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 501–600 of 1,002
Evolution of the diagnostic frontiers of Alzheimer’s disease and new therapeutic possibilities
Si, G. (2022) · S S Korsakov Journal of Neurology and Psychiatry · doi:10.17116/jnevro202212211238 · Cited by 5
Integrated Multimodal Omics and Dietary Approaches for the Management of Neurodegeneration
Murai, T., & Matsuda, S. (2023) · Epigenomes · doi:10.3390/epigenomes7030020 · Cited by 5
The Cracked Potential of Boron-containing Compounds in Alzheimer’s Disease
Soriano-Ursua, M. A., & Farfán‐García, E. D. (2023) · Central Nervous System Agents in Medicinal Chemistry · doi:10.2174/0118715249264888230920060941 · Cited by 5
Real‐world performance of plasma p‐tau181 in a heterogeneous memory clinic cohort
Parvizi, T., Wurm, R., König, T., Silvaieh, S., Altmann, P., Klotz, S., Regelsberger, G., Traub‐Weidinger, T., Gelpí, E., & Stögmann, E. (2024) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.52116 · Cited by 5
The Biomarkerization of Alzheimer’s Disease: From (Early) Diagnosis to Anticipation?
Boenink, M., & van der Molen, L. H. (2024) · Philosophy and medicine · doi:10.1007/978-3-031-62241-0_11 · Cited by 6
Leng, F., Hinz, R., Gentleman, S., Dani, M., Brooks, D. J., & Edison, P. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-230442 · Cited by 5
Vagiakis, I., Bakirtzis, C., Andravizou, A., & Pirounides, D. (2024) · Healthcare · doi:10.3390/healthcare12161589 · Cited by 6
“The diagnosis of AD is primarily clinical [7].”
BackgroundComparative mapping of single‐cell transcriptomic landscapes in neurodegenerative diseases
Shwab, E. K., Man, Z., Gingerich, D. C., Gamache, J., Garrett, M. E., Serrano, G. E., Beach, T. G., Crawford, G. E., Ashley‐Koch, A. E., & Chiba‐Falek, O. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70012 · Cited by 7
“7,102 On the other hand, motor symptoms are not typically associated with AD, 101 and PD is commonly associated with mild or absent cognitive decline, specifically in the early disease stages.”
Sabermahani, F., Almasi‐Dooghaee, M., & Sheikhtaheri, A. (2022) · Studies in health technology and informatics · doi:10.3233/shti220366 · Cited by 6
“Alzheimer's disease (AD) is one of the age-related disorders, with the incidence of AD increasing with the number of senior persons in the society [1].”
BackgroundWang, Q., Li, X., Teng, N., & Li, X. (2022) · Psychogeriatrics · doi:10.1111/psyg.12869 · Cited by 5
He, Q., Shi, L., Luo, Y., Wan, C., Malone, I. B., Mok, V., Cole, J. H., & Anatürk, M. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.932125 · Cited by 5
Sensi, S. L., Russo, M., & Tiraboschi, P. (2023) · Handbook of clinical neurology · doi:10.1016/b978-0-323-85538-9.00015-8 · Cited by 5
Nihashi, T., Sakurai, K., Kato, T., Kimura, Y., Ito, K., Nakamura, A., & Terasawa, T. (2024) · Diagnostic and Prognostic Research · doi:10.1186/s41512-024-00167-3 · Cited by 5
“The current diagnostic criteria necessitate confirmation of brain accumulation of both Aβ and tau through positron emission tomography (PET) or central spinal fluid (CSF) testing [4].”
BackgroundAD and its comorbidities: An obstacle to develop a clinically efficient treatment?
