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]
Citations
Cites
McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D., & Stadlan, E. M. (1984) · Neurology · doi:10.1212/wnl.34.7.939 · Cited by 27,915
McKhann, G. M., Knopman, D. S., Chertkow, H., Hyman, B. T., Jack, C. R., Kawas, C. H., Klunk, W. E., Koroshetz, W. J., Manly, J. J., Mayeux, R., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.005 · Cited by 18,657
NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease
Jack, C. R., Bennett, D. A., Blennow, K., Carrillo, M. C., Dunn, B., Haeberlein, S. B., Holtzman, D. M., Jagust, W., Jessen, F., Karlawish, J., et al. (2018) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2018.02.018 · Cited by 10,537
Self-citationAmyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D. (2013) · Neurodegenerative Diseases · doi:10.1159/000337230 · Cited by 10,359
Albert, M. S., DeKosky, S. T., Dickson, D., Dubois, B., Feldman, H. H., Fox, N. C., Gamst, A., Holtzman, D. M., Jagust, W. J., Petersen, R. C., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.008 · Cited by 10,152
Self-citationEuropean Guidelines on cardiovascular disease prevention in clinical practice (version 2012)
Authors/Task Force Members:, Perk, J., De Backer, G., Gohlke, H., Graham, I., Reiner, Ž., Verschuren, M., Albus, C., Benlian, P., Boysen, G., et al. (2012) · European Heart Journal · doi:10.1093/eurheartj/ehs092 · Cited by 8,490
Alzheimer's disease: the amyloid cascade hypothesis
Hardy, J. A., & Higgins, G. A. (1992) · Science · doi:10.1126/science.1566067 · Cited by 7,484
Sperling, R. A., Aisen, P. S., Beckett, L. A., Bennett, D. A., Craft, S., Fagan, A. M., Iwatsubo, T., Jack, C. R., Kaye, J., Montine, T. J., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.003 · Cited by 7,155
Self-citationClassification of primary progressive aphasia and its variants
Gorno-Tempini, M. L., Hillis, A. E., Weintraub, S., Kertesz, A., Mendez, M., Cappa, S. F., Ogar, J. M., Rohrer, J. D., Black, S., Boeve, B. F., et al. (2011) · Neurology · doi:10.1212/wnl.0b013e31821103e6 · Cited by 5,141 · cited 1×
“phenotypes) are: the amnestic syndrome of the hippocampal type 66 (typical), the posterior cortical atrophy variant 67 , and the logopenic variant primary progressive aphasia 68,69 (Supplementary Figure 1).”
BackgroundSelf-citationDiagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB Consortium
McKeith, I. G., Boeve, B. F., Dickson, D. W., Halliday, G., Taylor, J.-P., Weintraub, D., Aarsland, D., Galvin, J., Attems, J., Ballard, C. G., et al. (2017) · Neurology · doi:10.1212/wnl.0000000000004058 · Cited by 4,476
Self-citation
Cited by
Sorted by citations
Items 601–700 of 1,002
Cognitive impairment in patients with chronic cerebral ischemia (discirculatory encephalopathy)
Parfenov, V. A., & Silina, E. V. (2025) · Neurology neuropsychiatry Psychosomatics · doi:10.14412/2074-2711-2025-3120-126 · Cited by 3
Гришина, Д. А., Борисовна, Л. А., & А., М. Е. (2025) · Neurology neuropsychiatry Psychosomatics · doi:10.14412/2074-2711-2025-3-84-91 · Cited by 3
Mi, J., Zhang, S., Lu, X., et al. (2025) · Brain Sciences · doi:10.3390/brainsci15070701 · Cited by 3
“Alzheimer’s disease (AD) is primarily characterized by progressive cognitive dysfunction and pathological changes in the brain, particularly β -amyloid (A β ) deposition and neuronal damage [1].”
Bommarito, G., Griffa, A., Michel, P., Caroline, H., Salvioni, C. P., Pistocchi, S., Alemán-Gómez, Y., Damian, D., Jreige, M., Prior John, O., et al. (2025) · Alzheimer s Research & Therapy · doi:10.1186/s13195-025-01805-8 · Cited by 4
“…criteria were: (i) MCI or dementia with a clinical profile compatible with AD and (ii) positive biomarkers based on cerebrospinal fluid levels of amyloid-beta-42 (Aβ42) or Aβ42/Aβ40 ratio and phosphorylated tau (p-tau), or positive amyloid-PET, according to the most recent published criteria [18].”
