Cited by 252Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsAdvanced Neuroimaging Techniques and Applications

The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.

Association of Amyloid Pathology With Myelin Alteration in Preclinical Alzheimer Disease

Open access

Dean, Douglas C., Hurley, Samuel A., Kecskemeti, Steven R., O’Grady, J. Patrick, Canda, Cristybelle, Davenport-Sis, Nancy J., Carlsson, Cynthia M., Zetterberg, Henrik, Blennow, Kaj, Asthana, Sanjay, Sager, Mark A., Johnson, Sterling C., Alexander, Andrew L., Bendlin, Barbara B.·2017·JAMA Neurology

DOI 10.1001/jamaneurol.2016.3232PMC PMC5195903

Open this paper in CoChat — free account

Abstract

IMPORTANCE: The accumulation of aggregated β-amyloid and tau proteins into plaques and tangles is a central feature of Alzheimer disease (AD). While plaque and tangle accumulation likely contributes to neuron and synapse loss, disease-related changes to oligodendrocytes and myelin are also suspected of playing a role in development of AD dementia. Still, to our knowledge, little is known about AD-related myelin changes, and even when present, they are often regarded as secondary to concomitant arteriosclerosis or related to aging. OBJECTIVE: To assess associations between hallmark AD pathology and novel quantitative neuroimaging markers while being sensitive to white matter myelin content. DESIGN, SETTING, AND PARTICIPANTS: Magnetic resonance imaging was performed at an academic research neuroimaging center on a cohort of 71 cognitively asymptomatic adults enriched for AD risk. Lumbar punctures were performed and assayed for cerebrospinal fluid (CSF) biomarkers of AD pathology, including β-amyloid 42, total tau protein, phosphorylated tau 181, and soluble amyloid precursor protein. We measured whole-brain longitudinal and transverse relaxation rates as well as the myelin water fraction from each of these individuals. MAIN OUTCOMES AND MEASURES: Automated brain mapping algorithms and statistical models were used to evaluate the relationships between age, CSF biomarkers of AD pathology, and quantitative magnetic resonance imaging relaxometry measures, including the longitudinal and transverse relaxation rates and the myelin water fraction. RESULTS: The mean (SD) age for the 19 male participants and 52 female participants in the study was 61.6 (6.4) years. Widespread age-related changes to myelin were observed across the brain, particularly in late myelinating brain regions such as frontal white matter and the genu of the corpus callosum. Quantitative relaxometry measures were negatively associated with levels of CSF biomarkers across brain white matter and in areas preferentially affected in AD. Furthermore, significant age-by-biomarker interactions were observed between myelin water fraction and phosphorylated tau 181/β-amyloid 42, suggesting that phosphorylated tau 181/β-amyloid 42 levels modulate age-related changes in myelin water fraction. CONCLUSIONS AND RELEVANCE: These findings suggest amyloid pathologies significantly influence white matter and that these abnormalities may signify an early feature of the disease process. We expect that clarifying the nature of myelin damage in preclinical AD may be informative on the disease's course and lead to new markers of efficacy for prevention and treatment trials.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