Baker, J., & Schott, J. M. (2022) · Revue Neurologique · doi:10.1016/j.neurol.2022.03.001 · Cited by 5
Sobek, J., Li, J., Combes, B. F., Gerez, J., Nilsson, K. P. R., Henrich, M. T., Geibl, F. F., Shi, K., Rominger, A., Oertel, W. H., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.03.12.531651 · Cited by 5
Self-citationAssessment of extracellular vesicle protein cargo as neurodegenerative disease biomarkersPreprint
Gilboa, T., Ter‐Ovanesyan, D., Wang, S., Whiteman, S. T., Kannarkat, G. T., Church, G. M., Chen‐Plotkin, A. S., & Walt, D. R. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.11.02.565137 · Cited by 4
The Great Debate in Diagnosing Alzheimer Disease
Villain, N., & Paretsky, M. S. (2024) · Neurology · doi:10.1212/wnl.0000000000209836 · Cited by 5
Self-citationFazeli, B., Botzenhardt, S., Bachhuber, F., Klassen, P., Klose, V., Dorst, J., Wiesenfarth, M., Uzelac, Ž., Jesse, S., Brenner, D., et al. (2025) · EBioMedicine · doi:10.1016/j.ebiom.2025.105930 · Cited by 5
“29 This diagnosis was further supported by the analysis of core CSF biomarkers (A: Abeta 42 to 40 ratio, T: phosphorylated tau 181 (pTau181), N: total tau), following the recommendations from the National Institute on Ageing and Alzheimer’s Association.”
Singh, R., Mishra, A., Kumar, V., Gupta, A., Zehra, S., Rani, N., Dhingra, R., Modi, G. P., Inampudi, K. K., Nikolajeff, F. K., et al. (2025) · Clinica Chimica Acta · doi:10.1016/j.cca.2025.120761 · Cited by 6
Titze‐de‐Almeida, R., Gomes, G. D. M. O., dos Santos, T. C., & Titze-de-Almeida, S. S. (2025) · Pharmaceuticals · doi:10.3390/ph19010026 · Cited by 5
“Other contributing factors to AD risk include depression, obesity, subjective cognitive decline, neurodegenerative markers visible on imaging, and co-pathologies [4–12].”
A deep joint-learning proteomics model for diagnosis of six conditions associated with dementia
An, L., Binette, A. P., Hristovska, I., Vilkaite, G., Xiao, Y., Zendehdel, R., Dong, Z., Smets, B., Saloner, R., Tasaki, S., et al. (2026) · Nature Medicine · doi:10.1038/s41591-026-04303-y · Cited by 11
“Given that there are multiple criteria for the diagnosis of AD 38,39 and multiple interpretations of those criteria, this issue will be present in any real-world application.”
Hansen, N., Hirschel, S., Teegen, B., Wiltfang, J., & Malchow, B. (2022) · Frontiers in Dementia · doi:10.3389/frdem.2022.975851 · Cited by 4
“” All patients shared the feature of a hippocampus-based memory dysfunction concurring with the classical AD phenotype (Dubois et al., 2021).”
BackgroundResultGraessel, E., & Lauer, N. (2023) · Zeitschrift für Evidenz Fortbildung und Qualität im Gesundheitswesen · doi:10.1016/j.zefq.2023.04.004 · Cited by 4
Chen, C., Wagn, K., & Hou, X. (2024) · Optics Express · doi:10.1364/oe.514894 · Cited by 4
Affinito, G., Salerno, V., Gennaro, M. D., Scafa, L., Russo, A., Fumo, M. G., Giordana, R., Falco, F., Pia, F. D., Cecca, A. D., et al. (2024) · Neuroepidemiology · doi:10.1159/000539031 · Cited by 5
“…prevalent cases and 70% of incident cases, possibly suggesting that the progressive uptake of pathology-based diagnosis of dementia has made the diagnosis of AD more precise and frequent in patients newly presenting with symptoms suggestive of dementia [25], when compared with historical cohorts.”