Zhang, P., & Ma, Y. (2025) · Neurological Research · doi:10.1080/01616412.2025.2529563 · Cited by 3
“In detail, clinical and cognitive tests lack sufficient sensitivity and specificity in the early pre-symptomatic stages of AD, often leading to delayed diagnosis [6].”
Smith, R. A., Shaw, L. M. J., Palmqvist, S., Mattsson, N., Klein, G., Tonietto, M., Initiative, A. D. N., Quijano‐Rubio, C., Rank, C. M., Andreadou, M., et al. (2025) · Neurology and Therapy · doi:10.1007/s40120-025-00798-8 · Cited by 4
Almarri, B. A. (2025) · PLoS ONE · doi:10.1371/journal.pone.0330085 · Cited by 3
“It progresses irreversibly and impairs individuals’ memory, reasoning abilities, and the ability to perform routine tasks [2].”
Morgado, B., Klafki, H., Bauer, C., Steiert, A., Waniek, K., Lachmann, I., Osterloh, D., Esselmann, H., Hansen, N., Schuchhardt, J., et al. (2025) · European Archives of Psychiatry and Clinical Neuroscience · doi:10.1007/s00406-025-02123-8 · Cited by 6
“…a clinical phenotype of Alzheimer's disease between MCI (n = 24) and mild dementia (n = 17) according to the criteria recommended by the international working group [ 26]) and 41 control subjects with cognitive impair - ment between MCI (n = 22) and mild dementia (n = 19) and normal CSF Aβ42/40.”
Are plasma markers for Alzheimer’s disease ready for clinical use?
Petersen, R. C. (2022) · Nature Aging · doi:10.1038/s43587-022-00176-1 · Cited by 2
Farooq, R., Jawad, U., Khan, I., Zia‐ur‐Rehman, M., Irfan, M. S., & Ullah, S. (2022) · Pakistan Journal of Medical and Health Sciences · doi:10.53350/pjmhs22162952 · Cited by 3
Sabermahani, F., Almasi‐Dooghaee, M., & Sheikhtaheri, A. (2022) · Informatics in Medicine Unlocked · doi:10.1016/j.imu.2022.101039 · Cited by 3
Lipton, R. B., Podger, L., Stewart, W. F., Gómez‐Ulloa, D., Rodriguez, W., Runken, M. C., Barnes, F. B., & Serrano, D. (2022) · Expert Review of Neurotherapeutics · doi:10.1080/14737175.2022.2149324 · Cited by 3
“There have also been tremendous advances in the use of neuroimaging and biomarkers, in both CSF and blood, as eligibility criteria and as outcomes [44,111,118,119].”
BackgroundCerebrospinal fluid YKL‐40 level evolution is associated with autoimmune encephalitis remission
Dorcet, G., Bénaiteau, M., Pariente, J., Ory‐Magne, F., Cheuret, E., Rafiq, M., Brooks, W. H., Puissant‐Lubrano, B., Fortenfant, F., Renaudineau, Y., et al. (2023) · Clinical & Translational Immunology · doi:10.1002/cti2.1439 · Cited by 4
“Samples of interest from the AIE cases were compared with sera of five healthy donors obtained from the French Blood Agency and sera and CSF of 5 control cases diagnosed for probable Alzheimer’s disease (AD) in our tertiary centre.(61) This study complies the Declaration of Helsinki on the Protection of Persons and wa…”
ResultSaposnik, G., Sánchez‐Benavides, G., García-Arcelay, E., Macías, E. F., Bensi, C., Carmelingo, S., Allegri, R., Pérez-Martínez, D. A., & Mauriño, J. (2023) · Neurology and Therapy · doi:10.1007/s40120-023-00466-9 · Cited by 4
“Second, our study will not cover the whole spectrum of patients with AD, as the clinical criteria for the use of anti-amyloid-b agents (as per clinical trials and labels) only include patients with early AD with AD core biomarkers [5, 6, 10, 11].”
BackgroundStrategies for translating proteomics discoveries into drug discovery for dementia
Halder, A., & Drummond, E. (2023) · Neural Regeneration Research · doi:10.4103/1673-5374.373681 · Cited by 4
“…testing for mutations in GRN and C9orf72 , there are currently no fluid biomarkers that permit diagnosis of sporadic FTD. Well-recognized AD biomarkers include amyloid and tau cerebrospinal fluid (CSF) levels and positron emission tomography (PET) scans (Fleisher et al., 2020; Dubois et al., 2021).”
