The DOI matches its Crossref record; 117 of the 119 references it cites were found in a registry or an index; 5 of the 67 sources its claims cite were checked for support.
Clinical diagnosis of Alzheimer’s disease: Recommendations of the International Working Group
Open accessAbstract
In 2018, the National Institute of Aging and the Alzheimer Association proposed a purely biological definition of Alzheimer’s disease (AD) relying on biomarkers. While the intended use of the framework was for research purposes, it has engendered debate and challenges regarding its application in everyday clinical practice. For instance, cognitively unimpaired individuals may have biomarker evidence of both amyloid and tau pathology, but may never develop clinical manifestations in their lifetime. Furthermore, a positive AD pattern may be observed in other brain diseases where AD pathology is present as co‐pathology. In this presentation, the international Working Group (IWG) presents what we consider to be the current limitations of biomarkers in the diagnosis of AD, and on the basis of this evidence we propose recommendations for how biomarkers should and should not be used for diagnosis of AD in a clinical setting. We recommend that AD diagnosis be restricted to the occurrence of positive biomarkers together with specific AD phenotypes, whereas biomarker positive cognitively unimpaired individuals should be considered only at‐risk for progression to AD.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
The International Working Group argues that a purely biological ATN definition of Alzheimer’s disease is not ready for clinical diagnosis and recommends restricting Alzheimer’s disease diagnosis to people with both a specific Alzheimer’s disease clinical phenotype and positive amyloid and tau biomarkers. Biomarker-positive cognitively unimpaired individuals should be considered at-risk for progression, not clinically diagnosed with Alzheimer’s disease.
Key findings
- The IWG recommends a clinical–biological diagnosis: a specific Alzheimer’s disease phenotype plus amyloid-positive and tau-positive biomarker evidence; biomarker-positive cognitively unimpaired people should be classified as at-risk, not as having Alzheimer’s disease.
- A purely biological definition has low predictive accuracy: cognitively unimpaired biomarker-positive individuals often do not progress, and best current estimates of lifetime dementia risk range from 5% to 42%.
- Alzheimer’s pathology is commonly mixed: pure Alzheimer’s disease pathology is found in 3–30% of neuropathological series of people with dementia of the Alzheimer type, and 50–60% of Alzheimer’s-type dementia is estimated to be attributable to copathologies such as α-synucleinopathy, vascular pathology, non-Alzheimer’s tauopathies, and TDP-43 pathology.
- Practical biomarker limitations include artificial thresholds, limited generalisability, and accessibility; Cochrane reviews could not recommend routine CSF or amyloid PET use in clinical practice, plasma biomarkers are not currently recommended, and biomarker investigation in cognitively unimpaired individuals is not recommended.
Methods
- Design: a Personal View and consensus recommendations from the International Working Group, not a primary empirical study.
- Data or sample: no new primary sample is reported; the paper synthesises prior diagnostic frameworks, biomarker literature, neuropathology evidence, Cochrane reviews, and cohort findings.
- Analysis: narrative evidence synthesis leading to expert recommendations, including proposed diagnostic criteria, biomarker measures, and a risk-stratification proposal for cognitively unimpaired biomarker-positive individuals.
Limitations
- The paper states that a purely biological definition risks confusion between Alzheimer’s disease lesions and Alzheimer’s disease, has low predictive accuracy, is complicated by copathologies, and faces uncertain pathogenesis, threshold, generalisability, accessibility, and ethical problems.
- The paper states that current individualised prediction models do not work sufficiently well in cognitively unimpaired people compared with people in the prodromal stage, and that disclosing individual patient-level risk would be premature and is to be avoided.
- Evident from the text: as a Personal View, the recommendations are expert consensus rather than a systematic review or meta-analysis; the proposed risk stratification is a starting point for research and requires validation studies on large cohorts with long follow-up, as the paper itself notes.
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Claims the paper makes
31 Not checked yet · 13 Own interpretation · 2 Partly supported · 1 Supported · 1 No basis given · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“In cognitively unimpaired individuals, self-reported complaints and complaints reported by an informant should be clearly distinguished, because informant complaints indicate that these individuals are at increased risk of progression110 and merit a closer follow-up with regular clinical and neuropsychological evaluations.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > IWG recommendations for clinical diagnosis of Alzheimer’s disease
What the sources say
- Supportedcites [110] Caselli, 2014, Subjective cognitive decline: self and informant comparisons, Alzheimers Dement source
The Methods (section 2.6) state that all participants were cognitively normal at entry. The Results (section 3) report that 9.4% of those with informant-endorsed decline developed MCI, compared with 2.2% of those without it (odds ratio 4.58, p<.05). The Discussion cautions that the number of converters was small. (LLM, conf=0.94)
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- Supported
In the paper
“For instance, cognitively unimpaired individuals can have biomarker evidence of both amyloid β and tau pathology but will often not develop clinical manifestations in their lifetime.”
- Also stated in: § Difficulty in classifying cognitively unimpaired biomarker-positive individuals · hedged
“Cognitively unimpaired individuals with biomarker positivity will not invariably experience subsequent cognitive decline; the best current estimates of lifetime dementia risk range from 5% to 42%.33”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Abstract
What the sources say
- Not checked yetcites [33] Brookmeyer, 2018, Estimation of lifetime risks of Alzheimer's disease dementia using biomarkers for preclinical disease, Alzheimers Dement source
plain- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Difficulty in classifying cognitively unimpaired biomarker-positive individuals · hedged
In the paper
“current individualised prediction models do not work sufficiently well in cognitively unimpaired people compared with people who are in the prodromal stage of Alzheimer’s disease.62”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Difficulty in classifying cognitively unimpaired biomarker-positive individuals
What the sources say
- Not checked yetcites [62] van Maurik, 2019, Personalized risk for clinical progression in cognitively normal subjects-the ABIDE project, Alzheimers Res Ther source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“In 2018, the US National Institute on Aging and the Alzheimer’s Association proposed a purely biological definition of Alzheimer’s disease that relies on biomarkers.”
- Also stated in: § Introduction · plain
“In 2018, the US National Institute on Aging (NIA) and the Alzheimer’s Association (AA) proposed the amyloid β, tau, neurodegeneration (ATN) research framework for the definition and diagnosis of Alzheimer’s disease (for a glossary of terms, see panel 1).1”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Abstract
What the sources say
- Not checked yetcites [1] Jack, 2018, NIA–AA research framework: toward a biological definition of Alzheimer's disease, Alzheimers Dement source
plain- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Introduction · plain
In the paper
“However, the follow-up of cognitively unimpaired biomarker-positive individuals suggests that the majority of these individuals do not progress over time (panel 2).”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Uncertainty about the pathogenesis model of Alzheimer’s disease
What the sources say
- Not checked yetcites panel 2
hedged- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The relationship between the coexistence of tau and amyloid β pathology on the one hand, and the development of cognitive decline and neurodegeneration on the other hand, remain uncertain at an individual level.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Uncertainty about the pathogenesis model of Alzheimer’s disease
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Several studies (panel 2) indicate that the presence of both tau and amyloid β positivity is insufficient to definitively predict the occurrence of symptoms (mild cognitive impairment or dementia) in individuals without clinical impairment.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Low predictive accuracy
What the sources say
- Not checked yetcites panel 2
hedged- Asserted: passes — The authors put it forward as true.