InfluentialSabermahani, F., Almasi‐Dooghaee, M., & Sheikhtaheri, A. (2024) · Games for Health Journal · doi:10.1089/g4h.2023.0106 · Cited by 4
Discovery of plasma biomarkers related to blood-brain barrier dysregulation in Alzheimer’s disease
Dan, Y. R., & Chiam, K. (2024) · Frontiers in Bioinformatics · doi:10.3389/fbinf.2024.1463001 · Cited by 5
Posterior Cortical Atrophy Due to Alzheimer Disease in a Person With Down Syndrome
Rodríguez‐Baz, Í., Benejam, B., Morcillo-Nieto, A. O., Vaqué‐Alcázar, L., Arriola‐Infante, J. E., Camacho, V., Aranha, M. R., Carmona‐Iragui, M., Videla, L., Barroeta, I., et al. (2024) · Neurology · doi:10.1212/wnl.0000000000210179 · Cited by 4
Self-citationChang, K. H., Wang, C., Qin, J., Katz, M. J., Byrd, D., Lipton, R. B., & Rabin, L. A. (2024) · Journal of the International Neuropsychological Society · doi:10.1017/s1355617724000729 · Cited by 4
Васильевна, Н. К., Shpilyukova, Y. A., Fedotova, E. Y., Burmak, A. G., Шабалина, А. А., & Illarioshkin, S. N. (2025) · S S Korsakov Journal of Neurology and Psychiatry · doi:10.17116/jnevro202512501191 · Cited by 4
Non-invasive biomarkers for early diagnosis of Alzheimer’s disease in bodily fluids
Коваленко, Е. А., Makhnovich, E. V., Pervunina, A. V., Gileva, E. A., & Bogolepova, A. N. (2025) · S S Korsakov Journal of Neurology and Psychiatry · doi:10.17116/jnevro20251250118 · Cited by 4
Fang, X., Xu, X., Liu, C., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.14525 · Cited by 4
“36 Our study exhibited selection bias in terms of gender and age, particularly an overrepresentation of elderly participants, similar to the trend seen in the Sweden study.”
Tasnády, K. R., Jehoul, R., de Ravé, M. G., Gijbels, M. J., Brône, B., Dewachter, I., Melotte, V., & Boesmans, W. (2025) · Neurogastroenterology & Motility · doi:10.1111/nmo.15016 · Cited by 5
Molvik, I., Kjelvik, G., Selbæk, G., & Rokstad, A. M. M. (2025) · BMC Health Services Research · doi:10.1186/s12913-025-12657-1 · Cited by 6
“In the context of dementia, a timely diagnosis is defined as providing an accurate diagnosis at a stage in the disease process when it can be most beneficial to individuals with dementia and their families [14–16].”
Medical risk factors, ApoE haplotype, and Alzheimer’s disease: a large-scale analysis
Elias, U., Gazit, L., Zucker, R., Stern, A., Linial, M., Allali, G., Ben‐Hur, T., Marshall, G. A., & Arzy, S. (2025) · The Journal of Prevention of Alzheimer s Disease · doi:10.1016/j.tjpad.2025.100301 · Cited by 7
“The quest for RFs associated with AD spans over 7,000 studies of varying validity, including interventional studies, meta-analyses, review articles, consensus conferences and working groups [6,10 – 13], with RFs mostly include vascular risk factors [14].”
Bujalance‐Fernández, J., Carro, E., Antequera, D., Jurado‐Sánchez, B., & Escarpa, A. (2025) · Analytical Chemistry · doi:10.1021/acs.analchem.5c03467 · Cited by 5
Virga, G., Marco, B., Blandino, V., & Piccoli, T. (2025) · Brain Sciences · doi:10.3390/brainsci15090924 · Cited by 4
“This biological approach has improved diagnostic precision and enabled more refined stratification of patients based on underlying pathophysiological mechanisms [12].”
Validity of CSF alpha-synuclein to predict psychosis in prodromal Alzheimer's disease
Monge-García, S., García‐Ayllón, M., Sánchez–Payá, J., Gasparini‐Berenguer, R., Cortés‐Gómez, M., Sáez‐Valero, J., & Monge-Argilés, J. A. (2023) · Frontiers in Neurology · doi:10.3389/fneur.2023.1124145 · Cited by 4
Dyer, A. H., Dolphin, H., O’Connor, A., Morrison, L., Sedgwick, G., McFeely, A., Killeen, E., Gallagher, C., Davey, N., Connolly, E., et al. (2023) · BMJ Open · doi:10.1136/bmjopen-2023-077772 · Cited by 5
Huang, X., Zhao, J., Wang, Q., Yan, T., Gou, S., Zhu, X., Liu, Y., Ye, F., Zhang, J., Wang, Y., et al. (2024) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.14606 · Cited by 6
Gu, Y., Chen, N., Zhu, L., Chen, X., Jiang, T., & Zhang, Y. (2024) · Current Neurovascular Research · doi:10.2174/0115672026305417240209062508 · Cited by 6
Compagnoni, G. M., Appollonio, I. M., & Ferrarese, C. (2024) · Neurological Sciences · doi:10.1007/s10072-024-07476-x · Cited by 4
Fluid biomarkers unveil signatures of pathological aging
Hansen, N., & Wiltfang, J. (2024) · Seizure · doi:10.1016/j.seizure.2024.05.019 · Cited by 3
What is "biological Alzheimer's disease"?
