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      Distinct medical and substance use histories associate with cognitive decline in Alzheimer’s Disease

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          Abstract

          INTRODUCTION:

          Phenotype clustering reduces patient heterogeneity and could be useful when designing precision clinical trials. We hypothesized that the onset of early cognitive decline in patients would exhibit variance predicated on the clinical history documented prior to an Alzheimer’s Disease (AD) diagnosis

          METHODS:

          Self-reported medical and substance use history (i.e., problem history) was used to cluster participants from the National Alzheimer’s Coordinating Centers (NACC) into distinct subtypes. Linear mixed effects modeling was used to determine the effect of problem history subtype on cognitive decline over two years.

          RESULTS:

          2754 individuals were partitioned into three subtypes: minimal (n = 1380), substance use (n = 1038), and cardiovascular (n = 336) subtypes. The cardiovascular problem history subtype had significantly worse cognitive decline over a two-year follow-up period (p = 0.013).

          DISCUSSION:

          Our study highlights the need to account for problem history to reduce heterogeneity of outcomes in AD clinical trials.

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          Most cited references53

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          FactoMineR: AnRPackage for Multivariate Analysis

          Sébastien Le Jan, Julie Josse, François Husson (2008)
          Article 0 comments Cited 2124 times – based on 0 reviews     Review now
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            Clinical diagnosis of Alzheimer's disease: Report of the NINCDS-ADRDA Work Group* under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease

            G. McKhann, D. Drachman, M. Folstein … (1984)
            Neurology, 34(7), 939-939
            Article 0 comments Cited 1728 times – based on 0 reviews     Review now
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              Lecanemab in Early Alzheimer’s Disease

              Christopher H van Dyck, Chad J. Swanson, Paul Aisen … (2022)
              The accumulation of soluble and insoluble aggregated amyloid-beta (Aβ) may initiate or potentiate pathologic processes in Alzheimer's disease. Lecanemab, a humanized IgG1 monoclonal antibody that binds with high affinity to Aβ soluble protofibrils, is being tested in persons with early Alzheimer's disease.
              Article 0 comments Cited 1394 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): medRxiv
                Journal ID (publisher-id): MEDRXIV
                Title: medRxiv
                Publisher: Cold Spring Harbor Laboratory
                Publication date (Electronic): 28 November 2024
                Electronic Location Identifier: 2024.11.26.24317918
                Affiliations
                [1. ]Department of Cell Biology and Physiology, University of Kansas Medical Center, 3901 Rainbow Blvd, Kansas City, KS, 66160
                [2. ]Department of Internal Medicine, Division of Medical Informatics, Division of Pulmonary Critical Care and Sleep Medicine, University of Kansas Medical Center, Kansas City, KS 66160
                [3. ]Alzheimer’s Disease Research Center, University of Kansas Medical Center, 4350 Shawnee Mission Pkwy, Mail Stop 6002, Fairway, KS, 66205
                [4. ]Department of Biostatistics and Data Science, University of Kansas Medical Center, 3901 Rainbow Blvd, Kansas City, KS, 66160
                Author notes
                [+ ]Corresponding Author
                Author information
                http://orcid.org/0000-0002-0135-7576
                Article
                DOI: 10.1101/2024.11.26.24317918
                PMC ID: 11623748
                PubMed ID: 39649607
                SO-VID: 15a0a766-2476-4d79-9c53-2a25381fc99e
                License:

                This work is licensed under a Creative Commons Attribution 4.0 International License, which allows reusers to distribute, remix, adapt, and build upon the material in any medium or format, so long as attribution is given to the creator. The license allows for commercial use.

                History
                Funding
                The NACC database is funded by NIA/NIH Grant U24 AG072122. NACC data are contributed by the NIA-funded ADRCs: P30 AG062429 (PI James Brewer, MD, PhD), P30 AG066468 (PI Oscar Lopez, MD), P30 AG062421 (PI Bradley Hyman, MD, PhD), P30 AG066509 (PI Thomas Grabowski, MD), P30 AG066514 (PI Mary Sano, PhD), P30 AG066530 (PI Helena Chui, MD), P30 AG066507 (PI Marilyn Albert, PhD), P30 AG066444 (PI John Morris, MD), P30 AG066518 (PI Jeffrey Kaye, MD), P30 AG066512 (PI Thomas Wisniewski, MD), P30 AG066462 (PI Scott Small, MD), P30 AG072979 (PI David Wolk, MD), P30 AG072972 (PI Charles DeCarli, MD), P30 AG072976 (PI Andrew Saykin, PsyD), P30 AG072975 (PI David Bennett, MD), P30 AG072978 (PI Neil Kowall, MD), P30 AG072977 (PI Robert Vassar, PhD), P30 AG066519 (PI Frank LaFerla, PhD), P30 AG062677 (PI Ronald Petersen, MD, PhD), P30 AG079280 (PI Eric Reiman, MD), P30 AG062422 (PI Gil Rabinovici, MD), P30 AG066511 (PI Allan Levey, MD, PhD), P30 AG072946 (PI Linda Van Eldik, PhD), P30 AG062715 (PI Sanjay Asthana, MD, FRCP), P30 AG072973 (PI Russell Swerdlow, MD), P30 AG066506 (PI Todd Golde, MD, PhD), P30 AG066508 (PI Stephen Strittmatter, MD, PhD), P30 AG066515 (PI Victor Henderson, MD, MS), P30 AG072947 (PI Suzanne Craft, PhD), P30 AG072931 (PI Henry Paulson, MD, PhD), P30 AG066546 (PI Sudha Seshadri, MD), P20 AG068024 (PI Erik Roberson, MD, PhD), P20 AG068053 (PI Justin Miller, PhD), P20 AG068077 (PI Gary Rosenberg, MD), P20 AG068082 (PI Angela Jefferson, PhD), P30 AG072958 (PI Heather Whitson, MD), P30 AG072959 (PI James Leverenz, MD).
                The Alzheimer’s Disease Genetic Consortium (ADGC) data is funded by NIA/NIH Grant U01 AG032984.
                This work was also performed with funding from NIH P30 AG072973 and T32 AG078114 (CM); NIH P20 GM130423 (OJV) and P30 AG035982 (OJV, RAH).
                Categories
                Subject: Article

                Keywords: alzheimer’s disease,phenotype clustering,cardiovascular disease,national alzheimer’s coordinating centers,clinical dementia rating,substance use,cognitive decline
                Data availability:
                Keywords: alzheimer’s disease, phenotype clustering, cardiovascular disease, national alzheimer’s coordinating centers, clinical dementia rating, substance use, cognitive decline

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