Integrity signals

Registry

Crossref · 10.1001/jamaneurol.2016.3232

Cites

44 of 44 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

R: A Language and Environment for Statistical Computing
R Core Team (2000) · doi:10.32614/r.manuals · Cited by 355,893
Controlling the False Discovery Rate: A Practical and Powerful Approach to Multiple Testing
Benjamini, Y., & Hochberg, Y. (1995) · Journal of the Royal Statistical Society Series B: Statistical Methodology · doi:10.1111/j.2517-6161.1995.tb02031.x · Cited by 109,482
“Mini-mental state”
Folstein, M. F., Folstein, S. E., & McHugh, P. R. (1975) · Journal of Psychiatric Research · doi:10.1016/0022-3956(75)90026-6 · Cited by 88,282 · cited 2×
“Cardiovascular health was assessed using the Framingham cardiovascular risk score and further inclusion was limited to participants who scored 27 or greater on the Mini-Mental State Examination.(19) Written informed consent was obtained from all study participants and the study procedureswereperformedunder guidelines…”
[Japanese version of the Neuropsychiatric Inventory--a scoring system for neuropsychiatric disturbance in dementia patients].
Hirono, N., Mori, E., Ikejiri, Y., Imamura, T., Shimomura, T., Hashimoto, M., Yamashita, H., & Ikeda, M. (1997) · PubMed · Cited by 21,012
Special Care Units and Traditional Care in Dementia: Relationship with Behavior, Cognition, Functional Status and Quality of Life - A Review
Kok, J. S., Berg, I. J., & Scherder, E. J. A. (2013) · Dementia and Geriatric Cognitive Disorders Extra · doi:10.1159/000353441 · Cited by 20,589
Older Adults' Reasons for Using Technology while Aging in Place
Peek, S. T. M., Luijkx, K. G., Rijnaard, M. D., Nieboer, M. E., van der Voort, C. S., Aarts, S., van Hoof, J., Vrijhoef, H. J., & Wouters, E. (2015) · Gerontology · doi:10.1159/000430949 · Cited by 19,852
Sensitivity and False Alarm Rate of a Fall Sensor in Long-Term Fall Detection in the Elderly
Kangas, M., Korpelainen, R., Vikman, I., Nyberg, L., & Jämsä, T. J. (2014) · Gerontology · doi:10.1159/000362720 · Cited by 19,007
The Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics
Hardy, J., & Selkoe, D. J. (2002) · Science · doi:10.1126/science.1072994 · Cited by 13,864
Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D. (2013) · Neurodegenerative Diseases · doi:10.1159/000337230 · Cited by 10,359
Brain development during childhood and adolescence: a longitudinal MRI study
Giedd, J. N., Blumenthal, J., Jeffries, N. O., Castellanos, F. X., Liu, H., Zijdenbos, A., Paus, T., Evans, A. C., & Rapoport, J. L. (1999) · Nature Neuroscience · doi:10.1038/13158 · Cited by 5,552