Nitríni, R. (2024) · Dementia & Neuropsychologia · doi:10.1590/1980-5764-dn-2024-e001 · Cited by 4
“The strongest opposition to the use of this concept in clinical practice came from the International Working Group, which holds that “biomarker-positive cognitively unimpaired individuals should be considered only at-risk for progression to Alzheimer’s disease” 5 .”
MethodAlzheimer’s Disease: Engaging with an Unstable Category
Daly, T. P., & Keuck, L. (2024) · Springer eBooks · doi:10.1007/978-94-017-8706-2_113-1 · Cited by 5
Chang, Z., Wang, Z., Luo, L., Xie, Z., Yue, C., Bian, X., Yang, H., & Wang, P. (2024) · Frontiers in Neuroscience · doi:10.3389/fnins.2024.1423892 · Cited by 4
Bendetowicz, D., Planche, V., Bézard, E., Dehay, B., & Meissner, W. G. (2025) · Journal of Parkinson s Disease · doi:10.1177/1877718x241313443 · Cited by 4
“77,78 The main argument of the IWG is the substantial amount of amyloid pathology in the asymptomatic ageing population (30% of cognitively healthy subjects aged 80 are amyloid-positive, as measured with PET or CSF biomarkers).”
Synthesis and Characterization of Thiazole Derivatives as Cholinesterase Inhibitors
Zhang, Z., Han, S., Mingyu, W., Zien, Y., Hu, P., He, R., Cao, Y., & Shi, D. (2025) · ChemistrySelect · doi:10.1002/slct.202500051 · Cited by 5
Liu, C., Su, Y., Yau, Y.-M., Lin, H., Chen, Y., Fang, W., Xu, N., & Wu, Z. (2025) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2025.1560032 · Cited by 5
Zhong, J., Wang, Q., Li, Q., Cui, S., Chen, K., Gu, T., Li, S., & Bai, P. (2025) · Sensors and Actuators B Chemical · doi:10.1016/j.snb.2025.137816 · Cited by 6
Din, N. U., Maronnat, F., Zolnowski‐Kolp, V., Otmane, S., & Belmin, J. (2025) · Age and Ageing · doi:10.1093/ageing/afaf204 · Cited by 5
“%) and is defined by specific criteria [2].”
Prediction of Cognitive Decline for Enrichment of Alzheimer's Disease Clinical Trials
Tam, A., Laurent, C., Gauthier, S. G., & Dansereau, C. L. (2022) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2022.49 · Cited by 29
“Enrichment strategies for enrolling likely decliners is especially important for preventative trials given that many individuals in earlier disease stages do not have detectable levels of pathology and that the presence of AD pathology has relatively low predictive accuracy of future decline in cognitively unimpaired…”
BackgroundIn vitro neuroprotective effects of allicin on Alzheimer’s disease model of neuroblastoma cell line
Okkay, U., & Okkay, I. F. (2022) · Journal of Surgery and Medicine · doi:10.28982/josam.1068336 · Cited by 4
“Pathophysiological characteristics of AD involve amnesia and cognitive deterioration [3].”
BackgroundMai, Y., Cao, Z., Xu, J., Yu, Q., Yang, S., Tang, J., Zhao, L., Fang, W., Luo, Y., Lei, M., et al. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.859492 · Cited by 5
“The pathological changes in AD, mainly Aβ deposition, tau protein phosphorylation, and neuronal necrosis, which lead to brain atrophy, can begin decades before the onset of clinical symptoms in patient with MCI (Hardy and Higgins, 1992; Dubois et al., 2021).”
Jessen, F. (2022) · Fortschritte der Neurologie · Psychiatrie · doi:10.1055/a-1808-6459 · Cited by 4
Fray, S., Achouri-Rassas, A., Belal, S., & Messaoud, T. B. (2022) · Journal of Genetics · doi:10.1007/s12041-022-01384-9 · Cited by 5
“We retained nonamnestic AD or atypical AD presentation when the initial neurocognitive impairment was primary progressive aphasia variants (leugopenic, nonfluent and semantic), posterior cortical atrophy, psychiatric and behavioural (frontal AD) or dysexecutive variants and corticobasal syndrome (Dubois et al. 2021).”
