The DOI matches its Crossref record; 213 of the 213 references it cites were found in a registry or an index.
Imaging the evolution and pathophysiology of Alzheimer disease
Open accessAbstract
Technologies for imaging the pathophysiology of Alzheimer disease (AD) now permit studies of the relationships between the two major proteins deposited in this disease - amyloid-β (Aβ) and tau - and their effects on measures of neurodegeneration and cognition in humans. Deposition of Aβ in the medial parietal cortex appears to be the first stage in the development of AD, although tau aggregates in the medial temporal lobe (MTL) precede Aβ deposition in cognitively healthy older people. Whether aggregation of tau in the MTL is the first stage in AD or a fairly benign phenomenon that may be transformed and spread in the presence of Aβ is a major unresolved question. Despite a strong link between Aβ and tau, the relationship between Aβ and neurodegeneration is weak; rather, it is tau that is associated with brain atrophy and hypometabolism, which, in turn, are related to cognition. Although there is support for an interaction between Aβ and tau resulting in neurodegeneration that leads to dementia, the unknown nature of this interaction, the strikingly different patterns of brain Aβ and tau deposition and the appearance of neurodegeneration in the absence of Aβ and tau are challenges to this model that ultimately must be explained.
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“These and other studies 13,24,133,134 strongly support the concept of AD as being an amyloid-provoked, or facilitated, tauopathy, although there is also evidence that both pathologies act in synergy 135 .”
From The amyloid hypothesis in Alzheimer disease: new insights from new therapeutics (2022) · cites this paper as [13]
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Items 201–213 of 213
Adams, J. N., Lockhart, S. N., Li, L., & Jagust, W. J. (2018) · Cerebral Cortex · doi:10.1093/cercor/bhy078 · Cited by 90
Self-citationEffect of intellectual enrichment on AD biomarker trajectories
Vemuri, P., Lesnick, T. G., Przybelski, S. A., Knopman, D. S., Machulda, M. M., Lowe, V. J., Mielke, M. M., Roberts, R. O., Gunter, J. L., Senjem, M. L., et al. (2016) · Neurology · doi:10.1212/wnl.0000000000002490 · Cited by 88
Effects of beta-amyloid accumulation on neural function during encoding across the adult lifespan
Kennedy, K. M., Rodrigue, K. M., Devous, M. D., Hebrank, A. C., Bischof, G. N., & Park, D. C. (2012) · NeuroImage · doi:10.1016/j.neuroimage.2012.03.077 · Cited by 87
The association between tau PET and retrospective cortical thinning in clinically normal elderly
LaPoint, M. R., Chhatwal, J. P., Sepulcre, J., Johnson, K. A., Sperling, R. A., & Schultz, A. P. (2017) · NeuroImage · doi:10.1016/j.neuroimage.2017.05.049 · Cited by 84
Association of hypometabolism and amyloid levels in aging, normal subjects
Lowe, V. J., Weigand, S. D., Senjem, M. L., Vemuri, P., Jordan, L. G., Kantarci, K., Boeve, B. F., Jack, C. R., Knopman, D. S., & Petersen, R. C. (2014) · Neurology · doi:10.1212/wnl.0000000000000467 · Cited by 83
Gray matter maturation and cognition in children with different APOE ε genotypes
Chang, L., Douet, V., Bloss, C. S., Lee, K., Pritchett, A., Jernigan, T. L., Akshoomoff, N. A., Murray, S. S., Frazier, J. A., Kennedy, D. N., et al. (2016) · Neurology · doi:10.1212/wnl.0000000000002939 · Cited by 81
Amyloid and tau PET demonstrate region-specific associations in normal older people
Lockhart, S. N., Schöll, M., Baker, S. L., Ayakta, N., Swinnerton, K. N., Bell, R. K., Mellinger, T. J., Shah, V. D., O’Neil, J. P., Janabi, M., et al. (2017) · NeuroImage · doi:10.1016/j.neuroimage.2017.02.051 · Cited by 80
Self-citationChanges in Aβ biomarkers and associations with APOE genotype in 2 longitudinal cohorts
Resnick, S. M., Bilgel, M., Moghekar, A., An, Y., Cai, Q., Wang, M., Thambisetty, M., Prince, J. L., Zhou, Y., Soldan, A., et al. (2015) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2015.04.001 · Cited by 65
Mormino, E. C., Papp, K. V., Rentz, D. M., Schultz, A. P., LaPoint, M. R., Amariglio, R. E., Hanseeuw, B. J., Marshall, G. A., Hedden, T., Johnson, K. A., et al. (2016) · JAMA Neurology · doi:10.1001/jamaneurol.2016.2237 · Cited by 63
Gautam, P., Cherbuin, N., Sachdev, P. S., Wen, W. X., & Anstey, K. J. (2011) · NeuroImage · doi:10.1016/j.neuroimage.2011.01.015 · Cited by 37
Physical Activity and AD-Related Pathology—Reply
Landau, S. M., & Jagust, W. J. (2012) · Archives of Neurology · doi:10.1001/archneurol.2012.510 · Cited by 18
Self-citationSolano (2000) · doi:10.1002/1531-8249(200002)47:2 · Cited by 3
Price (1999) · doi:10.1002/1531-8249(199903)45:3
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Hallmarks of neurodegenerative diseases
Wilson, D. M., Cookson, M. R., Van Den Bosch, L., Zetterberg, H., Holtzman, D. M., & Dewachter, I. (2023) · Cell · doi:10.1016/j.cell.2022.12.032 · Cited by 1,789
Synergy between amyloid-β and tau in Alzheimer’s disease
Busche, M. A., & Hyman, B. T. (2020) · Nature Neuroscience · doi:10.1038/s41593-020-0687-6 · Cited by 1,242
López, J. A., González, H. M., & Léger, G. C. (2019) · Handbook of clinical neurology · doi:10.1016/b978-0-12-804766-8.00013-3 · Cited by 884
The amyloid hypothesis in Alzheimer disease: new insights from new therapeutics
Karran, E., & De Strooper, B. (2022) · Nature Reviews Drug Discovery · doi:10.1038/s41573-022-00391-w · Cited by 742
The Role of NMDA Receptors in Alzheimer’s Disease
Liu, J., Chang, L., Song, Y., Li, H., & Wu, Y. (2019) · Frontiers in Neuroscience · doi:10.3389/fnins.2019.00043 · Cited by 535
Metadata
- Authors
- Jagust, W.
- Affiliations
- Lawrence Berkeley National Laboratory (US)
- Corresponding author
- Jagust, William
- ORCID
- Jagust, William
- Venue
- Nature Reviews Neuroscience
- Published
- 2018-09-28
- Volume
- 19
- Issue
- 11
- Pages
- 687-700
- ISSN
- 1471-003X (ISSN-L)
- 1471-0048
- PMC
- PMC7032048
- OpenAlex
- W2894357926
- Cited by
- 604
- References
- 213
- Citations by year
- 2026: 73 · 2025: 85 · 2024: 89 · 2023: 94 · 2022: 76 · 2021: 85 · 2020: 58 · 2019: 40 · 2018: 2
- FWCI
- 7.13
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (R01AG045611, R01AG062542, P01AG019724, R01AG034570)
- 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
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloid-beta, tau protein, neurodegeneration, brain atrophy, hypometabolism, medial parietal cortex, medial temporal lobe, cognitive decline, dementia, disease progression
- MeSH terms
- Aging, Alzheimer Disease, Brain, Humans, Amyloid beta-Peptides, tau Proteins, Disease Progression, Multimodal Imaging
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