Lesions without symptoms: understanding resilience to Alzheimer disease neuropathological changes
Open accessAbstract
Since the original description of amyloid-β plaques and tau tangles more than 100 years ago, these lesions have been considered the neuropathological hallmarks of Alzheimer disease (AD). The prevalence of plaques, tangles and dementia increases with age, and the lesions are considered to be causally related to the cognitive symptoms of AD. Current schemes for assessing AD lesion burden examine the distribution, abundance and characteristics of plaques and tangles at post mortem, yielding an estimate of the likelihood of cognitive impairment. Although this approach is highly predictive for most individuals, in some instances, a striking mismatch between lesions and symptoms can be observed. A small subset of individuals harbour a high burden of plaques and tangles at autopsy, which would be expected to have had devastating clinical consequences, but remain at their cognitive baseline, indicating 'resilience'. The study of these brains might provide the key to understanding the 'black box' between the accumulation of plaques and tangles and cognitive impairment, and show the way towards disease-modifying treatments for AD. In this Review, we begin by considering the heterogeneity of clinical manifestations associated with the presence of plaques and tangles, and then focus on insights derived from the rare yet informative individuals who display high amounts of amyloid and tau deposition in their brains (observed directly at autopsy) without manifesting dementia during life. The resilient response of these individuals to the gradual accumulation of plaques and tangles has potential implications for assessing an individual's risk of AD and for the development of interventions aimed at preserving cognition.
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AsymAD individuals have neuritic plaque and NFTs Braak stages at autopsy comparable to those of AD subjects with dementia.
“These individuals have neuritic plaque and NFTs Braak stages at autopsy comparable to those of AD subjects with dementia, and the literature refers to them as resilient [31], Nondemented with AD Neuropathology (NDAN) [83], or asymptomatic AD (AsymAD) [22, 42].”
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 [31]
The ‘Neuronal and synaptic loss’ section reports that a selected group of resilient individuals without dementia was matched to a group with AD dementia for plaque and tangle burden and regional distribution at autopsy. It does not establish that asymptomatic individuals generally have comparable neuritic-plaque and NFT Braak stages; the same section describes another study in which the resilient group had fewer tangles in one region. No page number is available in our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe absence of dementia in AsymAD individuals is partly due to synaptic preservation and, hence, neuron survival.
“It is well established that the absence of dementia in AsymAD individuals is partly due to synaptic preservation and, hence, neuron survival [31, 67].”
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 [31]
In “Putative mechanisms of resilience > Neuronal and synaptic loss” (page not available), the review reports preserved synaptic markers and neuron numbers in people with AD pathology but no dementia. It says these findings favour identifying resilient brains by preservation of both neurons and synapses; it does not establish that synaptic preservation causes neuron survival, as the claim’s “hence” implies. (LLM, conf=0.86)
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“These individuals have neuritic plaque and NFTs Braak stages at autopsy comparable to those of AD subjects with dementia, and the literature refers to them as resilient [31], Nondemented with AD Neuropathology (NDAN) [83], or asymptomatic AD (AsymAD) [22, 42].”
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- Authors
- Gómez-Isla, T., & Frosch, M. P.
- Affiliations
- Massachusetts General Hospital (US)
- Venue
- Nature Reviews Neurology
- Published
- 2022-03-24
- Volume
- 18
- Issue
- 6
- Pages
- 323-332
- ISSN
- 1759-4758 (ISSN-L)
- 1759-4766
- PMC
- PMC10607925
- OpenAlex
- W4220661917
- Cited by
- 96
- References
- 136
- Citations by year
- 2026: 20 · 2025: 31 · 2024: 19 · 2023: 18 · 2022: 8
- FWCI
- 2.61
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Reviews Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Eli Lilly and Company
- National Institute on Aging (R01AG043511, P30AG062421)
- 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, tau tangles, lesion burden, cognitive resilience, dementia risk, disease-modifying therapy, clinical heterogeneity, postmortem neuropathology, cognitive preservation
- MeSH terms
- Alzheimer Disease, Brain, Humans, Amyloid beta-Peptides, Neurofibrillary Tangles, tau Proteins, Plaque, Amyloid
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