Hansen, N., Rentzsch, K., Hirschel, S., Bartels, C., Wiltfang, J., & Malchow, B. (2023) · Antibodies · doi:10.3390/antib12020034 · Cited by 3
“The latest diagnostic guidelines were followed to diagnose Alzheimer’s disease (AD), considering both clinical [21] and laboratory factors [22].”
MethodMICROGLIAL PHAGOCYTOSIS IN RATS WITH DIFFERENT MODELS OF ALZHEIMER'S DISEASE
Nefedova, A. (2023) · Biotechnologia Acta · doi:10.15407/biotech16.01.057 · Cited by 3
EXTRATOS FLORAIS DO DOMÍNIO CERRADO E INIBIÇÃO DA ACETILCOLINESTERASE
Filho, A. C. P. D. M., Ventura, M. V. A., Alves, I., et al. (2023) · Nativa · doi:10.31413/nat.v11i2.14555 · Cited by 3
Brain Imaging in Routine Psychiatric Practice.
Vogel, A. C., & BLACK, K. J. (2024) · PubMed Central · Cited by 4
Impaired lexical access for unique entities in individuals with subjective cognitive decline
Macoir, J., Tremblay, P., Beaudoin, S., Parent, M., & Hudon, C. (2024) · Applied Neuropsychology Adult · doi:10.1080/23279095.2024.2344636 · Cited by 3
“Moreover, as the aging population continues to grow, the prevalence of MNCD is expected to persistently rise (Alzheimer Association, 2023).”
InfluentialStereotactic surgery and its application in Alzheimer’s disease rat models
Tekin, E. (2024) · Journal of Surgery and Medicine · doi:10.28982/josam.7643 · Cited by 3
“AD, which is the most common cause of dementia, currently does not have a definitive treatment [3].”
BackgroundZou, Q., Shang, J., Liu, J.-X., & Gao, R. (2024) · IEEE Journal of Biomedical and Health Informatics · doi:10.1109/jbhi.2024.3442468 · Cited by 4
Signal-amplified detection of amyloid-β aggregates based on plasmon-enhanced fluorescence
Sun, W. C., Li, C., Yu, J., Liang, X., Gao, X., Shen, B., & Yang, Y. (2024) · Microchemical Journal · doi:10.1016/j.microc.2024.111541 · Cited by 3
Nabizadeh, F., & Initiative, A. D. N. (2025) · Cerebral Cortex · doi:10.1093/cercor/bhaf053 · Cited by 3
Christianson, K., Prabhu, M., Popp, Z., Rahman, S., Drane, J., Lee, M., Lathan, C., Lin, H., Au, R., Sunderaraman, P., et al. (2025) · Exploration of Medicine · doi:10.37349/emed.2025.1001356 · Cited by 3
“…diagnostic considerations, the traditional approach for characterizing cognitive symptoms consists of a single session of intensive neuropsychological (NP) testing to determine if generalized impairment and/or disorder-specific patterns of dispersion across cognitive domains are observable [4, 5].”
Positron Emission Tomography in Animal Models of Alzheimer’s Disease AmyloidosisPreprint
Ni, R. (2021) · Preprints.org · doi:10.20944/preprints202110.0222.v1 · Cited by 2
Early Detection of AD Biomarkers and the Ethical Criteria for Screening Programs
Tromp, K., Bunnik, E. M., Smedinga, M., et al. (2021) · AJOB Neuroscience · doi:10.1080/21507740.2021.1941407 · Cited by 3
“However, for the clinical context arguments have been made that symptoms of cognitive decline need to be present in order to diagnose AD and that biomarkers alone do not justify a clinical diagnosis, not least because many people with abnormal biomarkers never develop symptoms of dementia (Dubois et al. 2021; Schermer…”
BackgroundAT(N) predicts near-term development of Alzheimer’s disease symptoms in unimpaired older adultsPreprint
Strikwerda‐Brown, C., Gonneaud, J., Hobbs, D. A., St‐Onge, F., Binette, A. P., Ozlen, H., Provost, K., Soucy, J., Buckley, R. F., Benzinger, T. L. S., et al. (2022) · medRxiv · doi:10.1101/2022.05.09.22274638 · Cited by 3
Self-citationHøilund‐Carlsen, P. F., Alavi, A. A., & Revheim, M.-E. R. (2023) · Clinical Nuclear Medicine · doi:10.1097/rlu.0000000000004509 · Cited by 3
Eratne, D., Li, Q., Lewis, C. C., et al. (2024) · medRxiv · doi:10.1101/2024.04.29.24306586 · Cited by 3
“For the purpose of this study, we defined AD based on classification of cerebrospinal fluid (CSF) AD proteins, recommended for diagnosis [19], and which have been validated against amyloid positron emission tomography (PET; currently considered ‘gold standard’ for a premortem diagnosis of AD) with…”
MethodSelf-citationProtein-Taggable Near-Infrared Photocages for Theranostics of Alzheimer’s Disease
Ma, M., & Zhao, Y. (2025) · ACS Central Science · doi:10.1021/acscentsci.5c00553 · Cited by 3
Mekulu, K., Aqlan, F., & Yang, H. Y. (2025) · medRxiv · doi:10.1101/2025.06.12.25329529 · Cited by 3
An, L., Binette, A. P., Hristovska, I., Vilkaite, G., Xiao, Y., Zendehdel, R., Dong, Z., Smets, B., Saloner, R., Tasaki, S., et al. (2025) · medRxiv · doi:10.1101/2025.06.27.25330344 · Cited by 3
“Given that there are multiple criteria for the diagnosis of AD 92–94 and multiple interpretations of those criteria, this issue will be present in any real-world application.”
