ReviewNature reviews. Neurology2022
Lesions without symptoms: understanding resilience to Alzheimer disease neuropathological changes.
Review in Nature reviews. Neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Asymptomatic Versus Symptomatic Alzheimer's Disease Neuropathology: A Systematic Review of Differences Reported in Post-Mortem Studies.Neuropathology and applied neurobiology · 2026Pooled it
- Joint impact of pathological burden and cognitive resilience on Alzheimer's disease risk.Nature medicine · 2026Article
- Brain pathology in relation to somatic diseases: Exploring the body-brain crosstalk.Journal of internal medicine · 2026Review
- Purpose in life and blood-based biomarkers of brain health.The journals of gerontology. Series B, Psychological sciences and social sciences · 2026Article
- The complement system in Alzheimer's disease: evaluating biomarker potential in a complex neuroimmune context.Journal of neuroinflammation · 2026Review
- Stable neuronal representations underlie cognitive resilience to Alzheimer's disease pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- CK2 inhibition suppresses glial inflammation in models of neuroinflammation and neurodegeneration.Nature communications · 2026Article
- AI guided discovery of a murine model of asymptomatic Alzheimer's disease.Acta neuropathologica communications · 2026Article
- Anemia and Blood Biomarkers of Alzheimer Disease in Dementia Development.JAMA network open · 2026Article
- Educational attainment is associated with reduced functional decline in Puerto Ricans with elevated pTau181.Journal of Alzheimer's disease : JAD · 2026Article
- Neurodevelopmental origins of age-related neurodegenerative diseases.EBioMedicine · 2026Review
- Stable neuronal representations to repeated stimulation underlie cognitive resilience in Alzheimer's disease pathology.bioRxiv : the preprint server for biology · 2025Article
- Specific proteolysis mediated by a p97-directed proteolysis-targeting chimera (p97-PROTAC).eLife · 2025Article
- Proteomic Insight Into Alzheimer's Disease Pathogenesis Pathways.Proteomics · 2025Review
- Inhibition of miR-4284 could reduce apoptosis and neuroinflammation by targeting APBA1/JAK1/STAT3 signaling in Alzheimer's disease.Cell & bioscience · 2025Article
- Neuronal gene profiling of tau oligomer-bearing cholinergic nucleus basalis neurons during the onset of Alzheimer's disease.Acta neuropathologica communications · 2025Article
- Alterations of structural-functional connectivity coupling in older adults with depressive symptoms.Psychological medicine · 2025Article
- Celebrating neuropathology's contributions to Alzheimer's Disease Research Centers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Super-resolution microscopy for structural biology.Nature methods · 2025Review
- Use of Amyloid Positron-Emission Tomography to Diagnose Alzheimer's Disease in Clinical Practice in South Korea: Expert Recommendations.Journal of clinical neurology (Seoul, Korea) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.