Flagged first, then by citations

Show all 44 references

Sorted by citations

Items 201–252 of 252

TREM2 impacts brain microglia, oligodendrocytes and endothelial co-expression modules revealing genes and pathways important in Alzheimer’s diseasePreprint
Carbajosa, G., Malki, K., Lawless, N., Wang, H., Ryder, J. W., Wozniak, E., Wood, K., Mein, C. A., Hodgkinson, A., Dobson, R., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.07.16.452732 · Cited by 1
“…dysfunction are a recognised feature of AD, even preceding clinical diagnosis (Gao et al., 2011; Benitez et al., 2014; Caso et al., 2015; Dean et al., 2017; Nasrabady et al., 2018; Mathys et al., 2019), although the underlying disease mechanisms in AD and its relationship with cells…”
Background
Transcriptional Coordination between Mitochondrial and Nuclear Genomes for Oxidative Phosphorylation Is Disrupted in Alzheimer’s BrainPreprint
Shang, Y., Yin, F., & Brinton, R. D. (2022) · Research Square · doi:10.21203/rs.3.rs-2122232/v1 · Cited by 1
Multimodal imaging of microstructural cerebral changes and loss of synaptic density in Alzheimer’s diseasePreprint
Moallemian, S., Salmon, É., Bahri, M. A., Beliy, N., Delhaye, E., Balteau, E., Phillips, C. L. M., & Bastin, C. (2023) · medRxiv · doi:10.1101/2023.04.14.23288516 · Cited by 1
“It is recognized that AD pathological processes unfold decades before the emergence of clinical signs of cognitive decline (Dean et al., 2017; Gonneaud and Chételat, 2018; Tan et al., 2014).”
Background
BrainVAE: Exploring the role of white matter BOLD in preclinical Alzheimer’s disease classificationPreprint
Li, Y., Xu, L., Zuo, L., Chang, Y., Ding, Z., Anderson, A. W., Schilling, K. G., Gore, J. C., Gao, Y., & Initiative, T. A. D. N. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.05.07.652697 · Cited by 1
Fus depleted oligodendrocytes reduce neuronal damage and attenuate AD progression in the App NL-G-F mousePreprint
Tung, T.-H., Babu, S., Tang, X., Sciutto, A., Romer, M. A., Racha, P., Fiesler, V. M., Saha, A., Saito, T., Saido, T. C., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.11.24.689041 · Cited by 1
Kv1.3 inhibition alleviates neuropathology via neuroinflammatory and resilience pathways in a mouse model of Aβ pathologyPreprint
Kumari, R., Bowen, C. A., Srivastava, U., Brandelli, A. D., Kumar, P., Kour, D., Malepati, S., Jang, W. E., Bromwich, M., Zeng, H., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2025.12.25.696456 · Cited by 2
Relationship between cerebral amyloid burden and cerebral microstructure measured by quantitative MRI in healthy aging
González, P. V., Chylinski, D., Narbutas, J., Egroo, M. V., Cerasuolo, M., Besson, G., Ghaemmaghami, P., Collette, F., Salmon, É., Baquero, K., et al. (2018) · Frontiers in Neuroscience · doi:10.3389/conf.fnins.2018.95.00056
“As expected (Dean et al., 2017), we observed a link between increased amyloid burden and increased iron content in frontal areas mainly but also in parietal and occipital areas.”
Background
Estudo da correlação entre a razão de transferência de magnetização e a volumetria em pacientes com lesão axonal traumática
Macruz, F. (2019) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/t.5.2019.tde-07052019-112605
The dark side of the brain, myelinating glia in central and peripheral nervous systems.
Chrast, R., & Castelo-Branco, G. (2021) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2021.05.006
¿Cómo contabilizar?: contabilidad de la liquidación de una empresa
Viguera, M. G. (2004) · Técnica contable
White matter integrity of the frontal brain and its relevance for catatonia and executive function
Arinrad, S. (2021) · eDiss (Georg-August-Universität Göttingen) · doi:10.53846/goediss-8974
La mielinización como un factor modulador de los circuitos de memoria
García-Montes, M. E., & Crespo, I. (2023) · Revista de Neurología · doi:10.33588/rn.7603.2022325 · Cited by 1
Rapid whole-brain high-resolution myelin water fraction mapping from extremely under-sampled magnetic resonance imaging data using deep neural networkPreprint
Gong, Z., Khattar, N., Kiely, M., Triebswetter, C., & Bouhrara, M. (2023) · medRxiv · doi:10.1101/2023.03.07.23286946
The Protective Effects of Flavonoids from Scutellaria Baicalensis Georgi Stems and Leaves on Oligodendrocyte Damage Induced by Aβ1-42
Song, T., Yao, Y., & Yazhen, S. (2024) · Pharmacology & Pharmacy · doi:10.4236/pp.2024.151001 · Cited by 1
The contribution of oligodendrocytes to amyloid and tau pathologies in mouse models of Alzheimer’s disease