Bayart, J., Villain, N., Planche, V., et al. (2025) · medRxiv · doi:10.64898/2025.12.19.25342412 · Cited by 3
Self-citationBabiloni, C., Güntekin, B., Yener, G., & Percio, C. D. (2023) · Neuromethods · doi:10.1007/978-1-0716-3545-2_4 · Cited by 3
Kaufmann, L., Grünbaum, T., Janssen, R. J., Weiss, E. M., Benke, T., Dal‐Bianco, P., Defrancesco, M., Ransmayr, G. N., Schmidt, R., Stögmann, E., et al. (2024) · PLoS ONE · doi:10.1371/journal.pone.0307111 · Cited by 2
Early diagnosis of Alzheimer’s disease: potential of 18F-FDG PET as a biomarker of neurodegeneration
Emelin, А. Y., Litvinenko, I., Lobzin, V. Y., Lupanov, I. A., Kolmakova, K. A., Дынин, П. С., & Boykov, I. V. (2024) · Russian Military Medical Academy Reports · doi:10.17816/rmmar636520 · Cited by 2
Goerttler, S., He, F., & Wu, M. (2024) · doi:10.1109/embc53108.2024.10782936 · Cited by 2
“The current clinical gold standard of Alzheimer’s disease (AD) diagnosis integrates criteria derived from cognitive testing and positron emission tomography biomarkers [1].”
BackgroundCognition Assessment with ICOPE-Monitor: Identifying Candidates for Novel Therapies
González-Bautista, E., Soto, M. E., Fourteau, M., Berbon, C., Vellas, B. J., Delrieu, J., & Angioni, D. (2025) · Journal of the American Medical Directors Association · doi:10.1016/j.jamda.2024.105483 · Cited by 2
Topic Issue: “Translational Advances in Neurodegenerative Dementias”
Antonioni, A., & Lorenzo, F. D. (2025) · Neurology International · doi:10.3390/neurolint17020031 · Cited by 2
Veljanoska, E., Gomes, S., Szende, Á., Cabra, A., Munter-Young, R., & Gordois, A. (2025) · Value in Health · doi:10.1016/j.jval.2025.02.011 · Cited by 2
de la Monte, S. M., Yang, Y., Prabhu, A., & Tong, M. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26094190 · Cited by 4
Alahmari, K. A., & Alshehri, S. (2025) · Journal of Clinical Medicine · doi:10.3390/jcm14134544 · Cited by 2
“The diagnostic classification was established using internationally recognized clinical criteria [11].”
Fluid Markers of Alzheimer Disease
Sutphen, C. L., Volluz, K., & Tarawneh, R. M. (2025) · Springer eBooks · doi:10.1007/978-3-031-80849-4_8 · Cited by 2
Clinimetrics: Towards a diagnostic neuropsychology grounded in Alzheimer's disease
Ilardi, C. R. (2025) · Journal of Neuropsychology · doi:10.1111/jnp.70008 · Cited by 2
Low Frequency of Dementia with Lewy Bodies Diagnosis in a Colombian Memory Clinic
Rodríguez, F. B., Escudero, J. M. S., Borda, M. G., Salazar‐Londoño, S., Cano, C. A., Aarsland, D., & COL‐DLB (2025) · Movement Disorders Clinical Practice · doi:10.1002/mdc3.70345 · Cited by 2
“12 For AD, we applied the International Working Group 2021 criteria 13 and the requirements from the American Psychiatric Association 14 for VaD.”
