Non-Demented Individuals with Alzheimer's Disease Neuropathology: Resistance to Cognitive Decline May Reveal New Treatment Strategies
Open accessAbstract
Alzheimer's disease (AD) is a terminal neurodegenerative disorder that is characterized by accumulation of amyloid plaques and neurofibrillary tangles in the central nervous system. However, certain individuals remain cognitively intact despite manifestation of substantial plaques and tangles consistent with what would be normally associated with fully symptomatic AD. Mechanisms that allow these subjects to escape dementia remain unresolved and understanding such protective biological processes could reveal novel targets for the development of effective treatments for AD. In this review article we discuss potential compensatory mechanisms that allow these individuals to remain cognitively intact despite the typical AD neuropathology.
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Lewy-related pathology and Alzheimer's disease-type pathology have been documented in cognitively healthy individuals upon autopsy.
“LRP [74] and AD-type pathology [75] have been documented in cognitively healthy individuals upon autopsy.”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [75]
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Reese, L. C., & Taglialatela, G. (2010) · Europe PMC (PubMed Central) · Cited by 24 · see citing works
Self-citationThe Relationship between Amyloid Deposition, Neurodegeneration, and Cognitive Decline in Dementia
Vandenberghe, R. R. (2014) · Current Neurology and Neuroscience Reports · doi:10.1007/s11910-014-0498-9 · Cited by 19 · see citing works
Serbinek, D., Ullrich, C., Pirchl, M., Hochstrasser, T., Schmidt‐Kastner, R., & Humpel, C. (2010) · Cardiovascular Psychiatry and Neurology · doi:10.1155/2010/106123 · Cited by 15 · see citing works
THE BIOLOGICAL RESTORATION OF CENTRAL NERVOUS SYSTEM ARCHITECTURE AND FUNCTION
Farin, A., Liu, C. Y., Langmoen, I. A., & Apuzzo, M. L. J. (2009) · Neurosurgery · doi:10.1227/01.neu.0000343539.15177.d1 · Cited by 7 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
α-synuclein in the pathophysiology of Alzheimer’s disease
Twohig, D., & Nielsen, H. M. (2019) · Molecular Neurodegeneration · doi:10.1186/s13024-019-0320-x · Cited by 374 · see citing works
Fracassi, A., Marcatti, M., Zolochevska, O., Tabor, N., Woltjer, R., Moreno, S., & Taglialatela, G. (2021) · The Journal of Neuroscience · doi:10.1523/jneurosci.0295-20.2020 · Cited by 81 · see citing works
Self-citationSingh, A., Allen, D., Fracassi, A., Tumurbaatar, B., Natarajan, C., Scaduto, P., Woltjer, R., Kayed, R., Limon, A., Krishnan, B., et al. (2020) · Journal of Alzheimer's Disease · doi:10.3233/jad-200716 · Cited by 56 · see citing works
Self-citationPolis, B., & Samson, A. O. (2024) · Journal of Alzheimer's Disease · doi:10.3233/jad-240058 · Cited by 43 · see citing works
- Authors
- Zolochevska, O., & Taglialatela, G.
- Affiliations
- The University of Texas Medical Branch at Galveston (US)
- ORCID
- Taglialatela, Giulio
- Venue
- Current Pharmaceutical Design
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2016-08-01
- Volume
- 22
- Issue
- 26
- Pages
- 4063-4068
- ISSN
- 1381-6128 (ISSN-L)
- PMC
- PMC6007878
- OpenAlex
- W2396757371
- Cited by
- 49
- References
- 91
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 8 · 2023: 2 · 2022: 5 · 2021: 11 · 2020: 8 · 2019: 6 · 2018: 1 · 2016: 1
- FWCI
- 2.15
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Current Pharmaceutical Design (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG042890)
- National Institute of Environmental Health Sciences (T32ES007254)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, cognitive resilience, amyloid plaques, neurofibrillary tangles, compensatory mechanisms, neurodegeneration, treatment goals
- MeSH terms
- Alzheimer Disease, Animals, Humans, Cognitive Dysfunction
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 ›
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