Sasmita, A. O. (2024) · eDiss (Georg-August-Universität Göttingen) · doi:10.53846/goediss-10403
Amyloid β oligomers dysregulate oligodendrocyte differentiation and myelination via PKC in the zebrafish spinal cordPreprint
Balantzategi, U., Gaminde‐Blasco, A., Bayón‐Cordero, L., Sánchez‐Gómez, M. V., Zugaza, J. L., Appel, B., & Alberdi, E. M. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.06.10.598246
“Only a few studies have investigated the role of OLs in AD and proposed Aβ as a candidate for promoting white matter dysfunction (Dean et al., 2017; Selkoe & Hardy, 2016), but the mechanisms remain unclear.”
Background
Role of individual structural and functional elements of myelin in Parkinson’s disease
Shulskaya, M. V., Slominsky, P. A., Shadrina, M. I., & Alieva, A. K. (2024) · Журнал высшей нервной деятельности им И П Павлова · doi:10.31857/s0044467724030011
Myelin Genes Whose Expression Is Linked with Parkinson’s Disease
Shulskaya, M. V., Slominsky, P. A., Shadrina, M. I., & Alieva, A. K. (2024) · Neuroscience and Behavioral Physiology · doi:10.1007/s11055-024-01733-4
“For example, in Alzheimer’s disease, myelin loss by axons occurs at the early clinical stages of the disease, long before the ﬁ rst symptoms appear [Altevogt et al., 2002; Dean et al., 2017; Papuc and Rejdak, 2020].”
Mapping Amyloid Networks in Alzheimer’s Disease: A High-Order ICA Approach to Gray and White Matter PathologyPreprint
Khasayeva, N., Jensen, K. M., Eierud, C., Petropoulos, H., Levey, A. I., Lah, J. J., Luo, R., Premi, E., Borroni, B., Chen, J., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.03.21.644614
“…studies have shown that white matter (WM) degeneration may be an integral component of AD’s pathological cascade rather than a mere comorbidity [7], with changes such as axonal myelin degradation emerging early in the disease course, even before significant GM atrophy becomes evident [8].”
[18F]Florbetapir Pet Uptake Differences in White Matter Across the Alzheimer's Disease Continuum: From Cognitively Normal to MCI and Dementia
Khasayeva, N., Jensen, K. M., Eierud, C., Petropoulos, H., Calhoun, V. D., & Iraji, A. (2025) · IEEE International Symposium on Biomedical Imaging (ISBI) · doi:10.1109/isbi60581.2025.10981043
Multiscale analysis of myelin alterations in skin biopsies from synucleinopathiesPreprint
Fabrizio, M. D., van der Gaag, B., Terzi, M., Aaron, E., Steerenberg, N. B., Bol, J. G. J. M., van de Berg, W. D. J., Stahlberg, H., & Lewis, A. J. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.05.15.654285
“Macroscopic-scale imaging and omics studies on myelin alterations in the central nervous system have shown axonal and myelin abnormalities to play a crucial role in the development of synucleinopathies 11–17 and other neurodegenerative diseases 18–21 .”
An eigenfunction approach to conversion of the Laplace transform of point masses on the real line to the Fourier domain
Mckenna, M. E., Mhaskar, H. N., & Spencer, R. G. S. (2025) · Applied and Computational Harmonic Analysis · doi:10.1016/j.acha.2025.101776
“MWF mapping is applied widely in the investigation of cognitive decline [16, 31], Alzheimer’s disease [24, 40], neurodegenerative diseases such as multiple sclerosis [43], and in studies of normative aging that are characterized by or exhibit myelin loss [10, 11, 12, 13, 16, 27, 43, 55, 69].”
APOE4 carriership status influences [11C]PiB white matter retention in cognitively healthy older adults
Tato-Fernández, C., Ekblad, L. L., Bucci, M., Tuisku, J., Parkkola, R. K., Helin, S., Rinne, J. O., & Snellman, A. (2025) · Neurobiology of Disease · doi:10.1016/j.nbd.2025.107140
Investigating urea is an ideal additive to the Accu-OptiClearing delipidation cocktail
Lai, M. S., Chick, W. M., Law, R. M. H., & Chang, R. C. (2025) · Scientific Reports · doi:10.1038/s41598-025-18231-3
Additional file 3 of Opposing effects of apoE2 and apoE4 on microglial activation and lipid metabolism in response to demyelination
Wang, N., Wang, M., Jeevaratnam, S., Rosenberg, C. L., Ikezu, T. C., Shue, F., Doss, S. V., Alnobani, A., Martens, Y. A., Wren, M. C., et al. (2022) · Figshare · doi:10.6084/m9.figshare.21622301
Additional file 4 of Opposing effects of apoE2 and apoE4 on microglial activation and lipid metabolism in response to demyelination
Wang, N., Wang, M., Jeevaratnam, S., Rosenberg, C. L., Ikezu, T. C., Shue, F., Doss, S. V., Alnobani, A., Martens, Y. A., Wren, M. C., et al. (2022) · Figshare · doi:10.6084/m9.figshare.21622304