Diagnosis and treatment of cognitive impairment in outpatient practice
Parfenov, V. A., Silina, E. V., & Danielyan, A. R. (2025) · Meditsinskiy sovet = Medical Council · doi:10.21518/ms2025-266 · Cited by 2
Alzheimer Syndrome or Age-Related Dementia—History, Therapy and Prevention
Bermejo‐Pareja, F., & del Ser, T. (2025) · Journal of Clinical Medicine · doi:10.3390/jcm14217752 · Cited by 2
“One group led by French neurologist Bruno Dubois and the International Working Group (IWG), explicitly promoted by Big Pharma, first proposed a nosological shift in AD: the biological AD diagnosis [20,120–123], although in the last formulation, it admitted some clinical modification [124].”
Amyloid PET Z Score Quantification and Correlation with Visual Semiquantitative Grading
Yadav, D., Knight‐Greenfield, A., Moirano, J., Nordvig, A. S., Salgado, M. W., Hamed, M. A., Lin, M., RoyChoudhury, A., Blum, S., Keil, S. A., et al. (2025) · American Journal of Neuroradiology · doi:10.3174/ajnr.a9079 · Cited by 2
Shim, S., Cho, H., Lee, J. H., Cho, W. W., Kim, J., Lee, S.-M., Lee, S.-M., & Shin, D. (2025) · Analytica Chimica Acta · doi:10.1016/j.aca.2025.344851 · Cited by 2
Xu, Y., Li, N., Xu, L., Cui, X., Ju, R., Li, M., Zhao, J., & Han, F. (2025) · Journal of Pharmaceutical and Biomedical Analysis · doi:10.1016/j.jpba.2025.117251 · Cited by 2
Salsabila, N. R., Azzahra, A. R., Zakiah, S., Zulva, A., Yudistira, N., & Muflikhah, L. (2025) · Journal of Computational Mathematics and Data Science · doi:10.1016/j.jcmds.2025.100129 · Cited by 2
Sacchi, L., Arcaro, M., Bocca, G., Schmid, L., Carandini, T., Ghezzi, L., Pintus, M., Pietroboni, A. M., Fenoglio, C., Serpente, M., et al. (2025) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2025.1688996 · Cited by 3
Liang, Z., Su, L., Shi, Y., et al. (2025) · Journal of Affective Disorders · doi:10.1016/j.jad.2025.120809 · Cited by 2
Suleman, M. U., Mursaleen, M., Khalil, U., Khan, S. A., Saboor, A., Hussnain, M. A., Zahir, M., Khan, U. A., Rehman, D. U., & Tabassum, S. N. (2025) · Annals of Medicine and Surgery · doi:10.1097/ms9.0000000000004505 · Cited by 2
“0 cleared (2024) for ARIA lesion quantification [ 12 ] .”
Advances in Diagnostics and Treatments for Alzheimer’s Disease
Sunderland, A., Thatcher, A. L., Rackley, E. V., & Kuruvilla, T. (2025) · British Journal of Hospital Medicine · doi:10.12968/hmed.2025.0492 · Cited by 4
Roveta, F., Pizzini, F. B., Natale, V., et al. (2025) · Neurology · doi:10.1212/wnl.0000000000214477 · Cited by 2
Self-citationAbdulaal, A. H., Valizadeh, M., & Amirani, M. C. (2026) · Biomedical Signal Processing and Control · doi:10.1016/j.bspc.2026.109559 · Cited by 2
Xie, P., Wang, X., Wang, H., Xue, H., He, S., Li, L., Wong, M. S., & Qiao, X. G. (2026) · Biosensors and Bioelectronics · doi:10.1016/j.bios.2026.118430 · Cited by 3
Defining Alzheimer’s disease: stipulations and the ethics of diagnostic change
Michalon, R., Planche, V., Lemoine, M., Keuck, L., & Villain, N. (2026) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp-2025-337832 · Cited by 2
“14 16 These revisions did not challenge the clinical–pathological foundation established by the 1970s stipulation.”
