Recognition memory and divergent cognitive profiles in prodromal genetic frontotemporal dementia
Open accessAbstract
Although executive dysfunction is the characteristic cognitive marker of behavioral variant frontotemporal dementia (bvFTD), episodic memory deficits are relatively common, and may be present even during the prodromal disease phase. In a cohort of mutation carriers with mild behavioral and/or cognitive symptoms consistent with prodromal bvFTD, we aimed to investigate patterns of performance on an abbreviated list learning task, with a particular focus on recognition memory. We further aimed to characterize the cognitive prodromes associated with the three major genetic causes of frontotemporal dementia, as emerging evidence suggests there may be subtle differences in cognitive profiles among carriers of different genetic mutations. Participants included 57 carriers of a pathogenic mutation in microtubule-associated protein tau (MAPT, N = 23), or progranulin (GRN, N = 15), or a or a hexanucleotide repeat expansion in chromosome 9 open reading frame 72 (C9orf72, N = 19), with mild cognitive and/or behavioral symptoms consistent with prodromal bvFTD. Familial non-carriers were included as controls (N = 143). All participants completed a comprehensive neuropsychological examination, including an abbreviated list learning test assessing episodic memory recall and recognition. MAPT mutation carriers performed worse than non-carriers in terms of list recall, and had difficulty discriminating targets from distractors on the recognition memory task, primarily due to the endorsement of distractors as targets. MAPT mutation carriers also showed nonverbal episodic memory and semantic memory dysfunction (object naming). GRN mutation carriers were variable in performance and overall the most dysexecutive. Slowed psychomotor speed was evident in C9orf72 repeat expansion carriers. Identifying the earliest cognitive indicators of bvFTD is of critical clinical and research importance. List learning may be a sensitive cognitive marker for incipient dementia in MAPT and potentially a subset of GRN carriers. Our results highlight that distinct cognitive profiles may be evident in carriers of the three disease-causing genes during the prodromal disease stage.
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For genetic bvFTD, mutation-specific cognitive profiles and trajectories have been identified: characterized decline of confrontational naming, episodic and semantic memory in MAPT carriers, variable deficits with frequent executive dysfunction in GRN carriers, and a global and relatively stable profile in C9ORF72 carriers.
“For genetic bvFTD, mutation-specific cognitive profiles and trajectories have been identified: characterized decline of confrontational naming, episodic and semantic memory in MAPT carriers, variable deficits (with frequent executive dysfunction) in GRN carriers, and a global and relatively stable profile (e.g., mildly slowed processing speed) in C9ORF72 carriers (Poos et al., 2020; Barker et al.,”
From The pursuit for markers of disease progression in behavioral variant frontotemporal dementia: a scoping review to optimize outcome measures for clinical trials (2024) · cites this paper as Barker et al., 2021
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Palacino, F., Manganotti, P., & Benussi, A. (2025) · International Journal of Translational Medicine · doi:10.3390/ijtm5040052 · Cited by 7 · see citing works
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Additional file 1 of Diagnostic accuracy of research criteria for prodromal frontotemporal dementia
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Self-citation
- Authors
- Barker, M. S., Manoochehri, M., Rizer, S. J., Appleby, B. S., Brushaber, D., Dev, S. I., Devick, K. L., Dickerson, B. C., Fields, J. A., Foroud, T. M., Forsberg, L. K., Galasko, D. R., Ghoshal, N., Graff-Radford, N. R., Grossman, M., Heuer, H. W., Hsiung, G.-Y., Kornak, J., Litvan, I., Mackenzie, I. R., Mendez, M. F., Pascual, B., Rankin, K. P., Rascovsky, K., Staffaroni, A. M., Tartaglia, M. C., Weintraub, S., Wong, B., Boeve, B. F., Boxer, A. L., Rosen, H. J., Goldman, J., Huey, E. D., & Cosentino, S.
- Affiliations
- Columbia University Irving Medical Center (US)
- Case Western Reserve University (US)
- Mayo Clinic (US)
- Harvard University (US)
- Indiana University Indianapolis (US)
- University of California San Diego (US)
- Washington University in St. Louis (US)
- University of Pennsylvania (US)
- University of California, San Francisco (US)
- University of British Columbia (CA)
- University of California, Los Angeles (US)
- University of Toronto (CA)
- Corresponding author
- Barker, Megan S.
- ORCID
- Barker, Megan S.
- Manoochehri, Masood
- Rizer, Sandra J.
- Appleby, Brian S.
- Brushaber, Danielle
- Dev, Sheena I.
- Devick, Katrina L.
- Dickerson, Bradford C.
- Fields, Julie A.
- Foroud, Tatiana M.
- Forsberg, Leah K.
- Galasko, Douglas R.
- Ghoshal, Nupur
- Grossman, Murray
- Heuer, Hilary W.
- Hsiung, Ging-Yuek
- Kornak, John
- Litvan, Irene
- Mackenzie, Ian R.
- Mendez, Mario F.
- Pascual, Belen
- Rankin, Katherine P.
- Staffaroni, Adam M.
- Tartaglia, Maria Carmela
- Wong, Bonnie
- Boeve, Bradley F.
- Boxer, Adam L.
- Rosen, Howard J.
- Goldman, Jill
- Huey, Edward D.
- Cosentino, Stephanie
- Venue
- Cortex
- Publisher
- Elsevier BV
- Published
- 2021-06
- Volume
- 139
- Pages
- 99-115
- ISSN
- 0010-9452 (ISSN-L)
- PMC
- PMC8119343
- OpenAlex
- W3138847939
- Cited by
- 29
- References
- 61
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 16 · 2023: 4 · 2022: 4 · 2021: 2
- FWCI
- 4.66
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Cortex (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- IUScholarWorks (Indiana University) (submittedVersion)
- Funders
- Centers for Disease Control and Prevention
- AbbVie
- National Institute on Aging
- University of California, San Diego
- National Institute of Neurological Disorders and Stroke (U54 NS092089)
- Alzheimer Society
- Roche
- Eisai
- Biogen
- National Institutes of Health (1R21NS114764-01A1, 2R01AG038791-06A, 5P50AG005131-33, P20GM109025, R25NS098999, U01NS090259, U01NS100610, U01NS80818, U19 AG063911-1)
- National Center for Advancing Translational Sciences (U01 AG045390)
- Association for Frontotemporal Degeneration
- Canadian Institutes of Health Research
- Novartis
- Parkinsonfonden
- Michael J. Fox Foundation for Parkinson's Research
- Parkinson Study Group
- Mayo Clinic
- Quest Diagnostics
- Bristol-Myers Squibb
- Rainwater Charitable Foundation
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- behavioral variant frontotemporal dementia, recognition memory, episodic memory, MAPT mutations, progranulin mutations, C9orf72 repeat expansion, list learning, executive dysfunction, semantic memory, object naming, psychomotor speed, mutation carriers
- MeSH terms
- Progranulins, Cognition, Heterozygote, Humans, Mutation, Neuropsychological Tests, Pick Disease of the Brain, Frontotemporal Dementia
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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