Additional file 5 of Opposing effects of apoE2 and apoE4 on microglial activation and lipid metabolism in response to demyelination
Wang, N., Wang, M., Jeevaratnam, S., Rosenberg, C. L., Ikezu, T. C., Shue, F., Doss, S. V., Alnobani, A., Martens, Y. A., Wren, M. C., et al. (2022) · Figshare · doi:10.6084/m9.figshare.21622307
Additional file 6 of Opposing effects of apoE2 and apoE4 on microglial activation and lipid metabolism in response to demyelination
Wang, N., Wang, M., Jeevaratnam, S., Rosenberg, C. L., Ikezu, T. C., Shue, F., Doss, S. V., Alnobani, A., Martens, Y. A., Wren, M. C., et al. (2022) · Figshare · doi:10.6084/m9.figshare.21622310
Additional file 2 of Opposing effects of apoE2 and apoE4 on microglial activation and lipid metabolism in response to demyelination
Wang, N., Wang, M., Jeevaratnam, S., Rosenberg, C. L., Ikezu, T. C., Shue, F., Doss, S. V., Alnobani, A., Martens, Y. A., Wren, M. C., et al. (2022) · Figshare · doi:10.6084/m9.figshare.21622298
Additional file 1 of Opposing effects of apoE2 and apoE4 on microglial activation and lipid metabolism in response to demyelination
Wang, N., Wang, M., Jeevaratnam, S., Rosenberg, C. L., Ikezu, T. C., Shue, F., Doss, S. V., Alnobani, A., Martens, Y. A., Wren, M. C., et al. (2022) · Figshare · doi:10.6084/m9.figshare.21622295
Prediction of Single-Frequency 2D Viscoelastic Brain White Matter Properties Using an Ensemble of Forward Machine Learning Regression Models
Agarwal, M., & Pelegri, A. A. (2026) · Journal of Engineering and Science in Medical Diagnostics and Therapy · doi:10.1115/1.4071025
Motion-robust myelin imaging in MRI using 1D projection gating
Park, J., Sedaghat, S., Oguz, K., Jung, Y., Fu, E., Wang, N., Liu, F., & Jang, H. (2026) · Scientific Reports · doi:10.1038/s41598-026-39238-4
CSF Proteomic Profiles Associated With White Matter Integrity in Cognitively Normal Older Adults With and Without Amyloid Pathology
Lorenzini, L., Tranfa, M., ten Kate, M., den Braber, A., Vermunt, L., Duits, F. H., Lageman, S. B., de Leeuw, D. M., Teunissen, C. E., Garbarino, S., et al. (2026) · Neurology · doi:10.1212/wnl.0000000000214675
Rôle de la voie de signalisation Sonic Hedgehog dans les cellules Glast positives du cerveau de souris adulte
Tirou, L. (2020) · theses.fr (ABES) · doi:10.70675/5a9de569zf953z4f2cz9ccaz89ba17ab8490
Le métabolisme astrocytaire de la L-sérine et ses implications dans la maladie d'Alzheimer : une potentielle approche thérapeutique
Vigneron, P.-A. (2020) · theses.fr (ABES) · doi:10.70675/dbc75a2ez00c0z4ac9z8ac7zc8e17f8fe480
Hétérogénéité de la réactivité astrocytaire dans la maladie d'Alzheimer
Guillemaud, O. (2020) · theses.fr (ABES) · doi:10.70675/038d98c5z55ccz4754z9af9z417e3826d282
Myelin alterations in early stages of Alzheimer's disease and preclinical assessment of the protective and therapeutic potential of neurosteroid 3α-O-allyl-allopregnanolone
Okechukwu, N. G. (2023) · theses.fr (ABES) · doi:10.70675/ec1ca2c3zfad7z48b7zba08z6bb3bb44334f
Associations of plasma phosphorylated tau217 with cognitive impairment and brain microstructural alterations in Alzheimer's disease
Rivas‐Fernández, M. Á., Basanta-Torres, S., Lindı́n, M., Zurrón, M., Dı́az, F., Pereiro, A. X., Lojo‐Seoane, C., Rodríguez‐Pérez, A. I., Labandeira-García, J. L., & Galdo‐Álvarez, S. (2026) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.70333
“15,16 ReducedMWFhasalsobeenrelatedtoplasmabiomarkersofastroglial activation.”
White matter 18F-florbetapir retention predicts cognitive decline and treatment response in Alzheimer’s disease
Lin, H., Zhang, Y., Ni, R., Wang, M., Men, J., Ge, J., Lu, J., Wang, J., Zhang, H., Yang, Y., et al. (2026) · Alzheimer s Research & Therapy · doi:10.1186/s13195-026-02098-1
“Survival analyses confirmed that elevated baseline NAWM FBP retention was a potent predictor of clinical progression, with hazard ratios comparable to those of established CSF biomarkers [42] and plasma p-tau217 [43, 44].”
Metabolic profile association with white matter hyperintensity in patients with mild cognitive impairment
Ariaei, A., Zamiri, R., Ghasemi, A., Rezayani, B., Rezayani, S., Ezatpour, A., Farshidi, N., Sheikhi, E. A., & Roghanian, A. (2026) · IBRO Neuroscience Reports · doi:10.1016/j.ibneur.2026.06.003
“Moreover, demyelination, loss of oligodendrocytes, and axonal damage could be classified as WMH (Dean et al., 2017; Gouw et al., 2011).”
Plasmalogens in Alzheimer’s Disease: A Narrative Review of Dietary Sources, Metabolism, and Neuroprotective Mechanisms