Self-citationNeuronal PPP2R5C in plasma is a potential biomarker for early diagnosis of Alzheimer’s disease
Luo, S., Liu, H., Xiao, T., Li, Y., Liu, X., Xiao, X., Liao, X., Liu, Y., Zhou, Y., Wang, J.-L., et al. (2026) · Cell Reports Medicine · doi:10.1016/j.xcrm.2026.102631 · Cited by 3
“…have shifted the treat-ment from the late stages of the disease toward the earlier stages, introducing the possibility of pre-symptomatic diagnosis, 7 especially for developing blood-based markers for AD early diagnosis has receiving considerable attention, 8–10 which is further reflected in…”
Burry, E., Plumacker, F., Villain, N., Amaral, S., Damier, P., Delrieu, J., Mackowiak, M.-A., Michalon, R., Mohr, S., Planche, V., et al. (2026) · Revue Neurologique · doi:10.1016/j.neurol.2026.01.267 · Cited by 5
Self-citationNanomaterials for Alzheimer’s disease: emerging strategies in diagnosis and therapy
Na, Y., Bai, J., Zhang, N., Geng, F., & Wang, X. (2026) · Journal of Nanobiotechnology · doi:10.1186/s12951-026-04281-w · Cited by 4
Andrews, D., Golchi, S., Collins, D. L., & Initiative, F. T. A. D. N. (2026) · Alzheimer s Research & Therapy · doi:10.1186/s13195-026-02024-5 · Cited by 6
“Unmeasured factors such as evolving AD diagnostic criteria could enhance differences between a modern Recruited Cohort and External Cohort drawn from years-old retrospective datasets [12–15].”
Temporal Interference Stimulation Enhances Neural Regeneration
Peressotti, S., Garrido, M. G., Dzialecka, P., Law, R. M. H., Lara, R. P., Geary, B., Faillace, E., Aslie, S. M.-N., Wojewska, M. J., Otero‐Jimenez, M., et al. (2026) · Advanced Science · doi:10.1002/advs.202524341 · Cited by 3
Omics-driven strategies for identifying biomarkers in Alzheimer’s disease
Khan, Y., Rekha, A., Ballal, S., Maharana, L., Maqbool, M., Goyal, K., Mishra, R., Uniyal, P., Alam, P., Aljarba, T. M., et al. (2026) · Metabolic Brain Disease · doi:10.1007/s11011-026-01873-1 · Cited by 3
“Multiple PET tracers, such as Florbetapir and Flutemetamol have affinity to Aβ plaques, thus allow - ing their visualization in vivo (Bai et al. 2021; Dubois et al. 2021).”
GRK5 Deficiency in the Hippocampus Leads to Cognitive Impairment via Abnormal Microglial Alterations
Shen, H., Zhang, T., Ji, Y., Zhang, Y., Wang, Y., Jiang, Y., Chen, X., Liang, Q., Wu, K., Lu, X., et al. (2022) · Molecular Neurobiology · doi:10.1007/s12035-022-03151-4 · Cited by 2
Alzheimer’s Disease: Not Just for the Aged?
Perry, G. L. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230016 · Cited by 4
“However, some results do not conform with the recent AD diagnostic criteria proposed by the National Institute on Aging-Alzheimer’s Association (NIA-AA) [5] and the International Working Group [6], such as negative PET results.”
ResultPathology vs pathogenesis: Rationale and pitfalls in the clinicopathology model of neurodegeneration
Donadio, V. A., Sturchio, A., Rizzo, G., Abu‐Rumeileh, S., Liguori, R., & Espay, A. J. (2023) · Handbook of clinical neurology · doi:10.1016/b978-0-323-85538-9.00001-8 · Cited by 2
The theoretical problems of “prodrome” and “phenoconversion” in neurodegeneration
Sturchio, A., & Espay, A. J. (2023) · Handbook of clinical neurology · doi:10.1016/b978-0-323-85538-9.00002-x · Cited by 2
Palomo, M. S. M., & Zea‐Sevilla, M. A. (2023) · Medicine - Programa de Formación Médica Continuada Acreditado · doi:10.1016/j.med.2023.03.002 · Cited by 4
Shpilyukova, Y. A., Protopopova, A. O., Abramycheva, N. Y., Fedotova, E. Y., & Illarioshkin, S. N. (2023) · Neurology neuropsychiatry Psychosomatics · doi:10.14412/2074-2711-2023-2-63-67 · Cited by 2
Li, Z., Lin, H.-S., Huang, X.-P., Zhang, S.-Q. Y., Shu, X., & Wu, X. (2023) · Ageing and Neurodegenerative Diseases · doi:10.20517/and.2023.04 · Cited by 2
Improving Clinical Trials of Antioxidants in Alzheimer’s Disease
Daly, T. P. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230308 · Cited by 2
Zilioli, A., Misirocchi, F., Pancaldi, B., Mutti, C., Ganazzoli, C., Morelli, N., Pellegrini, F. F., Messa, G., Scarlattei, M., Mohanty, R., et al. (2023) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2023.122806 · Cited by 2
“Furthermore, its importance in AD detection is underscored by the latest proposed criteria for AD diagnosis [57].”
