 08036, Spain. allado@ 123456clinic.cat
                [1]

                These authors share senior authorship.

                [2]

                These authors share co-first authorship.

                Article
                Publisher Item ID: S2665-945X(23)00012-8 Publisher ID: 100084
                DOI: 10.1016/j.crneur.2023.100084
                PMC ID: 10313877
                PubMed ID: 37397807
                SO-VID: d9d0e2fa-9f97-4b09-9e55-c69d345feb94
                Copyright © © 2023 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 17 January 2023
                Date revision received : 27 February 2023
                Date accepted : 14 March 2023
                Categories
                Subject: Articles from the special issue: Integrating thalamocortical functions from sensation to cognition, edited by Mathieu Wolff and Anna Mitchell

                Keywords: thalamus,thalamic nuclei,early onset alzheimer's disease,late onset alzheimer's disease,thomas-dl
                Data availability:
                Keywords: thalamus, thalamic nuclei, early onset alzheimer's disease, late onset alzheimer's disease, thomas-dl

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