Hippocampal-occipital connectivity reflects autobiographical memory deficits in aphantasia.


Journal

eLife
ISSN: 2050-084X
Titre abrégé: Elife
Pays: England
ID NLM: 101579614

Informations de publication

Date de publication:
26 Sep 2024
Historique:
medline: 26 9 2024
pubmed: 26 9 2024
entrez: 26 9 2024
Statut: epublish

Résumé

Aphantasia refers to reduced or absent visual imagery. While most of us can readily recall decade-old personal experiences (autobiographical memories, AM) with vivid mental images, there is a dearth of information about whether the loss of visual imagery in aphantasics affects their AM retrieval. The hippocampus is thought to be a crucial hub in a brain-wide network underlying AM. One important question is whether this network, especially the connectivity of the hippocampus, is altered in aphantasia. In the current study, we tested 14 congenital aphantasics and 16 demographically matched controls in an AM fMRI task to investigate how key brain regions (i.e. hippocampus and visual-perceptual cortices) interact with each other during AM re-experiencing. All participants were interviewed regarding their autobiographical memory to examine their episodic and semantic recall of specific events. Aphantasics reported more difficulties in recalling AM, were less confident about their memories, and described less internal and emotional details than controls. Neurally, aphantasics displayed decreased hippocampal and increased visual-perceptual cortex activation during AM retrieval compared to controls. In addition, controls showed strong negative functional connectivity between the hippocampus and the visual cortex during AM and resting-state functional connectivity between these two brain structures predicted better visualization skills. Our results indicate that visual mental imagery plays an important role in detail-rich vivid AM, and that this type of cognitive function is supported by the functional connection between the hippocampus and the visual-perceptual cortex.

Identifiants

pubmed: 39325034
doi: 10.7554/eLife.94916
pii: 94916
doi:
pii:

Banques de données

Dryad
['10.5061/dryad.fbg79cp48']

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Deutsche Forschungsgemeinschaft
ID : MC244/3-1
Organisme : Deutsches Zentrum für Neurodegenerative Erkrankungen
ID : BN059K

Informations de copyright

© 2024, Monzel, Leelaarporn et al.

Déclaration de conflit d'intérêts

MM, PL, TL, JS, SB, MR, CM No competing interests declared

Auteurs

Merlin Monzel (M)

Department of Psychology, University of Bonn, Bonn, Germany.
German Center for Neurodegenerative Diseases, Bonn, Germany.

Pitshaporn Leelaarporn (P)

German Center for Neurodegenerative Diseases, Bonn, Germany.
Department of Old Age Psychiatry and Cognitive Disorders, University Hospital Bonn, Bonn, Germany.

Teresa Lutz (T)

German Center for Neurodegenerative Diseases, Bonn, Germany.

Johannes Schultz (J)

Center for Economics and Neuroscience, University of Bonn, Bonn, Germany.
Institute of Experimental Epileptology and Cognition Research, Medical Faculty, University of Bonn, Bonn, Germany.

Sascha Brunheim (S)

German Center for Neurodegenerative Diseases, Bonn, Germany.

Martin Reuter (M)

Department of Psychology, University of Bonn, Bonn, Germany.

Cornelia McCormick (C)

German Center for Neurodegenerative Diseases, Bonn, Germany.
Department of Old Age Psychiatry and Cognitive Disorders, University Hospital Bonn, Bonn, Germany.

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Classifications MeSH