Dissecting phenotypic traits linked to human resilience to Alzheimer’s pathology
Open accessAbstract
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 AD subjects with dementia, no phosphorylated tau accumulation occurs within synapses of AsymAD brains.
“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]
The Results and Discussion report increased synaptic hyperphosphorylated tau in demented Alzheimer’s cases, but not in the non-demented high-pathology “mismatches” compared with controls. The claim’s absolute wording, “no phosphorylated tau accumulation,” goes beyond the paper’s finding of no significant or aberrant increase; it does not establish that phosphorylated tau is absent from those synapses. (LLM, conf=0.87)
Experimental — accuracy not yet measuredAsymAD cases exhibit an overall deficiency in oligomeric and soluble phospho-tau species, indicating fewer pathological tau species in these cases than in AD cases.
“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]
The Results report that soluble hyperphosphorylated tau monomers and multimers accumulated in synapses in demented AD cases but not in high-probability mismatches. This supports fewer of those synaptic tau species in the asymptomatic cases, but not an overall deficiency in pathological tau: the Results also say neurofibrillary tangle counts did not significantly differ between the groups. (LLM, conf=0.86)
Experimental — accuracy not yet measuredVery few studies reported using stereology to complete their cell counts.
“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]
AsymAD brains exhibit decreased numbers of activated microglia and astrocyte cells compared with AD brains.
“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]
AsymAD brains exhibit no signs of notorious synaptic or neuronal deterioration.
“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]
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.
“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
The Results and Discussion (pages unavailable) compare amyloid-β plaques and tau pathology in the superior temporal sulcus, chiefly in relation to dementia and neuronal damage. Searches for their regional distributions and a weak correlation between them found no passage addressing that relationship or stating that their direct connection is poorly understood. (LLM, conf=0.74)
Experimental — accuracy not yet measuredIn resilient AD cases, the number of neurofibrillary tangles is the same as in typical AD patients, although neuronal and synaptic loss is minimal.
“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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Synergy between amyloid-β and tau in Alzheimer’s disease
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Self-citationReligious Orders Study and Rush Memory and Aging Project
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The Intersection of Amyloid Beta and Tau at Synapses in Alzheimer’s Disease
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Self-citationRoles of tau protein in health and disease
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Clinical diagnosis of Alzheimer’s disease: Recommendations of the International Working Group
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“…have comparable burden of AD brain lesions, confirmed with large post-mortem cohorts using quantification and digital neuropathological methods 88,89 All stages AD brain lesions (including both amyloid and tau lesions) are found in 2/3 of subjects aged of 70 years in systematic post-mortem…”
MethodA new era for understanding amyloid structures and disease
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Interaction between Aβ and Tau in the Pathogenesis of Alzheimer’s Disease
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At the interface of sensory and motor dysfunctions and Alzheimer’s disease.
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Self-citationHopperton, K. E., Mohammad, D., Trépanier, M. O., Giuliano, V, & Bazinet, R. P. (2018) · Molecular Psychiatry · doi:10.1038/mp.2017.246 · Cited by 567 · see citing works
Type I interferon response drives neuroinflammation and synapse loss in Alzheimer disease
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Cascading network failure across the Alzheimer’s disease spectrum
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Self-citationMicroglial activation and tau propagate jointly across Braak stages
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Synaptic degeneration in Alzheimer disease
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TDP-43 is a key player in the clinical features associated with Alzheimer’s disease
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Self-citationThe antimicrobial protection hypothesis of Alzheimer’s disease
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Association of Dual-Task Gait With Incident Dementia in Mild Cognitive Impairment
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Resistance vs resilience to Alzheimer disease
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The clinical promise of biomarkers of synapse damage or loss in Alzheimer’s disease
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Self-citationBeyond the neuron–cellular interactions early in Alzheimer disease pathogenesis
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Self-citationThe identity and function of microglia in neurodegeneration
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Beta-amyloid deposition in chronic traumatic encephalopathy
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Self-citationThe amyloid cascade hypothesis: an updated critical review
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The role of microglia in processing and spreading of bioactive tau seeds in Alzheimer’s disease
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Self-citationSynaptic Tau Seeding Precedes Tau Pathology in Human Alzheimer’s Disease Brain
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Self-citationDeciphering the astrocyte reaction in Alzheimer's disease
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Self-citationA systems approach to stress, stressors and resilience in humans
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Alzheimer's Disease-Like Pathology Induced by Amyloid-β Oligomers in Nonhuman Primates
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Challenges for Alzheimer's Disease Therapy: Insights from Novel Mechanisms Beyond Memory Defects
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The role of innate immune genes in Alzheimer's disease
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Multiscale causal networks identify VGF as a key regulator of Alzheimer’s disease
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Synaptic pathology: A shared mechanism in neurological disease
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Hippocampal plasticity during the progression of Alzheimer’s disease
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Tau Oligomers: The Toxic Player at Synapses in Alzheimer’s Disease
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Self-citationNeuroinflammation, gut microbiome, and Alzheimer's disease
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Is Alzheimer’s Disease Risk Modifiable?
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PSD-95 protects synapses from β-amyloid
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Quaternary Structure Defines a Large Class of Amyloid-β Oligomers Neutralized by Sequestration
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Self-citationThe foundation and architecture of precision medicine in neurology and psychiatry
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Markers of neuroinflammation associated with Alzheimer’s disease pathology in older adults
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Removing endogenous tau does not prevent tau propagation yet reduces its neurotoxicity
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Distinct cytokine profiles in human brains resilient to Alzheimer's pathology
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Self-citationMolecular and cellular pathophysiology of preclinical Alzheimer’s disease
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Astrocytes and neuroinflammation in Alzheimer's disease
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Synaptic Amyloid-β Oligomers Precede p-Tau and Differentiate High Pathology Control Cases
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The metabolic brain signature of cognitive resilience in the 80+: beyond Alzheimer pathologies
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Self-citationTau Oligomer–Containing Synapse Elimination by Microglia and Astrocytes in Alzheimer Disease
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Self-citation[F-18]-AV-1451 binding correlates with postmortem neurofibrillary tangle Braak staging
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Untangling Tau and Iron: Exploring the Interaction Between Iron and Tau in Neurodegeneration
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The interactions of p53 with tau and Aß as potential therapeutic targets for Alzheimer’s disease
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Lesions without symptoms: understanding resilience to Alzheimer disease neuropathological changes
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Self-citationDown syndrome and Alzheimer's disease: common molecular traits beyond the amyloid precursor protein
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Aβ propagation and strains: Implications for the phenotypic diversity in Alzheimer's disease
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Dendritic Spines: Mediators of Cognitive Resilience in Aging and Alzheimer’s Disease
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Improving the resistance and resilience framework for aging and dementia studies
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Self-citationNanoscale structure of amyloid-β plaques in Alzheimer’s disease
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- 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
- 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, 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
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.
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