Zhang, Y., Chen, J., Jiang, J., Yang, N., Guo, S., Gao, F., Zhang, C., Weng, Q., Xiao, H., Luo, J., et al. (2026) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.6c05250
Amyloid-β1-42 oligomers compromise oligodendrocyte precursor cells and disrupt blood–brain barrier integrity in vitro
Toyokawa, M., Yasuda, K., Kikuya, A., Asada‐Utsugi, M., Hida, M., Nakamura, Y., Yanagida, N., Toda, S., Kaji, S., Kinoshita, Y., et al. (2026) · Brain Research · doi:10.1016/j.brainres.2026.150436
Role of E3 Ubiquitin Ligases in Oligodendrocyte Health and Disease
Mabb, A. M., Pyaram, D. N., & Samanta, J. (2026) · ASN NEURO · doi:10.1080/17590914.2026.2682220
“…studies in human AD and AD mouse models show changes in OL density and myelin integrity alongside myelin injury that precede A b and tau pathology (Behrendt et al., 2013; Dean et al., 2017), indicating that dysfunctional OLs may more directly contribute to AD pathogenesis (Jian et al., 2026).”
White matter abnormalities in Alzheimer's disease: Implications for pathophysiology, diagnosis, and treatment
Chen, Z., Yang, K., Lin, F., Tang, W., Shi, Y., Zhou, S., Liu, J. S., & You, Y. (2026) · Ageing Research Reviews · doi:10.1016/j.arr.2026.103229
Plaque-associated oligodendrocyte proteostatic failure underlies myelin loss in Alzheimer’s diseasePreprint
Shin, J., Joshi, N., Miller, B., Vellarikkal, S., Huang, J., Wu, F., Cui, Y., Murali, A., Chason, J., Campbell, C. S., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.07.08.737318
Sequential associations of myelin dysfunction with Aβ and Tau pathology in Alzheimer's disease: a dynamic myelin perturbation
Wen, J., Lan, G., Fu, Y., Jiang, W., Xu, B., Zhang, J., & Initiative, A. D. N. (2026) · Alzheimer s Research & Therapy · doi:10.1186/s13195-026-02139-9
“Recent neuroimaging studies have increasingly highlighted the frequent occurrence of macrostructural and microstructural white matter (WM) abnormalities in AD, with the loss of myelin integrity emerging as one of the most prominent pathological features [3, 4].”
Amyloid‐β–Related Cortical Susceptibility Alterations in Individuals Under Assessment for Alzheimer's Disease: A χ‐Separation Study
Tatekawa, H., Oura, T., Takeda, A., Omori, A., Atsukawa, N., Matsushita, S., Horiuchi, D., Takita, H., Mitsuyama, Y., Ban, Y., et al. (2026) · Journal of Magnetic Resonance Imaging · doi:10.1002/jmri.70458
Translational imaging evidence for rapid reversal of amyloid and myelin pathology following deep cervical lymphatic–venous anastomosis in Alzheimer's disease
Wang, X., Liu, Y., Liu, J., Wang, R., Zheng, J., Deng, Z., Song, K., Zhang, D., Wang, C., Zhu, K., et al. (2026) · Nuclear Medicine and Biology · doi:10.1016/j.nucmedbio.2026.109675
Myelin maturation failure and oligodendrocyte precursor loss underlie default mode network disruption in a humanized APP knock-in model of Alzheimer’s diseasePreprint
Unaran, E., Adebiyi, O. E., Krishnan, M. R., Bussey, T. J., Saksida, L. M., Prado, M. A., Prado, V. F., & Menon, R. S. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.08.12.744193
When myelin breaks, tau aggregates — a new perspective on Alzheimer's disease
Tiane, A., van den Hove, D., & Vanmierlo, T. (2026) · Alzheimer s & Dementia · doi:10.1002/alz.71774
“32–34 These observations argue against a model in which microglia-driven myelin loss is merely a downstream consequence of tau aggregation and instead support the notion that myelin damage may represent an early and upstream event in the disease process.”
T1 mapping in Alzheimer’s disease: a quantitative MRI study with amyloid-PET correlation
Gualco, L., Montobbio, N., Losa, M., Costagli, M., Massa, F., Orso, B., Argenti, L., Peira, E., Chincarini, A., Morbelli, S. D., et al. (2026) · European Radiology Experimental · doi:10.1186/s41747-026-00792-1
“A study by Dean et al showed that core CSF AD biomarkers are associated with lower longitudinal relaxation rates in the WM in AD, likely re ﬂ ecting myelin loss [24], and similar changes could involve intracortical myelinated ﬁ bers.”
Beyond Histamine Blockade: Clemastine Fumarate as a Promoter of Myelin Regeneration, Inflammatory Regulation, and Neuroimmune Modulation in CNS Disorders
Singh, R. K., Banerjee, C., & Mehan, S. (2026) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-026-10321-x
“Early AD is associated with reduced oligodendrocyte numbers, depletion of OPCs, impaired oligodendrocyte maturation, decreased MBP, and accumulation of degraded MBP indicating defective myelin maintenance (Dean et al., 2017).”