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In the paper
“Pure Alzheimer’s disease pathology is the exception rather than the rule (found in 3–30% of neuropathological series of people with dementia of the Alzheimer type, depending on age40) at post-mortem examination.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Presence of other pathologies
What the sources say
- Not checked yetcites [40] Robinson, 2018, Neurodegenerative disease concomitant proteinopathies are prevalent, age-related and APOE4-associated, Brain source
plain- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“50–60% of Alzheimer’s-type dementia (dementia defined clinically as Alzheimer’s disease) is estimated to be attributable to these copathologies.40,42–45”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Presence of other pathologies
What the sources say
- Not checked yetcites [40] Robinson, 2018, Neurodegenerative disease concomitant proteinopathies are prevalent, age-related and APOE4-associated, Brain source
- Not checked yetcites [42] Yokota, 2018, Neuropathological comorbidity associated with argyrophilic grain disease, Neuropathology source
- Not checked yetcites [43] Ossenkoppele, 2020, Assessment of demographic, genetic, and imaging variables associated with brain resilience and cognitive resilience to pathological tau in patients with Alzheimer disease, JAMA Neurol source
- Not checked yetcites [44] Karanth, 2020, Prevalence and clinical phenotype of quadruple misfolded proteins in older adults, JAMA Neurol source
- Not checked yetcites [45] Nelson, 2019, Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report, Brain source
hedgedstates a cause- Asserted: passes — The authors put it forward as true.
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In the paper
“Furthermore, a positive Alzheimer’s disease pattern of biomarkers can be observed in other brain diseases in which Alzheimer’s disease pathology is present as a comorbidity.”
- Also stated in: § Presence of other pathologies · hedged
“Another challenge with using a biomarker-only diagnosis of Alzheimer’s disease is that the in-vivo presence of biomarkers of Alzheimer’s disease lesions could certify Alzheimer’s disease as the primary diagnosis, because such lesions are commonly found in people who have other neurodegenerative diseases, most often dementia with Lewy bodies.40”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Abstract
What the sources say
- Not checked yetcites [40] Robinson, 2018, Neurodegenerative disease concomitant proteinopathies are prevalent, age-related and APOE4-associated, Brain source
plainstates an association- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Presence of other pathologies · hedged
- It may state two separate claims as one. 19
- Probably not a substantial claim. 7
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Biomarker thresholds also depend on their intended use (eg, to identify the first signs of amyloid β pathology, or to predict the occurrence of clinical symptoms) and no consensus on the context of use (eg, in asymptomatic vs symptomatic individuals; in people who complain about subjective cognitive decline vs non-complainers) is currently available.1”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Biomarker thresholds
What the sources say
- Partly supportedcites [1] Jack, 2018, NIA–AA research framework: toward a biological definition of Alzheimer's disease, Alzheimers Dement sourceExperimental — accuracy not yet measured
The Implementation section says cut points should fit the research question, giving early detection and high diagnostic certainty as examples. It also says universal biomarker standards have not been established, but does not specifically establish a lack of consensus on thresholds for asymptomatic versus symptomatic people or subjective cognitive decline complainants versus non-complainants. No page numbers were provided for these passages. (LLM, conf=0.83)
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It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The positivity of both amyloid and tau biomarkers is required because an amnestic phenotype with only amyloid positivity is not specific to Alzheimer’s disease and is seen in other neurodegenerative diseases with amyloid copathology (including LATE and dementia with Lewy bodies1,40,41,100) or in patients with cerebral amyloid angiopathy and amnestic vascular cognitive impairment101 (appendix p 2).”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > IWG recommendations for clinical diagnosis of Alzheimer’s disease
What the sources say
- Partly supportedcites [1] Jack, 2018, NIA–AA research framework: toward a biological definition of Alzheimer's disease, Alzheimers Dement sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Partly supportedcites [40] Robinson, 2018, Neurodegenerative disease concomitant proteinopathies are prevalent, age-related and APOE4-associated, Brain sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Partly supportedcites [41] McKeith, 2017, Diagnosis and management of dementia with Lewy bodies: fourth consensus report of the DLB Consortium, Neurology sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plainstates a cause- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Partly supported
None of the sources cited for this claim have been checked yet.
In the paper
“Most of all, this binary threshold does not reflect the reality of amyloid β and tau pathology, which is continuous and present at a minimal extent in almost all people older than 70 years,17 with important discrepancies between pathology burden and clinical symptoms at intermediate extents (panel 2).”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Biomarker thresholds
What the sources say
- Not checked yetcites [17] Braak, 2011, Stages of the pathologic process in Alzheimer disease: age categories from 1 to 100 years, J Neuropathol Exp Neurol source
- Not checked yetcites panel 2
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The clear-cut separation between negative and positive patients in relation to a given biomarker is somewhat artificial and differs between sites and studies.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Biomarker thresholds
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, amyloid β and tau biomarkers are not sufficient to confidently predict progression to prodromal Alzheimer’s disease or Alzheimer’s disease dementia, or to define a person’s position on the Alzheimer’s disease continuum, without clinical input.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Uncertainty about the pathogenesis model of Alzheimer’s disease
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Cognitively unimpaired individuals with biomarker positivity will not invariably experience subsequent cognitive decline; the best current estimates of lifetime dementia risk range from 5% to 42%.33”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Difficulty in classifying cognitively unimpaired biomarker-positive individuals
What the sources say
- Not checked yetcites [33] Brookmeyer, 2018, Estimation of lifetime risks of Alzheimer's disease dementia using biomarkers for preclinical disease, Alzheimers Dement source
hedged- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“For physicians, Alzheimer’s disease equates with Alzheimer’s disease neuropathological changes, whereas for patients, Alzheimer’s disease equates with dementia, dependency, and death.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Ethical concerns
What the sources say
- Not checked yetcites [12] Frisoni, 2019, Re-aligning scientific and lay narratives of Alzheimer's disease, Lancet Neurol source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“CSF investigation is prioritised because it provides simultaneous information on the two types of biomarkers (amyloid β and tau) and is less expensive than amyloid PET, tau PET, or both.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > IWG recommendations for clinical diagnosis of Alzheimer’s disease
plainstates a cause- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may state two separate claims as one.
In the paper
“However, this increased sensitivity in the detection of cognitive decline comes at the expense of a reduced specificity, and numerous other causes than neurodegeneration or Alzheimer’s disease can be responsible for the observed changes, such as metabolic disorders, psychiatric disorders, or sleep apnoea.72”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Biomarker thresholds
What the sources say
- Not checked yetcites [72] Chipi, 2019, Biomarker-based signature of alzheimer's disease in pre-MCI individuals, Brain Sci source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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In the paper
“In both situations, pathophysiological Alzheimer’s disease biomarkers can be positive.111”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > IWG recommendations for clinical diagnosis of Alzheimer’s disease
What the sources say
- Not checked yetcites [111] Niemantsverdriet, 2018, Added diagnostic value of cerebrospinal fluid biomarkers for differential dementia diagnosis in an autopsy-confirmed cohort, J Alzheimers Dis source
hedgedstates an association- Asserted: passes — The authors put it forward as true.
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In the paper
“As shown in panel 2, the effect of biomarker positivity on clinical progression remains weak to moderate and was established using selected volunteers from research cohorts.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Generalisability and accessibility in clinical practice
What the sources say
- Not checked yetcites panel 2
plainstates an association- Asserted: passes — The authors put it forward as true.
