Delineating the neural substrates of autobiographical memory impairment in Huntington's disease.

Autor: Horne K; Brain and Mind Centre, The University of Sydney, Sydney, New South Wales, Australia.; School of Psychology, The University of Sydney, Sydney, New South Wales, Australia., Carmichael A; School of Psychological Sciences, Turner Institute for Brain and Mental Health, Monash University, Clayton, Australia., Mercieca EC; School of Psychological Sciences, Turner Institute for Brain and Mental Health, Monash University, Clayton, Australia., Glikmann-Johnston Y; School of Psychological Sciences, Turner Institute for Brain and Mental Health, Monash University, Clayton, Australia., Stout JC; School of Psychological Sciences, Turner Institute for Brain and Mental Health, Monash University, Clayton, Australia., Irish M; Brain and Mind Centre, The University of Sydney, Sydney, New South Wales, Australia.; School of Psychology, The University of Sydney, Sydney, New South Wales, Australia.
Jazyk: angličtina
Zdroj: The European journal of neuroscience [Eur J Neurosci] 2024 Nov; Vol. 60 (10), pp. 6509-6524. Date of Electronic Publication: 2024 Oct 17.
DOI: 10.1111/ejn.16576
Abstrakt: Emerging evidence suggests that autobiographical memory (ABM) is altered in Huntington's disease (HD). While these impairments are typically attributed to frontostriatal dysfunction, the neural substrates of ABM impairment in HD remain unexplored. To this end, we assessed ABM in 30 participants with genetically confirmed HD (18 premanifest, 12 manifest) and 24 age-matched healthy controls. Participants completed the Autobiographical Interview to assess free and probed ABM recall and underwent structural brain imaging. Whole-brain voxel-based morphometry (VBM) was used to explore voxel-wise associations between ABM performance and grey matter intensity (False Discovery Rate corrected at q = 0.05). Relative to controls, HD participants displayed significantly less detailed ABM retrieval across free and probed recall conditions, irrespective of disease stage. Recall performance did not differ significantly between manifest and premanifest HD groups. VBM analyses indicated that poorer ABM performance was associated with atrophy of a distributed cortico-subcortical network. Key regions implicated irrespective of ABM condition included the bilateral occipital cortex, left precuneus, right parahippocampal gyrus and right caudate nucleus. In addition, probed ABM recall was associated with the superior and inferior frontal gyri, frontal pole, right hippocampus, nucleus accumbens, paracingulate gyrus and cerebellum. Overall, our findings indicate that ABM impairments in HD reflect the progressive degeneration of a distributed cortico-subcortical brain network comprising medial temporal, frontal, striatal and posterior parietal cortices. Our findings advance our understanding of the neurocognitive profile of HD, providing an important foundation for future interventions to support memory function in this population.
(© 2024 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.)
Databáze: MEDLINE
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