BackgroundAmyloid-β and tau PET scans predict clinical progression in cognitively unimpaired people
(2022) · Nature Medicine · doi:10.1038/s41591-022-02071-z · Cited by 4
van den Bos, M. A. J., Menon, P., & Vucic, S. (2022) · Expert Review of Neurotherapeutics · doi:10.1080/14737175.2022.2170784 · Cited by 4
“their lifetimes, and biomarkers can be present in patients where AD is a comorbidity[27].”
BackgroundHausmann, A., Chiabotti, P. S., Nasuti, M., Rouaud, O., & Allali, G. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.13092 · Cited by 4
“This study highlights the need for an extensivebiomarkerworkupinPPApatients,followingthemostrecent recommendations 2 as well as the need for trials of disease-modifying drugs in non-amnestic AD presentations.”
BackgroundMarcolini, S., Mondragón, J. D., Dominguez‐Vega, Z. T., Deyn, P. P. D., Maurits, N. M., & Initiative, A. D. N. (2024) · European Journal of Neurology · doi:10.1111/ene.16235 · Cited by 3
“Previous studies have found that the assessment of cognitive domains, such as attention, processing speed, executive function, memory, and language, can help identify biological disease stages [10, 11].”
InfluentialNeurological Disorders and Challenges in Their Theranostics
Kumar, P., Zelena, D., & Gautam, A. (2023) · Springer eBooks · doi:10.1007/978-981-99-9510-3_1 · Cited by 6
Omics‐derived biological modules reflect metabolic brain changes in Alzheimer's disease
Povala, G., Bastiani, M. A. D., Bellaver, B., Ferreira, P. C. L., Ferrari‐Souza, J. P., Lussier, F. Z., Souza, D. O., Rosa‐Neto, P., Pascoal, T. A., Zatt, B., et al. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14095 · Cited by 3
Naturally occurring Alzheimer’s disease in rhesus monkeysPreprint
Li, Z., He, X., Wu, S., Huang, R., Li, H., Wang, Z., Wang, L., Qin, D., Kong, Y., Guo, Y., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.10.20.513120 · Cited by 5
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) · medRxiv · doi:10.1101/2024.08.06.24311577 · Cited by 4
Sohn, B., Chung, S. J., Lee, J. R., Hwang, D., Xie, W., Chan, L. L., Choi, Y. S., Study, H. B. I., Initiative, J. A. D. N., & Initiative, A. D. N. (2024) · Radiology Advances · doi:10.1093/radadv/umae021 · Cited by 3
Success stories: impactful applications of cancer biomarkers
Theivendren, P., Kunjiappan, S., Pavadai, P., Shanmugam, A., Karunanithi, K., Gopal, M., & Kiruthiga, N. (2025) · Elsevier eBooks · doi:10.1016/b978-0-443-29279-8.00015-6 · Cited by 3
Bolcato, V., Poloni, T. E., Basile, G., Davin, A., Ferrari, R. R., Negro, G., Ceretti, A., Guaita, A., & Tronconi, L. (2025) · Neurological Sciences · doi:10.1007/s10072-025-08214-7 · Cited by 3
“This approach is the basis for searching and validating biological markers for early diagnosis and identification of specific therapeutic targets that lead to personalized therapies [3–5].”
Núñez‐Cortés, R., Calatayud, J., Calonge‐Pascual, S., Andersen, L. L., Bláfoss, R., López‐Gil, J. F., & López‐Bueno, R. (2025) · International Journal of Geriatric Psychiatry · doi:10.1002/gps.70137 · Cited by 3
“Nevertheless, international recommendations indicate that some factors need further confirmation, including lifestyle factors such as physical activity [31].”
Serio, M. A., Dethloff, D. R., Curry, G. C., Beesley, M. L., Shekoohi, S., & Kaye, A. D. (2025) · Advances in Therapy · doi:10.1007/s12325-025-03337-x · Cited by 4
“In 2018, the National Institute on Aging and Alzheimer’s Association (NIA-AA) research defined AD with only biomarkers, while the 2021 International Working Group (IWG) criteria used a combination of clinical diagnosis and biomarkers [48, 49].”
