ArticleBehavioral and brain functions : BBF2024
White matter alterations and their associations with biomarkers and behavior in subjective cognitive decline individuals: a fixel-based analysis.
Article in Behavioral and brain functions : BBF, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- The causal relationship between immune cells, white matter microstructure and dementia: a Mendelian randomization study and co-localization analysis.European archives of psychiatry and clinical neuroscience · 2026Article
- Advanced diffusion MRI tract signatures in Alzheimer's disease, dementia with Lewy bodies, and the FTD/PPA spectrum.NeuroImage · 2026Review
- Genetically inferred effects of brain structure and gene expression on neurodegenerative diseases: a Mendelian randomization study.Archives of medical science : AMS · 2026Article
- Utility of Harmonisation for Fixel-Based Metrics in Travelling Subjects and Alzheimer's Disease Data.Human brain mapping · 2025Article
- Eight-Year Longitudinal Study on the Assay Stability of Plasma Amyloid Beta 1-42 Peptide and Total Tau Protein Using Immunomagnetic Reduction.Molecular neurobiology · 2025Article
- Cerebral white matter damage in patients with end-stage kidney disease associates with cognitive impairment.Clinical kidney journal · 2025Article
- Structural and microstructural changes in white and gray matter across the Alzheimer's disease continuum.Frontiers in aging neuroscience · 2025Review
- Fixel-based analysis and free-water metrics in subjective cognitive decline and cognitive impairment no dementia.Alzheimer's & dementia (Amsterdam, Netherlands)Article
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Authors and funding
13 authors.
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Abstract
backgroundSubjective cognitive decline (SCD) is an early stage of dementia linked to Alzheimer's disease pathology. White matter changes were found in SCD using diffusion tensor imaging, but there are known limitations in voxel-wise tensor-based methods. Fixel-based analysis (FBA) can help understand changes in white matter fibers and how they relate to neurodegenerative proteins and multidomain behavior data in individuals with SCD.
methodsHealthy adults with normal cognition were recruited in the Northeastern Taiwan Community Medicine Research Cohort in 2018-2022 and divided into SCD and normal control (NC). Participants underwent evaluations to assess cognitive abilities, mental states, physical activity levels, and susceptibility to fatigue. Neurodegenerative proteins were measured using an immunomagnetic reduction technique. Multi-shell diffusion MRI data were collected and analyzed using whole-brain FBA, comparing results between groups and correlating them with multidomain assessments.
resultsThe final enrollment included 33 SCD and 46 NC participants, with no significant differences in age, sex, or education between the groups. SCD had a greater fiber-bundle cross-section than NC (pFWE < 0.05) at bilateral frontal superior longitudinal fasciculus II (SLFII). These white matter changes correlate negatively with plasma Aβ42 level (r = -0.38, p = 0.01) and positively with the AD8 score for subjective cognitive complaints (r = 0.42, p = 0.004) and the Hamilton Anxiety Rating Scale score for the degree of anxiety (Ham-A, r = 0.35, p = 0.019). The dimensional analysis of FBA metrics and blood biomarkers found positive correlations of plasma neurofilament light chain with fiber density at the splenium of corpus callosum (pFWE < 0.05) and with fiber-bundle cross-section at the right thalamus (pFWE < 0.05). Further examination of how SCD grouping interacts between the correlations of FBA metrics and multidomain assessments showed interactions between the fiber density at the corpus callosum with letter-number sequencing cognitive score (pFWE < 0.01) and with fatigue to leisure activities (pFWE < 0.05).
conclusionBased on FBA, our investigation suggests white matter structural alterations in SCD. The enlargement of SLFII's fiber cross-section is linked to plasma Aβ42 and neuropsychiatric symptoms, which suggests potential early axonal dystrophy associated with Alzheimer's pathology in SCD. The splenium of the corpus callosum is also a critical region of axonal degeneration and cognitive alteration for SCD.
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