Marco, M. D., Wright, L., Valera‐Bermejo, J. M., & Ferguson, C. E. (2023) · Neuropsychologia · doi:10.1016/j.neuropsychologia.2023.108741 · Cited by 3
“First, although we applied a robust set of exclusion criteria to minimise aetiological variability, we did not rely on biological criteria (e.g., Dubois et al., 2021).”
Les phases prodromique et préclinique de la maladie d’Alzheimer
Planche, V., & Villain, N. (2024) · Pratique Neurologique - FMC · doi:10.1016/j.praneu.2024.01.005 · Cited by 2
Self-citationPressman, P. (2024) · Elsevier eBooks · doi:10.1016/b978-0-323-95702-1.00119-6 · Cited by 2
Chang, H., Huang, K., Huang, C.-G., Huang, C., Huang, S., Lin, K., & Chang, C. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25115607 · Cited by 2
“Participants who fulfilled the updated NIA-AA 2018 criteria [1] were considered to have AD [50].”
MethodXu, C., Wu, W., Fan, Y., & Zhu, S. (2024) · Frontiers in Neurology · doi:10.3389/fneur.2024.1401880 · Cited by 2
Low-dose diazepam improves cognitive function in APP/PS1 mouse models: Involvement of AMPA receptors
Chen, J., Zhang, M., Shen, Z., Tang, M., Zeng, Y., Bai, D., Zhao, P., & Jiang, G. (2024) · Brain Research · doi:10.1016/j.brainres.2024.149207 · Cited by 3
Timing of biomarker changes preceding Alzheimer’s disease: for diagnosis, treatment or prevention?
Quan, M. (2024) · Science China Life Sciences · doi:10.1007/s11427-024-2733-7 · Cited by 2
“These criteria stipulate that the presence of objective cognitive impairment (MCI or dementia) in conjunction with positive AD biomarkers is required for a clinical diagnosis of AD (Dubois et al., 2021).”
Alzheimer's disease: part 2 – the present
Nitríni, R. (2024) · Arquivos de Neuro-Psiquiatria · doi:10.1055/s-0044-1791755 · Cited by 3
Graham, M., Rossor, M., Lawlor, B., & Naci, L. (2024) · Journal of Alzheimer's Disease · doi:10.1177/13872877241292370 · Cited by 2
“…information about modi fi able risk factors to research participants (e.g., those captured in dementia risk scores like CAIDE) has not been discussed in previous recommendations, 17 despite recent studies showing that these factors are strongly associated with reduced brain health in mid-life.”
Ultra-fast [18F]florbetapir PET imaging using the uMI Panorama PET/CT system
Yang, X., Wu, M., Liang, M., Zhang, H., Li, B., Mao, C., Dong, L., Wang, Y., Xing, H., Ren, C., et al. (2024) · EJNMMI Physics · doi:10.1186/s40658-024-00712-5 · Cited by 2
The deprivation cascade hypothesis of dementia
Daly, T. P. (2025) · Aging and Health Research · doi:10.1016/j.ahr.2024.100219 · Cited by 4
OAS1: A Protective Mechanism for Alzheimer’s Disease? An Exploration of Data and Possible Mechanisms
Elsworthy, R. J., Pearce, A., Masoudzadeh, F., Koska, K., Lodhiya, H., Meher, G., Adjej, J., & Brookes, K. J. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26020524 · Cited by 3
Haag, L., Lancini, E., Yakupov, R., Ziegler, G., Yi, Y., Lüsebrink, F., Glanz, W., Peters, O., Spruth, E. J., Altenstein, S., et al. (2024) · Brain Communications · doi:10.1093/braincomms/fcaf031 · Cited by 2
Self-citationDeveloping non-invasive molecular markers for early risk assessment of Alzheimer's disease
Sur, T. K., Mondal, T., Noreen, Z., Johnson, J., Nunlee‐Bland, G., Loffredo, C. A., Korba, B. E., Chandra, V., Jana, S. S., Kwabi‐Addo, B., et al. (2025) · Biomarkers in Neuropsychiatry · doi:10.1016/j.bionps.2025.100120 · Cited by 3
“…change, (iii) A+T−N− as AD, (iv) A+T−N + as AD, (v) A+T−N + as Alzheimer’s and concomitant suspected non-AD pathological change, (vi) A−T−N− as non-AD pathological change, (vii) A−T−N + as non-AD pathological change, and (viii) A−T + N + as non-AD pathological change (Dubois et al., 2021).”