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In the paper
“This deep difference in use and understanding of the term can adversely affect the therapeutic alliance.12”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Ethical concerns
What the sources say
- Not checked yetcites [12] Frisoni, 2019, Re-aligning scientific and lay narratives of Alzheimer's disease, Lancet Neurol source
plainstates a possible cause- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“The current in-vivo detection of tau positivity using 18F-flortaucipir PET seems to correspond only to widespread tau pathology in the brain (ie, Braak stages ≥IV),69 whereas CSF phosphorylated tau elevation can reflect earlier stages of tauopathy.70”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Biomarker thresholds
What the sources say
- Not checked yetcites [69] Fleisher, 2020, Positron emission tomography imaging with [18F]flortaucipir and postmortem assessment of Alzheimer disease neuropathologic changes, JAMA Neurol source
- Not checked yetcites [70] Mattsson-Carlgren, 2020, Aβ deposition is associated with increases in soluble and phosphorylated tau that precede a positive tau PET in Alzheimer's disease, Sci Adv source
hedgedstates an association- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“If a person decides to receive the results and the results are positive, they should be counselled that they are at risk for subsequent clinical progression to prodromal Alzheimer’s disease or Alzheimer’s disease dementia, but are not clinically diagnosed as having Alzheimer’s disease.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > IWG recommendations for clinical diagnosis of Alzheimer’s disease
plainstates an association- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
In the paper
“As underscored by the Cochrane reviews, the prognostic value of a diagnosis based on biomarkers remains limited, first because there is a high variability of decline rate among individuals with biomarker-positive Alzheimer’s disease,79 and second because non-Alzheimer’s disease neurodegenerative diseases contribute to cognitive decline.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Generalisability and accessibility in clinical practice
What the sources say
- Not checked yetcites [79] Jang, 2019, Prediction of fast decline in amyloid positive mild cognitive impairment patients using multimodal biomarkers, Neuroimage Clin source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In symptomatic patients, the identification of the specific clinical phenotype (interfering or not with independence in everyday activities) is a major step in diagnosis, because it expresses the brain dysfunction that the biomarkers are signalling.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Difficulty in classifying cognitively unimpaired biomarker-positive individuals
plainstates a cause- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“Subjective cognitive decline might be a risk factor of clinical progression,24 but the ability of subjective cognitive decline to predict progression to objective cognitive decline (ie, mild cognitive decline, or dementia, or both) remains low (OR 1·5–3·081).”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Generalisability and accessibility in clinical practice
What the sources say
- Not checked yetcites [24] Ebenau, 2020, ATN classification and clinical progression in subjective cognitive decline: the SCIENCe project, Neurology source
- Not checked yetcites [81] Slot, 2019, Subjective cognitive decline and rates of incident Alzheimer's disease and non-Alzheimer's disease dementia, Alzheimers Dement source
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“However, an isolated amnestic syndrome of the hippocampal type with only tau biomarker positivity can occur in primary age-related tauopathy37,38 or in atypical presentations of mixed 3 repeat or 4 repeat tau frontotemporal lobar degeneration100,102 (appendix p 2).”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > IWG recommendations for clinical diagnosis of Alzheimer’s disease
What the sources say
- Not checked yetcites [37] Toledo, 2015, Alzheimer's disease cerebrospinal fluid biomarker in cognitively normal subjects, Brain source
- Not checked yetcites [38] Bell, 2019, Neuropathologic, genetic, and longitudinal cognitive profiles in primary age-related tauopathy (PART) and Alzheimer's disease, Alzheimers Dement source
- Not checked yetcites [100] Villain, 2019, Alzheimer's disease including focal presentations, Semin Neurol source
plainstates an association- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Subjective memory complaints and subjective cognitive decline, if isolated and not supported by objective cognitive impairment, are not specific enough to be considered part of the Alzheimer’s disease phenotype.109”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > IWG recommendations for clinical diagnosis of Alzheimer’s disease
What the sources say
- Not checked yetcites [109] Jessen, 2020, Prediction of dementia of Alzheimer type by different types of subjective cognitive decline, Alzheimers Dement source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“individuals included in such longitudinal cohorts are usually recruited by advertisement and do not represent the variety of individuals to whom the biomarker investigations would be applied in clinical practice.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Generalisability and accessibility in clinical practice
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In clinical practice, such an extension to earlier thresholds in amyloid or tau biomarkers might lengthen the duration of the asymptomatic stages and decrease the lifetime probability of clinical progression.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Biomarker thresholds
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Overall, evidence for the use of biomarkers in clinical practice remains highly disputed and suffers from a dearth of evidence-based data to recommend biomarker assessments for cognitively unimpaired individuals.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Generalisability and accessibility in clinical practice
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although the definition of Alzheimer’s disease based exclusively on biological markers has gained substantial traction in research settings, emerging studies suggest that the biomarker definition is not ready for application in clinical settings and for diagnosis of individuals without cognitive impairment.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Conclusion
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
A specific clinical phenotype of Alzheimer’s disease can be reliably identified in clinical practice.
“It requires the presence of both a specific clinical phenotype of Alzheimer’s disease (phenotype positive) and biomarker evidence of Alzheimer’s disease pathology (amyloid-positive and tau positive).”
The paper relies on this without support.
Biomarkers are currently unavailable for the pathological changes that underlie the non-Alzheimer’s neurodegenerative diseases often found in people with dementia.
“Unfortunately, biomarkers are currently unavailable for the pathological changes that underlie the non-Alzheimer’s neurodegenerative diseases often found in people with dementia, and disentangling Alzheimer’s disease from other neurodegenerative diseases continues to depend on phenotype or postmortem examination.”
The paper relies on this without support.
In some complex cases, only post-mortem evaluation will provide definitive information about whether Alzheimer's disease is the primary pathology or a copathology.
“In some complex cases, only post-mortem evaluation will provide definitive information.”
The paper relies on this without support.
Biomarker investigations can be limited by the availability, cost, and health-care payment coverage of biomarkers across countries, centres, and clinical situations.
“Biomarker investigations can also be limited by the availability, cost, and health-care payment coverage of biomarkers across countries, centres, and clinical situations.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Disease onset can occur at < 65 (familial early-onset) or > 65 years of age (sporadic late-onset), with the latter afflicting more than 95% of patients [87, 213]”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [87]
Experimental — accuracy not yet measuredIn the citing paper
“In 2021, new recommendations for the clinical diagnosis of AD were proposed by the International working group, highlighting that the diagnosis of AD should be restricted to people who have positive biomarkers together with specific AD phenotypes. Cognitively unimpaired individuals who are only positive to biomarkers should be considered at-risk for progression to AD [10].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [10]
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“However, these 2 methods are incompatible with community health centers [6] due to their high costs and safety concerns [7,8].”
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“The use of positron emission tomography (PET) with Aβ and tau imaging ligands has facilitated the early/differential diagnosis of AD [3].”
MethodSelf-citationAdvances of therapy for Alzheimer's disease: An updated review
Mei, C., Zhan, J., Zhu, S., Zhang, Y., Xiong, C., Wang, J., Xu, Y. J., Zhong, H., & Cheng, J. (2024) · Brain‐X · doi:10.1002/brx2.68 · Cited by 15
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“10 Here, neuropsychology comes into play.”
BackgroundLi, Z., Yin, S., Wang, S., Wang, Y., Qiang, W., & Jiang, J. (2024) · Journal of Advanced Research · doi:10.1016/j.jare.2024.11.018 · Cited by 15
“…solution to address the current gap in severe and irreversible diseases from screening to management, such as AD, in which early diagnosis relies on a complex series of cognitive, clinical, and cerebrospinal fluid biomarker evidence, with the definitive diagnosis only confirmed post mortem [99].”
