ApoE influences regional white-matter axonal density loss in Alzheimer's disease
Open accessAbstract
Mechanisms underlying phenotypic heterogeneity in young onset Alzheimer disease (YOAD) are poorly understood. We used diffusion tensor imaging and neurite orientation dispersion and density imaging (NODDI) with tract-based spatial statistics to investigate apolipoprotein (APOE) ε4 modulation of white-matter damage in 37 patients with YOAD (22, 59% APOE ε4 positive) and 23 age-matched controls. Correlation between neurite density index (NDI) and neuropsychological performance was assessed in 4 white-matter regions of interest. White-matter disruption was more widespread in ε4+ individuals but more focal (posterior predominant) in the absence of an ε4 allele. NODDI metrics indicate fractional anisotropy changes are underpinned by combinations of axonal loss and morphological change. Regional NDI in parieto-occipital white matter correlated with visual object and spatial perception battery performance (right and left, both p = 0.02), and performance (nonverbal) intelligence (WASI matrices, right, p = 0.04). NODDI provides tissue-specific microstructural metrics of white-matter tract damage in YOAD, including NDI which correlates with focal cognitive deficits, and APOEε4 status is associated with different patterns of white-matter neurodegeneration.
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A post mortem AD study in humans revealed a decrease in NDI in the white matter of APOE4 carriers, suggesting a loss of axons.
“A post mortem AD study in humans revealed a decrease in NDI in the white matter of APOE4 carriers, suggesting a loss of axons. 56”
From Apolipoprotein ε4 exacerbates white matter impairment in a mouse model of Aβ amyloidosis by decreasing actively myelinating oligodendrocytes (2025) · cites this paper as [56]
The Results report reduced white-matter NDI in APOE ε4-positive patients with young-onset Alzheimer’s disease relative to controls, and the Discussion interprets reduced NDI as modeling axonal loss. But this was a clinical MRI study, not a post-mortem study; the Discussion says post-mortem verification is needed. (LLM, conf=0.91)
Experimental — accuracy not yet measuredODI decreases are thought to indicate loss of crossing fibers and decreased dendritic arborizations evident in various central nervous system disorders.
“ODI decreases are thought to indicate loss of crossing fibers 50,51 and decreased dendritic arborizations evident in various central nervous system disorders.45,47”
From White Matter Changes after Neurobehavioral Therapy for Functional Seizures (2023) · cites this paper as [50]
In young-onset Alzheimer's disease, NDI is reduced in the parieto-occipital WM in both ε4+ and ε4- patients relative to controls, with the reduction more widespread in ε4+ patients.
“With NODDI, (Slattery et al., 2017) reported reduced NDI in the parieto-occipital WM in both ε4+ and ε4-patients with young-onset Alzheimer's disease relative to controls, with the reduction more widespread in ε4+ patients.”
From NODDI in clinical research (2020) · cites this paper as Slattery et al., 2017
NODDI has improved sensitivity over DTI in young-onset Alzheimer's disease, with parallel reductions of NDI and ODI in some WM regions that had no observable changes in FA.
“(Slattery et al., 2017) also demonstrated improved sensitivity of NODDI over DTI, reporting parallel reductions of NDI and ODI in some WM regions that had no observable changes in FA.”
From NODDI in clinical research (2020) · cites this paper as Slattery et al., 2017
NDI of the parieto-occipital WM is correlated with visuospatial and visuoperceptual cognitive performance in young-onset Alzheimer's disease.
“NDI of the parieto-occipital WM was also correlated with visuospatial and visuoperceptual cognitive performance, a marker of parietal cortex function.”
From NODDI in clinical research (2020) · cites this paper as Slattery et al., 2017
NODDI revealed putative neuronal damage beyond limitations of DTI in diseases like Alzheimer's disease and iNPH.
“Disentangling these factors beyond NODDI is expected to further improve our understanding of the brain and diseases, just as NODDI revealed the putative neuronal damage beyond limitations of DTI in diseases like Alzheimer's disease (Slattery et al., 2017) and iNPH (Kamiya et al., 2017).”
From NODDI in clinical research (2020) · cites this paper as Slattery et al., 2017
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- Authors
- Slattery, C. F., Zhang, J., Paterson, R. W., Foulkes, A. J. M., Carton, A., Macpherson, K., Mancini, L., Thomas, D. L., Modat, M., Toussaint, N., Cash, D. M., Thornton, J. S., Henley, S. M. D., Crutch, S. J., Alexander, D. C., Ourselin, S., Fox, N. C., Zhang, H., & Schott, J. M.
- Affiliations
- UCL Queen Square Institute of Neurology (GB)
- University College London (GB)
- University College London Hospitals NHS Foundation Trust (GB)
- Corresponding author
- Slattery, Catherine F.
- ORCID
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2017-09
- Volume
- 57
- Pages
- 8-17
- ISSN
- 0197-4580 (ISSN-L)
- PMC
- PMC5538347
- OpenAlex
- W2610402968
- Cited by
- 102
- References
- 61
- Citations by year
- 2026: 4 · 2025: 11 · 2024: 12 · 2023: 15 · 2022: 11 · 2021: 10 · 2020: 9 · 2019: 15 · 2018: 14 · 2017: 1
- FWCI
- 8.19
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Neurobiology of Aging (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Research Portal (King's College London) (submittedVersion, other-oa)
- Funders
- Alzheimer's Society (ARUK-PG2014-1946, AS‐PG‐15‐025)
- Alzheimer Society (AS-PG-15-025)
- National Institute for Health and Care Research (CL-2016-18-004, NF-SI-0513-10134, BRC10269, ES/L001810/1, EP/J020990/1)
- Brain Research Trust
- University College London (EP/J020990/1, EP/H046410/1, PR/ylr/18575)
- European Commission (EU-FP7, 601055, 666992, ICT-2011, FP7-ICT-2011-9, FP7‐ICT‐2011)
- Wolfson Foundation (PR/ylr/18575)
- China Scholarship Council
- University College London Hospitals NHS Foundation Trust
- Medical Research Council (MR/L023784/2, CSUB19166, MR/M023664/1, MR/J01107X/, MR/M009106/1, FP7-ICT-2011-9-601055, MR/J01107X/1)
- Engineering and Physical Sciences Research Council (EP/L022680/1, EP/H046410, H046410, MR/J01107X/1, EP/J020990/1, EP/M020533/1, EP/N018702/1, EP/G007748/1, EP/M006093/1, EP/H046410/1, L022680, FP7-ICT-2011-9-601055, J020990, M006093)
- Economic and Social Research Council (ES/L001810/1)
- FP7 Information and Communication Technologies (FP7‐ICT‐2011‐9‐601055)
- Topics
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Advanced Neuroimaging Techniques and Applications
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- APOE ε4, early-onset Alzheimer's disease, axonal loss, neurite density index, NODDI, fractional anisotropy, white matter microstructure, cognitive impairment, visual object recognition, spatial perception, nonverbal intelligence, phenotypic heterogeneity
- MeSH terms
- Aged, Alzheimer Disease, Axons, Female, Humans, Intelligence, Male, Middle Aged, Phenotype, Neurites, Apolipoprotein E4, Diffusion Tensor Imaging, Genetic Association Studies, Spatial Processing, White Matter
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