Authors: Dean, D. C., Hurley, S. A., Kecskemeti, S. R., O’Grady, J. P., Canda, C., Davenport-Sis, N. J., Carlsson, C. M., Zetterberg, H., Blennow, K., Asthana, S., Sager, M. A., Johnson, S. C., Alexander, A. L., & Bendlin, B. B.
Affiliations: University of Wisconsin–Madison (US)
University of Oxford (GB)
Alzheimer Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison4Wisconsin Alzheimer Institute, University of Wisconsin School of Medicine and Public Health, Madison
UCL Queen Square Institute of Neurology (GB)
University of Gothenburg (SE)
Corresponding author: Dean, Douglas C.
ORCID: Dean, Douglas C.
Hurley, Samuel A.
Kecskemeti, Steven R.
Carlsson, Cynthia M.
Zetterberg, Henrik
Blennow, Kaj
Asthana, Sanjay
Johnson, Sterling C.
Alexander, Andrew L.
Bendlin, Barbara B.
Venue: JAMA Neurology
Publisher: American Medical Association (AMA)
Published: 2017-01-01
Volume: 74
Issue: 1
Pages: 41
ISSN: 2168-6149 (ISSN-L)
DOI: 10.1001/jamaneurol.2016.3232
PMC: PMC5195903
OpenAlex: W2554389950
Cited by: 252
References: 44
Citations by year: 2026: 26 · 2025: 40 · 2024: 33 · 2023: 36 · 2022: 34 · 2021: 17 · 2020: 19 · 2019: 16 · 2018: 17 · 2017: 13
FWCI: 13.62
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: JAMA Neurology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
UCL Discovery (University College London) (submittedVersion)
Funders: National Institutes of Health (UL1TR000427)
National Institute on Aging (R01AG037639, P50AG033514, R01AG021155, R01AG027161, R56AG037639)
National Center for Research Resources (UL1RR025011)
National Center for Advancing Translational Sciences
Eunice Kennedy Shriver National Institute of Child Health and Human Development (R21HD078119, P30HD003352, T32HD007489)
Topics: Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Advanced Neuroimaging Techniques and Applications
Keywords: preclinical Alzheimer's disease, amyloid pathology, white matter, myelin water fraction, relaxometry, cerebrospinal fluid biomarkers, phosphorylated tau 181, amyloid-beta 42, tau protein, corpus callosum, neuroimaging biomarkers
MeSH terms: Age Factors, Aged, Alzheimer Disease, Apolipoproteins E, Female, Humans, Image Processing, Computer-Assisted, Magnetic Resonance Imaging, Male, Middle Aged, Myelin Sheath, Peptide Fragments, Phosphorylation, Statistics as Topic, Water, Cohort Studies, Biomarkers, Amyloid beta-Peptides, tau Proteins, Disease Progression, Plaque, Amyloid

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

Association of Amyloid Pathology With Myelin Alteration in Preclinical Alzheimer Disease

Abstract

Overview

Integrity signals

Verification

Claims the paper makes

Claims other papers make about this one

Self-check

Citations

Cites

Cited by

Related

Metadata

Record

About these checks