Wang, Y., Wang, Q., Luo, D., Zhao, P., Zhong, S.-S., Dai, B., Wang, J.-J., Wan, Y.-T., Liu, Z., & Yang, H. (2023) · Chinese Journal of Integrative Medicine · doi:10.1007/s11655-023-3592-5 · Cited by 14
“The 2018 World Alzheimer Report revealed that there were about 50 million patients with dementia globally.((6,7)) With the aging of the population, the incidence of AD is becoming increasingly serious and is therefore an important global medical challenge.”
BackgroundAsken, B. M., Curiel, R. E., Crocco, E., Armstrong, M. J., Levy, S.-A. T., Arias, F., Rosselli, M., Vélez-Uribe, I., Barker, W., Matusz, E. F., et al. (2025) · The Journal of Prevention of Alzheimer s Disease · doi:10.1016/j.tjpad.2024.100011 · Cited by 14
“Both the Alzheimer’s Association [ 5 ] and International Working Group [ 29 ] recommendations for AD diagnosis require biomarker support for presence of AD pathology, while the former emphasizes the separation of syndrome (symptoms) and disease biology (etiology) and allows for AD diagnosis based…”
Advances in the genetics and pathology of Lewy body dementia
Scholz, S. W., Okubadejo, N. U., Prakash, P., Liddelow, S. A., Ryten, M., & Halliday, G. M. (2025) · The Lancet Neurology · doi:10.1016/s1474-4422(25)00363-1 · Cited by 22
Epileptic activity in Alzheimer's disease: emerging insights and therapeutic implications
Vossel, K. A., Johnson, E. L., Cretin, B., & Matsumoto, R. (2026) · The Lancet Neurology · doi:10.1016/s1474-4422(25)00425-9 · Cited by 15
Xu, Y., Jiang, H., Zhu, B., Cao, M., Feng, T., Sun, Z., Du, G., & Zhao, Z. (2023) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.14238 · Cited by 11
White Matter Changes as an Independent Predictor of Alzheimer’s Disease
Yan, Y., Wu, Y., Xiao, G., Wang, L., Zhou, S., Wei, L., Tian, Y., Wu, X., Hu, P., & Wang, K. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-221037 · Cited by 14
“…size = 361 voxels), right anterior thalamic radiations (peak t-value = 5.51, MNI coordinates = [21, 30, 9], cluster size = 54 voxels), and left forceps minor (peak t-value = 5.15, MNI coordinates = [–12, 30, 3], cluster size = 20 voxels) were lower than those in the HC group (all p 0.05) (Figs.”
InfluentialChen, H. M., Chen, H. M., Li, K. Y., et al. (2023) · Journal of Dentistry · doi:10.1016/j.jdent.2023.104570 · Cited by 12
Multipredictor risk models for predicting individual risk of Alzheimer’s disease
Hou, X., Suckling, J., Shen, X., Liu, Y., Zuo, C., Huang, Y., Li, H., Wang, H.-F., Tan, C., Cui, M., et al. (2023) · Journal of Translational Medicine · doi:10.1186/s12967-023-04646-x · Cited by 12
“The diagnosis of AD was recommended by the International Working Group to be restricted to people who have both positive biomarkers and specific AD phenotypes in the newly published article which highlight the importance of biomarkers in the clinical diagnosis of AD [31].”
MethodRomagnoli, M., Amore, G., Avanzini, P., Carelli, V., & Morgia, C. L. (2024) · Frontiers in Psychology · doi:10.3389/fpsyg.2023.1295129 · Cited by 13
“The current recommendations for AD diagnosis include tau/ amyloid cerebrospinal fluid (CSF) and positron emission tomography (PET) imaging (Dubois et al., 2021), but there is a still unmet need for easily accessible and objective biomarkers either for biological definition of AD and its prodromal…”
BackgroundMethodFocusing on earlier diagnosis of Alzheimer's disease
Frederiksen, K. S., Morató, X., Zetterberg, H., Gauthier, S. G., Boada, M., Pytel, V., Hahn-Pedersen, J. H., Tarazona, L. R. S., & Mattke, S. (2024) · Future Neurology · doi:10.2217/fnl-2023-0024 · Cited by 14
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Lu, J., Wang, J., Wu, J., Zhang, H., Ma, X., Zhu, Y., Wang, J., Yang, Y., Xiao, Z., Li, M., et al. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14245 · Cited by 12
Ghadami, R., & Rahebi, J. (2025) · Diagnostics · doi:10.3390/diagnostics15030377 · Cited by 16
Neuropsychology of Alzheimer’s disease: From preclinical phase to dementia
Buyukiscan, E. S. (2025) · Applied Neuropsychology Adult · doi:10.1080/23279095.2025.2469236 · Cited by 15
Conca, F., Esposito, V., Rundo, F., Quaranta, D., Muscio, C., Manenti, R., Caruso, G., Lucca, U., Galbussera, A. A., Tella, S. D., et al. (2022) · Alzheimer s Research & Therapy · doi:10.1186/s13195-022-01056-x · Cited by 15
Self-citationKlafki, H.-W., Vogelgsang, J. S., Manuilova, E., Bauer, C., Jethwa, A., Esselmann, H., Jahn‐Brodmann, A., Osterloh, D., Lachmann, I., Breitling, B., et al. (2022) · Alzheimer s Research & Therapy · doi:10.1186/s13195-022-01071-y · Cited by 14
“To that end, and considering the recent recommendations of Dubois and colleagues [23], the study participants were classified on the basis of available clinical, psychometric and neuroimaging biomarker data (including amyloid-PET and fluorodeoxyglucose (FDG) PET, for n = 16 subjects and 36 subjects respectively) plus…”
BackgroundMethodCirculating Biomarkers for the Early Diagnosis of Alzheimer’s Disease
Nunkoo, V. S., Jurcău, A., Les, M., Cristian, A., Militaru, M., Marge, C., Iovanovici, D. C., & Jurcău, M. C. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26157268 · Cited by 13
Titze-de-Almeida, S. S., Marina, C. L., Ramos, M. V., Silva, L. D. D. S., Brandão, P. R. D. P., Bispo, D. D. D. C., von Glehn, F., & Titze‐de‐Almeida, R. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26178246 · Cited by 13
“Depression, obesity, subjective cognitive decline, neurodegenerative markers on imaging, and co-pathologies also contribute to AD risk [5–13].”
α-synuclein as an emerging pathophysiological biomarker of Alzheimer’s disease
Beatino, M. F., Luca, C. D., Campese, N., Belli, E., Piccarducci, R., Giampietri, L., Martini, C., Perugi, G., Siciliano, G., Ceravolo, R., et al. (2022) · Expert Review of Molecular Diagnostics · doi:10.1080/14737159.2022.2068952 · Cited by 11
“diagnosis [50], while recent research on blood-basedbiosignatures led to the exploration of alternative proteins, such as”
BackgroundMethodEndophytic fungi: a potential source for drugs against central nervous system disorders
Pant, A., & Vasundhara, M. (2023) · Brazilian Journal of Microbiology · doi:10.1007/s42770-023-00997-1 · Cited by 10
“These signs are thought to induce oxidative damage and inflammation to cause AD [27, 28].”
