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Dissecting phenotypic traits linked to human resilience to Alzheimer’s pathology
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Clinico-pathological correlation studies and positron emission tomography amyloid imaging studies have shown that some individuals can tolerate substantial amounts of Alzheimer's pathology in their brains without experiencing dementia. Few details are known about the neuropathological phenotype of these unique cases that might prove relevant to understanding human resilience to Alzheimer's pathology. We conducted detailed quantitative histopathological and biochemical assessments on brains from non-demented individuals before death whose brains were free of substantial Alzheimer's pathology, non-demented individuals before death but whose post-mortem examination demonstrated significant amounts of Alzheimer's changes ('mismatches'), and demented Alzheimer's cases. Quantification of amyloid-β plaque burden, stereologically-based counts of neurofibrillary tangles, neurons and reactive glia, and morphological analyses of axons were performed in the multimodal association cortex lining the superior temporal sulcus. Levels of synaptic integrity markers, and soluble monomeric and multimeric amyloid-β and tau species were measured. Our results indicate that some individuals can accumulate equivalent loads of amyloid-β plaques and tangles to those found in demented Alzheimer's cases without experiencing dementia. Analyses revealed four main phenotypic differences among these two groups: (i) mismatches had striking preservation of neuron numbers, synaptic markers and axonal geometry compared to demented cases; (ii) demented cases had significantly higher burdens of fibrillar thioflavin-S-positive plaques and of oligomeric amyloid-β deposits reactive to conformer-specific antibody NAB61 than mismatches; (iii) strong and selective accumulation of hyperphosphorylated soluble tau multimers into the synaptic compartment was noted in demented cases compared with controls but not in mismatches; and (iv) the robust glial activation accompanying amyloid-β and tau pathologies in demented cases was remarkably reduced in mismatches. Further biochemical measurements of soluble amyloid-β species-monomers, dimers and higher molecular weight oligomers-in total brain homogenates and synaptoneurosomal preparations failed to demonstrate significant differences between mismatches and demented cases. Together, these data suggest that amyloid-β plaques and tangles do not inevitably result in neural system derangement and dementia in all individuals. We identified distinct phenotypic characteristics in the profile of brain fibrillar and soluble amyloid-β and tau accrual and in the glial response that discriminated demented and non-demented individuals with high loads of Alzheimer's pathology. Amyloid-β deposition in the form of fibrillar plaques and intimately related oligomeric amyloid-β assemblies, hyperphosphorylated soluble tau species localized in synapses, and glial activation emerged in this series as likely mediators of neurotoxicity and altered cognition, providing further insight into factors and pathways potentially involved in human susceptibility or resilience to Alzheimer's pathological changes.
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“unlike in the brains of AD subjects with dementia, no phosphorylated tau accumulation occurs within the synapses of AsymAD brains [73, 83].”
From Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer’s disease (2024) · cites this paper as [73]
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“Consistent with our findings, previous studies have shown that AsymAD cases exhibit an overall deficiency in oligomeric and soluble phospho-tau species, indicating fewer pathological tau species in these cases than in AD cases [8, 73, 83].”
From Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer’s disease (2024) · cites this paper as [73]
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“Very few studies reported using stereology to complete their cell counts,54, 70, 83, 84, 122 the gold standard for quantifying cells in a tissue without bias.”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [83]
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“AsymAD brains have also been found to exhibit a neuroinflammatory profile distinct from that of AD brains, with decreased numbers of activated microglia and astrocyte cells [73]”
From Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer’s disease (2024) · cites this paper as [73]
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“studies have demonstrated that AsymAD brains exhibit no signs of notorious synaptic or neuronal deterioration [8, 42, 73]”
From Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer’s disease (2024) · cites this paper as [73]
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“The direct connection between Aβ and MAPT pathology is poorly understood, as shown by the weak correlation between the distribution of Aβ pathology and the distribution of MAPT pathology in humans (Serrano-Pozo et al., 2011; Perez-Nievas et al., 2013; Scheltens et al., 2021).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Perez-Nievas et al., 2013
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“Moreover, in rare instances of AD in which cognition is relatively preserved (resilient cases), the number of neurofibrillary tangles is the same as in typical AD patients, although the amount of neuronal and synaptic loss is minimal (17).”
From All the Tau We Cannot See (2023) · cites this paper as [17]
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Self-citation
Metadata
- Authors
- Perez-Nievas, B. G., Stein, T. D., Tai, H.-C., Dols-Icardo, O., Scotton, T. C., Barroeta-Espar, I., Fernandez-Carballo, L., de Munain, E. L., Perez, J., Marquie, M., Serrano-Pozo, A., Frosch, M. P., Lowe, V., Parisi, J. E., Petersen, R. C., Ikonomovic, M. D., López, O. L., Klunk, W., Hyman, B. T., & Gómez-Isla, T.
- Affiliations
- Harvard University (US)
- Mayo Clinic (US)
- University of Pittsburgh (US)
- ORCID
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-07-03
- Volume
- 136
- Issue
- 8
- Pages
- 2510-2526
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- PMC
- PMC3722351
- OpenAlex
- W1978991736
- Cited by
- 387
- References
- 67
- Citations by year
- 2026: 30 · 2025: 27 · 2024: 28 · 2023: 38 · 2022: 34 · 2021: 46 · 2020: 37 · 2019: 29 · 2018: 36 · 2017: 18 · 2016: 18 · 2015: 22 · 2014: 20 · 2013: 3
- FWCI
- 14.58
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- U.S. Department of Veterans Affairs (I01 CX001038)
- National Institutes of Health
- National Institute on Aging (AG-005133, R01AG043511, P50AG005133, U01AG016976, P50AG005134, P30AG062421, P50AG016574)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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, amyloid plaques, neurofibrillary tangles, tau hyperphosphorylation, soluble amyloid-beta oligomers, synaptic integrity, axon morphology, glial activation, superior temporal sulcus, association cortex, dementia
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Brain, Cognition, Humans, Neuroglia, Neurons, Phenotype, Neurofibrillary Tangles, tau Proteins, Resilience, Psychological, Plaque, Amyloid
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