An AI-assisted multiplex fluorescence sensing platform for grading diagnosis of Alzheimer's disease
Liu, Y., Zhou, Z., Liu, X., et al. (2025) · Journal of Materials Chemistry B · doi:10.1039/d5tb01103e · Cited by 3
ADAgent: LLM Agent for Alzheimer’s Disease Analysis with Collaborative Coordinator
Hou, W., Yang, G., Du, Y., Lau, Y., Liu, L., He, J., Long, L., & Wang, S. (2025) · Lecture notes in computer science · doi:10.1007/978-3-032-06004-4_3 · Cited by 5
Aging, Alzheimer's disease, and stroke: A 25-year longitudinal analysis of U.S. mortality trends
Ali, M. F., Ahmad, H. F., Hemida, M. F., Tahir, M., Qadeer, T., Rasheed, S., Rashid, Z., Malik, M. H. B. A., Ahmed, A. O. E., Morden, A., et al. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251380689 · Cited by 3
“27,28 The adoption of more sensitive diagnostic criteria, such as the 2011 National Institute on Aging – Alzheimer ’ s Association (NIA-AA) guidelines and the increasing use of neuroimaging and cerebrospinal fl uid biomarkers, has led to earlier and more accurate identi fi cation of AD.”
Athanasaki, A., Tsantzali, I., Theodorou, A., Michalopoulou, A., Constantinides, V. C., Boufidou, F., Tzartos, J. S., Tsalouchidou, P., Zompola, C., Paraskevas, S. G., et al. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26199531 · Cited by 3
“Thus, there are still debates over the definition and biomarker profile of AD, i.e., amongst the 2018 NIA-AA criteria [41], 2024 AA revised criteria [43], and IWG criteria [42,44].”
Hosseinpour-Mashkani, S. M., Bishop, D. P., Adlard, P. A., et al. (2025) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2025.09.010 · Cited by 3
Bachmann, D., Wybitul, M., Buchmann, A., Gericke, C., Saake, A., Studer, S. T., Rauen, K., Gruber, E., Blennow, K., Zetterberg, H., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70802 · Cited by 5
“41,42 Some studies reported a specific early decline in episodic memory, 43,44 while othersobserveddeclineacrossmultiplecognitivedomains.”
Self-citationVisualising dementia in news media: reinforcing ageing, dependency and stigma
Nurmi, S., Halkoaho, A., Krüger, J., Nikumaa, H., Mäki‐Petäjä‐Leinonen, A., Katisko, K., & Solje, E. (2025) · Age and Ageing · doi:10.1093/ageing/afaf305 · Cited by 4
“Although some images captured elements of the daily experiences of people living with dementia, the overall negative and stereotypical nature of the portrayals reinforces stigma and overlooks the complexity of the condition [40–42].”
Simon, K. E., Gruen, M. E., & Olby, N. J. (2025) · Frontiers in Veterinary Science · doi:10.3389/fvets.2025.1685430 · Cited by 5
The challenging concept of preclinical Alzheimer's disease
Wallon, D., & Garnier‐Crussard, A. (2025) · Revue Neurologique · doi:10.1016/j.neurol.2025.07.016 · Cited by 6
Chudhary, M. (2025) · Chemical Papers · doi:10.1007/s11696-025-04532-4 · Cited by 4
Multimodal neural correlates of cognitive awareness in aging and Alzheimer’s disease
Cacciamani, F., Houot, M., du Montcel, S. T., Thibeau–Sutre, E., Vannini, P., & Migliaccio, R. (2025) · NeuroImage Clinical · doi:10.1016/j.nicl.2025.103922 · Cited by 3
Utilizing multimodal models to forecast Alzheimer's disease progression and clinical subtypes
Ren, H., Jing, F., Zhou, Y., Luo, Z., Yu, X., Jin, W., & Chen, L. (2025) · Health Information Science and Systems · doi:10.1007/s13755-025-00407-w · Cited by 3
“Traditional diagnostic approaches for AD mainly rely on clinical assessments and neuropsychological testing [15, 16].”
Miao, X., Luo, K., Li, Y., Zhou, Y., Wei, M., Zhang, T., Hu, Y., Wang, H., & Jia, J. (2025) · Molecular Neurobiology · doi:10.1007/s12035-025-05574-1 · Cited by 3
“Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by memory impairment and cognitive deficiencies [1, 2].”