BackgroundSpatial–temporal patterns of brain disconnectome in Alzheimer 's disease
Liang, L., Zhou, P., Ye, C., Yang, Q., & Ma, T. (2023) · Human Brain Mapping · doi:10.1002/hbm.26344 · Cited by 9
“…disease is increasingly considered as a progressive degenerative disease, associated with the aggregation of heterogeneous pathologies, including pathological proteins, cortical atrophy, metabolic dysfunction, cerebrovascular alterations and so on (Dubois et al., 2021; Sweeney et al., 2019).”
BackgroundArioz, B. I., Cotuk, A., Yaka, E. C., & Genç, Ş. (2023) · European Journal of Neuroscience · doi:10.1111/ejn.16226 · Cited by 12
“The most accepted fluid biomarkers are decreased levels of A β 42 and increased levels of t-tau and p-tau in CSF (Dubois et al., 2021).”
BackgroundLeiris, N. D., Perret, P., Lombardi, C., Gözel, B., Chierici, S., Millet, P., Debiossat, M., Bacot, S., Tournier, B. B., Chames, P., et al. (2024) · Journal of Translational Medicine · doi:10.1186/s12967-024-04987-1 · Cited by 10
“It consists of a continuum, starting from an asymptomatic preclinical stage, and progressing to a clinically identifiable disease characterized by means of cognitive and memory tests [3].”
BackgroundZhang, M., Wang, Y., Jiang, J., Jiang, Y., & Song, D. (2024) · Critical Reviews in Analytical Chemistry · doi:10.1080/10408347.2024.2324460 · Cited by 11
“[45,46] It is worth noting that the incidence of AD has increased globally, which suggests the need for further investigation into its pathogenesis and potential therapeutic interventions.”
Katsipis, G., Tzekaki, E. E., Andreadou, E. G., Mouzakidis, C., Baldimtsi, E. N., Karathanasi, E. M., Hassandra, M., Galanis, E., Hatzigeorgiadis, A., Γούδας, Μ., et al. (2024) · Neuroscience Applied · doi:10.1016/j.nsa.2024.104085 · Cited by 12
“However, biofluid biomarker analysis is imperative to increase the diagnosis ’ s availability, sensitivity, and specificity, as suggested in the recent diagnostic criteria (Dubois et al., 2021).”
Filippini, T., Costanzini, S., Chiari, A., Urbano, T., Despini, F., Tondelli, M., Bedin, R., Zamboni, G., Teggi, S., & Vinceti, M. (2024) · International Journal of Health Geographics · doi:10.1186/s12942-024-00384-5 · Cited by 11
Understanding the Molecular Impact of Physical Exercise on Alzheimer’s Disease
Cantón-Suárez, A., Sánchez-Valdeón, L., Bello-Corral, L., Cuevas, M. J., & Estébanez, B. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252413576 · Cited by 16
Toward alpha‐synuclein seed amplification assay in clinical practice
Verdurand, M., Kaczorowski, F., Dautricourt, S., Desestret, V., Formaglio, M., Mollion, H., Petitnicolas, G., Afifi, A., Fourier, A., Garnier‐Crussard, A., et al. (2025) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.70066 · Cited by 11
Diagnostic Accuracy of the Five-Word Test for Mild Cognitive Impairment Due to Alzheimer’s Disease
Fornari, C., Mori, F., Zoppi, N., Libri, I., Silvestri, C., Cosseddu, M., Turrone, R., Maffi, M., Caratozzolo, S., Borroni, B., et al. (2022) · Neurology International · doi:10.3390/neurolint14020029 · Cited by 11
“The evaluation of biomarkers in the CSF or with amyloid‐PET imaging are now wide‐ spread tools in clinical practice for the diagnosis of AD [20].”
BackgroundMethodInfluentialRodriguez, E., García‐Alba, J., Novell, R., & Esteba‐Castillo, S. (2023) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph20065096 · Cited by 11
“In this sense, a subjective cognitive decline (SCD) stage has been proposed as a risk condition announcing possible dementia [16,17], but it must be supported by objective cognitive impairment to be considered part of the AD continuum [18].”
BackgroundZhou, W., Zhou, Y., & Li, J. (2023) · Journal of Clinical Medicine · doi:10.3390/jcm12103589 · Cited by 12
Facial emotion expressivity in patients with Parkinson’s and Alzheimer’s disease
Cannavacciuolo, A., Paparella, G., Salzillo, M., Colella, D., Canevelli, M., Costa, D. D., Birreci, D., Angelini, L., Guerra, A., Ricciardi, L., et al. (2023) · Journal of Neural Transmission · doi:10.1007/s00702-023-02699-2 · Cited by 11
“Parkinson’s disease (PD) and Alzheimer’s disease (AD) are two of the most common neurodegenerative disorders with some overlapping clinical features (Martin 1999; Pos-tuma et al. 2015; Schirinzi et al. 2020; Dubois et al. 2021).”
BackgroundThe Potential of a Stratified Approach to Drug Repurposing in Alzheimer’s Disease
Anderson, C., Bucholc, M., McClean, P. L., & Zhang, S. (2023) · Biomolecules · doi:10.3390/biom14010011 · Cited by 13
“Firstly, the relationship between pathological burden and disease progression is unclear [192,193].”
BackgroundConsensus on rapid screening for prodromal Alzheimer’s disease in China
Huang, L., Li, Q., Lu, Y., Pan, F., Cui, L., Wang, Y., Miao, Y., Chen, T., Li, Y., Wu, J., et al. (2024) · General Psychiatry · doi:10.1136/gpsych-2023-101310 · Cited by 12
Comprehensive characterization of elevated tau PET signal in the absence of amyloid-beta
Weigand, A. J., Edwards, L., Thomas, K. R., Bangen, K. J., Bondi, M. W., & Initiative, A. D. N. (2022) · Brain Communications · doi:10.1093/braincomms/fcac272 · Cited by 13
“The International Working Group on the diagnosis of Alzheimer’s disease recommended that its diagnosis ‘be restricted to people who have positive biomarkers together with specific Alzheimer’s disease phenotypes, whereas biomarker positive cognitively unimpaired individuals should be considered only at-risk for progres…”
BackgroundHao, Z., Liu, K., Zhou, L., & Chen, P. (2023) · Frontiers in Physiology · doi:10.3389/fphys.2023.1193031 · Cited by 10
“AD is a neurodegenerative disease with insidious onset and progressive development, characterized by cognitive impairment, psycho-behavioral abnormalities and reduced social life functions (Dubois et al., 2021).”
BackgroundXie, R., Chen, F., Ma, Y., Hu, W., Zheng, Q., Cao, J., & Wu, Y. (2023) · Frontiers in Pharmacology · doi:10.3389/fphar.2023.1249632 · Cited by 12
“Many studies have demonstrated that the incidence of AD signi fi cantly increases with age (Dubois et al., 2021).”
BackgroundRequired improvements for cerebrospinal fluid-based biomarker tests of Alzheimer’s disease
Gaetani, L., Chiasserini, D., Paoletti, F. P., Bellomo, G., & Parnetti, L. (2023) · Expert Review of Molecular Diagnostics · doi:10.1080/14737159.2023.2276918 · Cited by 10
“These results can be used in conjunction with neuropsychological evaluation according to international diagnostic guidelines [7,98].”
MethodLi, Q.-M., Han, H., Zang, D., Zha, X., Zhou, A., Zhang, F.-Y., & Luo, J. (2024) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.3c08664 · Cited by 10
Kurihara, M., Kondo, S., Ohse, K., Nojima, H., Kikkawa-Saito, E., & Iwata, A. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-240185 · Cited by 10
“Clinical diagnosis is not sufficiently specific [1] and biological confirmation via biomarkers is important [2, 3].”