InfluentialSalman, Y., Huyghe, L., Quenon, L., Ghysens, O., Malotaux, V., Tomé, S. O., Thal, D. R., & Hanseeuw, B. J. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251314199 · Cited by 2
“28 resonance imaging (MRI).”
InfluentialSchinke, H., Jonsson, M. F., Gummesson, M., Nilsson, R., Gaupp, S., Manuilova, E., McIlwrick, S., Weinberger, J.-P., Rutz, S., Carboni, M., et al. (2025) · Clinical Chemistry and Laboratory Medicine (CCLM) · doi:10.1515/cclm-2024-1476 · Cited by 2
“…Group on the clinical diagnosis of AD suggest that the assessment of biological parameters, such as cerebrospinal fl uid (CSF) biomarkers and amyloid positivity by positron emission tomography (PET) imaging, may help detect biological changes before symptom onset and aid in early AD diagnosis [9].”
Mestre, T., & Sampaio, C. M. (2025) · Movement Disorders · doi:10.1002/mds.30173 · Cited by 2
Criminal Behavior in Early Onset Neurodegenerative Diseases
Soppela, H., Aaltonen, M., Aho, K., Heikkinen, S. V., Kivisild, A., Lehtonen, A., Leppänen, L., Mäki‐Petäjä‐Leinonen, A., Rinnankoski, I., Tervonen, L., et al. (2025) · European Journal of Neurology · doi:10.1111/ene.70134 · Cited by 3
“The diagnoses were based on the previously published criteria [19–25].”
The International Working Group recommendations on cognitively unimpaired individuals
Villain, N., Frisoni, G. B., Feldman, H., et al. (2025) · The Lancet Neurology · doi:10.1016/s1474-4422(25)00162-0 · Cited by 2
Self-citationListerin Alleviates Alzheimer's Disease through IRE1‐mediated Decay of TLR4 mRNA
Qin, F., Cao, R., Bai, X., Yuan, J., Sun, W., Zheng, Y., Qi, X., Zhao, W., Liu, B., & Gao, C. (2025) · Advanced Science · doi:10.1002/advs.202414956 · Cited by 2
Wang, Y., Zhu, T., Cheng, Q., Cui, X., Zhang, P.-F., Lu, Z., & Initiative, A. D. N. (2025) · Journal of Alzheimer s Disease Reports · doi:10.1177/25424823251331110 · Cited by 2
The biological diagnosis of Alzheimer’s disease using blood-based biomarkers: A Canadian prospective
Kumar, P., Mousavi, A., & Frykman, H. (2025) · Clinical Biochemistry · doi:10.1016/j.clinbiochem.2025.110980 · Cited by 2
Singh, R. K., Bekena, S., Damera, N., Zhu, Y., Trani, J., & Babulal, G. M. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251365219 · Cited by 4
“8 The limitations of current diagnostic approaches are further exempli fi ed by studies indicating that 16% of patients with a clinical diagnosis of AD are amyloid-negative, calling into question the accuracy of existing diagnostic frameworks.”
Detection of Alzheimer’s Disease Using Extreme Band Powers in EEG Data
Sarkar, S., Chakraborty, A., Sinha, A., et al. (2025) · IEEE Applied Sensing Conference (APSCON) · doi:10.1109/apscon63569.2025.11144072 · Cited by 2
“The diagnosis of AD is done using a combination of multiple methods like physical and neurological examination, cognitive tests batteries, neuropsychological testing, brain imaging like positron emission tomography, functional magnetic resonance imaging etc. [3].”
Coppinger, J., West, T., Kirmess, K. M., Fogelman, I., Ray, S., Aurora, S. K., Verghese, P. B., Braunstein, J. B., Yarasheski, K. E., & (ADNI), T. A. D. N. I. (2025) · npj Dementia · doi:10.1038/s44400-025-00026-y · Cited by 2
“…leaders and expert panels convened by the World Health Organization (WHO), Global CEO Initiative on AD (CEOi), and the Alz-heimer ’ s Association outlined diagnostic performance characteristics that should be considered with fl uid biomarkers targeted for use in clinical settings 8,12,24 – 27 .”
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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