ArticleFrontiers in neuroscience2024
Greater white matter degeneration and lower structural connectivity in non-amnestic vs. amnestic Alzheimer's disease.
Article in Frontiers in neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 3 citations in OpenAlex.
- Disrupted interhemispheric communication in primary progressive aphasia: a multimodal MRI study of homotopic connectivity.NeuroImage. Clinical · 2026Article
- Semantic control across Alzheimer's disease phenotypes: cognitive mechanisms and neural correlates.Frontiers in aging neuroscience · 2026Article
- EEG-based stroke severity classification using higher-order topological features and graph convolutional networks.Frontiers in neuroscience · 2026Article
- Juvenile Myoclonic Epilepsy Imaging Endophenotypes and Relationship With Cognition and Resting-State EEG.Human brain mapping · 2025Article
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Authors and funding
13 authors at 2 institutions in 1 country.
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Abstract
Introduction: Multimodal evidence indicates Alzheimer's disease (AD) is characterized by early white matter (WM) changes that precede overt cognitive impairment. WM changes have overwhelmingly been investigated in typical, amnestic mild cognitive impairment and AD; fewer studies have addressed WM change in atypical, non-amnestic syndromes. We hypothesized each non-amnestic AD syndrome would exhibit WM differences from amnestic and other non-amnestic syndromes. Materials and methods: Participants included 45 cognitively normal (CN) individuals; 41 amnestic AD patients; and 67 patients with non-amnestic AD syndromes including logopenic-variant primary progressive aphasia (lvPPA, Results: Both amnestic and non-amnestic patients exhibited lower WM connection strength than CN participants in corpus callosum, cingulum, and inferior and superior longitudinal fasciculi. Overall, non-amnestic patients had more WM disease than amnestic patients. LvPPA patients had left-lateralized WM degeneration; PCA patients had reductions in connections to bilateral posterior parietal, occipital, and temporal areas. Topological analysis showed the non-amnestic but not the amnestic group had more connected components than controls, indicating persistently lower connectivity. Longer disease duration and cognitive impairment were associated with more connected components and fewer cycles in individuals' brain graphs. Discussion: We have previously reported syndromic differences in GM degeneration and tau accumulation between AD syndromes; here we find corresponding differences in WM tracts connecting syndrome-specific epicenters. Determining the reasons for selective WM degeneration in non-amnestic AD is a research priority that will require integration of knowledge from neuroimaging, biomarker, autopsy, and functional genetic studies. Furthermore, longitudinal studies to determine the chronology of WM vs. GM degeneration will be key to assessing evidence for WM-mediated tau spread.
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