BackgroundMilos, T., Vuić, B., Balic, N., Farkaš, V., Erjavec, G. N., Štrac, D. Š., Perković, M. N., & Pivac, N. (2024) · Expert Review of Neurotherapeutics · doi:10.1080/14737175.2024.2400683 · Cited by 11
“Determination of CSF amyloid beta (Aβ), total tau (t-tau), and phosphorylated tau (p-tau) levels has been included in both clinical and research diagnostic criteria [18,19,21].”
Longitudinal Assessment of Retinal Microvasculature in Preclinical Alzheimer's Disease
Curro‐Tafili, K. R., van Nispen, R. M. A., den Braber, A., van de Giessen, E., van de Kreeke, J. A., Tan, H. S., Visser, P. J., Bouwman, F. H., & Verbraak, F. D. (2024) · Investigative Ophthalmology & Visual Science · doi:10.1167/iovs.65.12.2 · Cited by 12
An Update of Salivary Biomarkers for the Diagnosis of Alzheimer’s Disease
Guo, H., RuiHuan, Y., Cheng, W., Li, Q., & Du, M. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26052059 · Cited by 14
“Notably, the clinical symptom, dementia, is required for an AD diagnosis according to the guidelines from NINCDS–ADRDA, while no clinical symptoms are required on the basis of recommendations from the NIA-AA [115].”
Bonarota, S., Caruso, G., Domenico, C. D., Sperati, S., Tamigi, F. M., Giulietti, G., Giove, F., Caltagirone, C., & Serra, L. (2025) · NeuroImage · doi:10.1016/j.neuroimage.2025.121264 · Cited by 11
“However, neuroimaging and cognitive biomarkers have been shown to aid both the early diagnostic and prognostic phases (Dubois et al., 2021).”
Lei, Y., Nougaisse, J., Malek, M., Mishu, M. M., Bai, Y., Denney, K., Du, Q., Stranahan, A. M., Garza, J. C., & Lu, X. (2025) · Molecular Psychiatry · doi:10.1038/s41380-025-03067-0 · Cited by 15
“Although cognitive impairment emerges later in the disease process, it remains a critical component for the clinical diagnosis of AD [17].”
Heterogeneity and Factorial Structure in Alzheimer’s Disease: A Cognitive Perspective
Zangrossi, A., Montemurro, S., Altoè, G., & Mondini, S. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210719 · Cited by 10
Blutbasierte Biomarker zur Optimierung der Früh- und Differentialdiagnostik der Alzheimer-Demenz
Hansen, N., Rauter, C. M., & Wiltfang, J. (2022) · Fortschritte der Neurologie · Psychiatrie · doi:10.1055/a-1839-6237 · Cited by 10
“Weniger häufig auftretende Phänotypen der Alzheimer Krankheit umfassen darüber hinaus die Verhaltensvariante (dysex-ekutive Variante), die kortiko-basale Variante oder andere Varian-ten der Primär Progressiven Aphasie [9].”
BackgroundInfluentialValidation study of “Santé-Cerveau”, a digital tool for early cognitive changes identification
Lesoil, C., Bombois, S., Guinebretiere, O., Houot, M., Bahrami, M., Lévy, M., Genthon, R., Bozon, F., Jean-Marie, H., Epelbaum, S., et al. (2023) · Alzheimer s Research & Therapy · doi:10.1186/s13195-023-01204-x · Cited by 12
“Hence, SCD-T can detect a mild cognitive impairment but, above all, an amnestic syndrome of the hippocampal type, a core phenotype of typical Alzheimer’s disease [15].”
BackgroundMethodSelf-citationWang, Y., Zhan, D., & Wang, L. (2023) · PubMed Central · Cited by 9
Ferreira, D. A., Macedo, L. B. C., & Foss, M. P. (2023) · The Clinical Neuropsychologist · doi:10.1080/13854046.2023.2273574 · Cited by 10
“Furthermore, studying NPS in individuals without cognitive impairment is crucial for identifying unique biomarkers for detecting cognitive decline and dementia in asymptomatic individuals (Dubois et al., 2021).”
BackgroundHazan, J., Liu, K. Y., Fox, N. C., & Howard, R. J. (2023) · Brain Communications · doi:10.1093/braincomms/fcad322 · Cited by 10
Blood and Cerebrospinal Fluid Biomarkers in Vascular Dementia and Alzheimer’s Disease
Gorelick, P. B. (2022) · Clinics in Geriatric Medicine · doi:10.1016/j.cger.2022.08.001 · Cited by 11
Liu, Q., He, Y., Wang, Q., Min, S., Geng, H., Liu, Y., & Xu, T. (2025) · Biosensors and Bioelectronics · doi:10.1016/j.bios.2025.118074 · Cited by 12
Diagnostic Tools for Alzheimer’s Disease: A Narrative Review Based on Our Own Research Experience
Park, S.-H., Kwon, K. J., Kim, M. Y., Kim, J., Moon, W., Ryu, H. J., Jang, J., Moon, Y., & K-ARPI (2023) · Dementia and Neurocognitive Disorders · doi:10.12779/dnd.2023.22.1.16 · Cited by 9
Liu, F., Shi, Y., Wu, Q., Chen, H., Wang, Y., Cai, L., & Zhang, N. (2023) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.14418 · Cited by 9
“Moreover, consistent a meta-analysis showing that amyloid PET had a sensitivity of 93% and a specificity of 56% for predicting MCI conversion to AD, 48 PiB results showed a high value in predicting AD dementia conversion from MCI at long-term follow-up with a median time of 32 months.”
BackgroundResultInfluentialChatGPT as a Diagnostic Aid in Alzheimer’s Disease: An Exploratory Study
Haj, M. E., Boutoleau‐Bretonnière, C., Gallouj, K., Wagemann, N., Antoine, P., Kapogiannis, D., & Chapelet, G. (2024) · Journal of Alzheimer s Disease Reports · doi:10.3233/adr-230191 · Cited by 9
Ahmadi, M., Javaheri, D., Khajavi, M., Danesh, K., & Hur, J. (2024) · PLoS ONE · doi:10.1371/journal.pone.0297996 · Cited by 10
Chen, H. M., Li, K. Y., Li, T. L., Wong, G. H. Y., Kwong, E., Ng, R. C.-L., Burrow, M. F., McGrath, C. P. J., & Chen, H. (2024) · Journal of Dentistry · doi:10.1016/j.jdent.2024.104967 · Cited by 9
Characterization of cerebrovascular changes in Alzheimer’s disease mice by photoacoustic imaging
Li, X., Zhang, Z., Shi, H., & Zhou, F. (2024) · Journal of Innovative Optical Health Sciences · doi:10.1142/s179354582450007x · Cited by 9
Molecular probes for super-resolution imaging of drug dynamics
Fang, H., Wang, M., Wei, P., Liu, Q., Su, Y. R., Liu, H., Chen, Y., Su, Z. G., & He, W. (2024) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2024.115330 · Cited by 10
Gonzalez, A. S., Savage, S. A., Alladi, S., Amaral‐Carvalho, V., Arshad, F., Camino, J., Caramelli, P., Comas‐Herrera, A., Cook, J., Cooper, C., et al. (2024) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph21060790 · Cited by 9
Childs, R., Karamacoska, D., Lim, C. K., & Steiner, G. Z. (2024) · Brain Behavior & Immunity - Health · doi:10.1016/j.bbih.2024.100819 · Cited by 9
“…gold standard diagnostic modalities for AD include expensive and largely inaccessible imaging modalities such as positron emission tomography (PET) and invasive collections of cerebrospinal fluid (CSF) by lumbar puncture to measure levels of A β and hyper-phosphorylated tau (Dubois et al., 2021).”
BackgroundAnalysis of individual alpha frequency in a large cohort from a tertiary memory center
Cecchetti, G., Agosta, F., Canu, E., et al. (2024) · European Journal of Neurology · doi:10.1111/ene.16424 · Cited by 9
“…clinical diagno - sis at hospital discharge, including amnestic MCI (aMCI) [ 7], nonam-nestic MCI, multidomain MCI, typical AD, early onset dementia due to AD [5, 8], behavioral variant frontotemporal dementia (bvFTD) [9 ], Lewy body dementia (LBD) [ 10 ], mixed AD, and vascular dementia [11].”
BackgroundHuang, L., Hu, W., Cui, L., Zhang, Z., Lu, Y., Li, Q., Huang, Q., Wang, L., Jiang, J., Guo, Q., et al. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14155 · Cited by 8
de la Monte, S. M., Yang, Y., & Tong, M. (2024) · Journal of Molecular Pathology · doi:10.3390/jmp5030025 · Cited by 10
“Incomplete understanding of the stepwise pathologies, optimum stages of therapeutic intervention, and biomarkers of disease remediation constitutes a major hurdle in the development of effective treatment and preventive measures for WM ARBD [60].”
Motolese, F., Norata, D., Iaccarino, G., Sapio, E., & Capone, F. (2024) · Behavioural Brain Research · doi:10.1016/j.bbr.2024.115289 · Cited by 10
Eratne, D., Li, Q.-X., Lewis, C. C., Dang, C., Kang, M. J., Grewal, J. K., Loi, S. M., Walterfang, M., Evans, A. H., Malpas, C. B., et al. (2024) · Journal of Neurology · doi:10.1007/s00415-024-12732-3 · Cited by 13
“This is likely a reflection of the real-world clinically heterogenous clinical cohort and ranges, that many non-AD disorders have A+T− and other abnormal CSF profiles [35, 36], as well as the recognised challenges (and inaccuracies) of in vivo clinical diagnosis [13, 24, 25, 29, 30].”
InfluentialSelf-citationLi, S., Lin, S., Tu, Y., Qiao, J., & Xiao, S. (2025) · Biomedical Signal Processing and Control · doi:10.1016/j.bspc.2025.107660 · Cited by 9
Wagemann, O., Nübling, G., Martínez-Murcia, F. J., Wlasich, E., Loosli, S. V., Sandkühler, K., Stockbauer, A., Prix, C., Katzdobler, S., Petrera, A., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70040 · Cited by 9
“In Alzheimer’s disease (AD), amyloid-plaques and neurofibrillary tau tangles (NFT) make up the pathophysiological hallmarks causing neurodegeneration, 1,2 known to cause decline in cognitive capacity and everyday functioning.”
Changing definitions of disease: Transformations in the diagnostic criteria for Alzheimer's disease
van der Molen, L. H., Boenink, M., van Lente, H., & Richard, E. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70133 · Cited by 12
“18,22,25,26,28,29 Remarkably,thisconfusionisnotmentionedinthe latest criteria document by the AA 1 .”
InfluentialMultimodal fusion architectures for Alzheimer’s disease diagnosis: An experimental study
Leony, F., & Lin, C. (2025) · Journal of Biomedical Informatics · doi:10.1016/j.jbi.2025.104834 · Cited by 9
Doxycycline: An essential tool for Alzheimer’s disease
Forloni, G. (2025) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2025.118159 · Cited by 11
Windon, C., Gatsonis, C. A., Carrillo, M. C., Romanoff, J., Hanna, L., Glavin, E. E., Gareen, I. F., Gutman, R., Hillner, B. E., March, A., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70504 · Cited by 11
Self-citationYang, C., Huang, K.-Y., Hsu, J., Hu, C., Lu, Y., & Kuan, Y. (2025) · Journal of NeuroEngineering and Rehabilitation · doi:10.1186/s12984-025-01738-1 · Cited by 13
“Third, while advances in biomarkers for AD diagnosis have been significant [69], our reliance on symptomatic clinical approaches may limit the internal validity of the study [70].”
Beyond Frailty in Alzheimer's Disease: Should We Move to the Concept of Intrinsic Capacity?
Garnier‐Crussard, A., Dauphinot, V., Zamudio-Rodriguez, A., & Krolak‐Salmon, P. (2022) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2022.75 · Cited by 9
“Twenty years later, the International Working Group added frailty in their recommendation for clinical diagnosis of AD as a “factor that can increase the risk of progression to Alzheimer ’s disease” (4).”
BackgroundBaldeiras, I., Silva‐Spínola, A., Lima, M., Leitão, M. J., Durães, J., Vieira, D., Tábuas‐Pereira, M., Cruz, V. T., da Rocha, R. P., Alves, L., et al. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220587 · Cited by 10
“Although the intended use of this framework was for research purposes, the challenges regarding its use in everyday clinical practice have been debated [11], and it is therefore important to address how it behaves in the clinical setting of memory clinics.”
InfluentialFang, X., Deng, Y., Xu, X., Shu, W., Tang, F., Li, S., Zhu, T., Zhang, L., Zhong, P., & Mao, R. (2022) · Frontiers in Surgery · doi:10.3389/fsurg.2022.977123 · Cited by 9
Woyk, K., Sahlmann, C. O., Hansen, N., Timäus, C., Müller, S. J., Khadhraoui, E., Wiltfang, J., Lange, C., & Bouter, C. (2022) · Journal of Neuroimaging · doi:10.1111/jon.13068 · Cited by 9
“ß-Amyloid 42 (Aß42) and ß-amyloid 40 (Aß40) were measured in the Neurochemistry Laboratory of the University Medical Center Göttingen using commercially available INNOTEST® β-AMYLOID (1-42) ELISA kit (Fujirebio) and ELISA from IBL (AMYLOID BETA [1-40]).”
MethodPre-targeting amyloid-β with antibodies for potential molecular imaging of Alzheimer's disease
Morgan, K. A., de Veer, M., Miles, L. A., Kelderman, C. A. A., McLean, C., Masters, C. L., Barnham, K. J., White, J. M., Paterson, B. M., & Donnelly, P. S. (2023) · Chemical Communications · doi:10.1039/d2cc06850h · Cited by 8
Moebius, H. J., & Church, K. J. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-220871 · Cited by 9
“For instance, persons with no cognitive impairment can demonstrate biomarker evidence of A pathology and may develop no clinical manifestations of AD in their lifetime [58].”
BackgroundThe Use of Diffusion Kurtosis Imaging for the Differential Diagnosis of Alzheimer’s Disease Spectrum
Zhang, H., Wang, Z., Chan, K., Shea, Y. F., Lee, C., Chiu, P. K., Cao, P., & Mak, H. K. (2023) · Brain Sciences · doi:10.3390/brainsci13040595 · Cited by 9
“Although AD diagnostic criteria have been improved, accurate AD staging for patients with early signs of cognitive symptoms remains challenging [7].”
BackgroundRecent advances in nanoenzymes for Alzheimer's disease treatment
Bi, X., Cao, N., & He, J. (2024) · Colloids and Surfaces B Biointerfaces · doi:10.1016/j.colsurfb.2024.114139 · Cited by 10
Calderón‐Garcidueñas, L. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2022.901447 · Cited by 9
Faldu, K. G., & Shah, J. (2022) · Expert Review of Molecular Diagnostics · doi:10.1080/14737159.2022.2104639 · Cited by 10
“tion and is not effective in preclinical AD (Figure 1) [19,20].”
BackgroundFeng, Y., Chen, X., Zhang, X. D., & Huang, C. (2023) · Genes · doi:10.3390/genes14061285 · Cited by 9
“Particularly, the US National Institute on Aging and the Alzheimer’s Association proposed using biomarkers as a purely biological definition of AD [5].”
BackgroundÖzge, A., Ghouri, R., Öksüz, N., & Taşdelen, B. (2023) · Frontiers in Neurology · doi:10.3389/fneur.2023.1239995 · Cited by 9
On the 2024 Alzheimer's Association Criteria: Still Not Ready for Clinical Use
Zhou, R. Z., Wimo, A. B., & Winblad, B. G. (2024) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2024.141 · Cited by 9
Slovak database of speech affected by neurodegenerative diseases
Rusko, M., Sabo, R., Trnka, M., Zimmermann, A., Malaschitz, R., Ružický, E., Brandoburová, P., Kevická, V., & Škorvánek, M. (2024) · Scientific Data · doi:10.1038/s41597-024-04171-6 · Cited by 21
Liu, Z., Guan, R., Bu, F., & Pan, L. (2022) · Medicine · doi:10.1097/md.0000000000032218 · Cited by 8
“But it turns out that, in any case, many clinical examinations relying on the amyloid beta hypothesis have proved unsuccessful.[56] Thus, the likelihood that many amyloid-beta proteins are no longer essential drivers of AD is enhanced.”
BackgroundLópez, E., Etxebarria‐Elezgarai, J., García‐Sebastián, M., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25094737 · Cited by 8
“According to the International Working Group (IWG), “The diagnosis of AD is clinical-biological and requires the presence of both a specific clinical phenotype of AD and biomarker evidence of AD pathology” [7].”
BackgroundGiuffrè, G. M., Quaranta, D., Citro, S., Morganti, T. G., Martellacci, N., Vita, M. G., Rossini, P. M., Calabresi, P., & Marra, C. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-240150 · Cited by 8
“Therefore, neuropsychological assessments sensitive to earliest signs of AD specific clinical phenotype remain pivotal in both research and clinical practice [3].”
Li, Z., Huang, C., Zhao, X., Gao, Y., & Tian, S. (2024) · Experimental Gerontology · doi:10.1016/j.exger.2024.112547 · Cited by 8
“MCI patients generally present with memory impairment more serious than that normally expected for their age group and cognitive impairment that is not sufficiently severe to meet the criteria for dementia (Dubois et al., 2021).”
BackgroundTreating Alzheimer’s Disease: Focusing on Neurodegenerative Consequences
Sun, M., & Alkon, D. L. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-240479 · Cited by 8
Impaired glymphatic clearance is an important cause of Alzheimer’s disease
Hazzard, I., Batiste, M., Luo, T., Cheung, C., & Lui, F. (2024) · Exploration of Neuroprotective Therapy · doi:10.37349/ent.2024.00091 · Cited by 9
Ikanga, J. N., Jean, K. R., Medina, P., Patel, S. S., Schwinne, M., Epenge, E., Gikelekele, G., Tshengele, N., Kavugho, I., Mampunza, S. M. M., et al. (2024) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2024.1477047 · Cited by 14
Metadata
- Authors
- Dubois, B., Villain, N., Frisoni, G. B., Rabinovici, G. D., Sabbagh, M., Cappa, S., Bejanin, A., Bombois, S., Epelbaum, S., Teichmann, M., Habert, M.-O., Nordberg, A., Blennow, K., Galasko, D., Stern, Y., Rowe, C. C., Salloway, S., Schneider, L. S., Cummings, J. L., & Feldman, H. H.
- Affiliations
- Sorbonne Université (FR)
- University of Geneva (CH)
- University of California, San Francisco (US)
- Cleveland Clinic (US)
- Istituto Universitario di Studi Superiori di Pavia (IT)
- Universitat Autònoma de Barcelona (ES)
- Inserm (FR)
- Institut national de recherche en sciences et technologies du numérique (FR)
- Centre National de la Recherche Scientifique (FR)
- Karolinska University Hospital (SE)
- Sahlgrenska University Hospital (SE)
- University of California San Diego (US)
- Columbia University (US)
- The University of Melbourne (AU)
- Brown University (US)
- University of Southern California (US)
- Corresponding author
- Dubois, Bruno
- ORCID
- Dubois, Bruno
- Villain, Nicolas
- Frisoni, Giovanni B
- Rabinovici, Gil D
- Cappa, Stefano
- Bejanin, Alexandre
- Bombois, Stéphanie
- Epelbaum, Stéphane
- Teichmann, Marc
- Habert, Marie-Odile
- Nordberg, Agneta
- Blennow, Kaj
- Galasko, Douglas
- Stern, Yaakov
- Rowe, Christopher C
- Salloway, Stephen
- Schneider, Lon S
- Cummings, Jeffrey L
- Feldman, Howard H
- Venue
- The Lancet Neurology
- Publisher
- Elsevier BV
- Published
- 2021-06
- Volume
- 20
- Issue
- 6
- Pages
- 484-496
- ISSN
- 1474-4422 (ISSN-L)
- PMC
- PMC8339877
- OpenAlex
- W3159530258
- Semantic Scholar
- dc5f525087f24d7c6a95d667de138557d460fc7e
- Cited by
- 1,051
- References
- 119
- Citations by year
- 2026: 146 · 2025: 272 · 2024: 237 · 2023: 209 · 2022: 153 · 2021: 33
- FWCI
- 28.16
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (am, 171 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- The Lancet Neurology (acceptedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion, other-oa)
- HAL (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Oskar-Bordeaux (Universite de Bordeaux) (submittedVersion)
- Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
- Funders
- National Institutes of Health
- Merck
- Rainwater Charitable Foundation
- U.S. Department of Defense
- Novartis
- National Health and Medical Research Council
- National Institute on Aging
- Roche
- Eisai
- National Institute of General Medical Sciences
- Medtronic
- Adamas Pharmaceuticals
- Johnson and Johnson
- UCB Pharma
- Abbott Laboratories
- American College of Radiology
- Alzheimer's Drug Discovery Foundation
- ACADIA Pharmaceuticals
- Eli Lilly and Company
- Avid Radiopharmaceuticals
- Genentech
- Merz Pharmaceuticals
- Biogen
- Sorbonne Université
- Alzheimer's Association
- GE Healthcare
- National Institute of Neurological Disorders and Stroke
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Oncology › Cancer-related cognitive impairment studies
- Keywords
- Alzheimer's disease, diagnosis, biomarkers, amyloid-beta, tau pathology, NIA-AA criteria, cognitively unimpaired individuals, prodromal Alzheimer's disease, at-risk individuals, comorbidities, diagnostic recommendations
- MeSH terms
- Alzheimer Disease, Humans, Phenotype, Biomarkers, Amyloid beta-Peptides, tau Proteins, Disease Progression, 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.
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