Usman, A. S., Manoharan, S. D., Nassir, C. M. N. C. M., Hamid, H. A., Hein, Z. M., Norazit, A., Murthy, J., Zainol, M., Kamaruzzaman, M. A., Chiroma, S. M., et al. (2026) · Molecular Neurobiology · doi:10.1007/s12035-025-05642-6 · Cited by 3
“According to NIH Alzheimer’s Disease Research Center (ADRC) guidelines, definitive models of AD typically demonstrate both amyloid (Aβ) and tau (p-Tau) deposition [73].”
Atomically Precise Clusterzymes: A Programmable Optoelectronic Platform for Neuroscience
Sun, S., Liu, D., Zhou, S., Wang, Y., Wang, H., Zheng, Z., & Zhang, X. (2026) · Advanced Science · doi:10.1002/advs.202519438 · Cited by 3
Wang, Y., Lv, R., Jiang, Z. H. E. N. G. M., Liu, Y., Zhang, J., Zhao, Z., Liu, Y., Zheng, Y., Liu, B., Clauw, D., et al. (2026) · Molecular Psychiatry · doi:10.1038/s41380-026-03542-2 · Cited by 8
“Behavioral assessments necessitate non-verbal or digital tools to circumvent social communication barriers inherent in traditional cognitive testing, while distinguishing overlapping manifestations between degenerative symptoms and ASD core features (e.g., intensi fi ed repetitive behaviors) [259].”
Otani, K., Ishihara, H., Nakamura, T., & KAWABE, K. (2026) · General Hospital Psychiatry · doi:10.1016/j.genhosppsych.2026.04.006 · Cited by 3
Sakakibara, R., Sawai, S., Ogata, T., & Iimura, A. (2022) · Neurology and Clinical Neuroscience · doi:10.1111/ncn3.12647 · Cited by 2
Visual disorders and driving ability in persons with dementia: A mini review
Papageorgiou, E., Tsirelis, D., Lazari, K., Siokas, V., Dardiotis, E., & Tsironi, E. E. (2022) · Frontiers in Human Neuroscience · doi:10.3389/fnhum.2022.932820 · Cited by 3
“Clinically, AD is mainly characterized by deficits in memory, language, executive, and visuospatial domains (Dubois et al., 2021; Graff-Radford et al., 2021).”
BackgroundAranha, M. R., Coutinho, A. M., Carneiro, C. D. G., Pastorello, B., Studart‐Neto, A., Guariglia, C., Tsunemi, M. H., Moreira, E. L. S., Ianof, J. N., Anghinah, R., et al. (2023) · Arquivos de Neuro-Psiquiatria · doi:10.1055/s-0043-1768666 · Cited by 3
Bibliometric analysis of global research on the role of apolipoprotein E in Alzheimer's disease
Wang, Z., Zhu, X., Wen, Y., & Shang, D. (2023) · Heliyon · doi:10.1016/j.heliyon.2023.e17987 · Cited by 6
Ly, M. T., Adler, J. S., Loy, A. F. T., Edmonds, E. C., Bondi, M. W., & Delano‐Wood, L. (2024) · Journal of the International Neuropsychological Society · doi:10.1017/s135561772301144x · Cited by 4
“However, critiques of a biologically-defined AD state that biomarkers alone are not sufficient to define an individual ’ s position on the AD continuum without clinical input (Dubois et al., 2021).”
BackgroundLing, Y., Hu, L., Chen, J., Zhao, M., & Dai, X. (2024) · Clinics · doi:10.1016/j.clinsp.2024.100373 · Cited by 3
Norman, B., Arjun, A. M., Vulpe, G., et al. (2024) · IEEE BioSensors Conference (BioSensors) · doi:10.1109/biosensors61405.2024.10712719 · Cited by 3
“Additionally, imaging techniques such as magnetic resonance imaging and positron emission tomography may be used to detect structural changes in the brain and assess the presence of beta-amyloid plaques[2].”
MethodChu, H., Huang, C., Xie, F., & Guo, Q. (2024) · Neurology and Therapy · doi:10.1007/s40120-024-00666-x · Cited by 3
“In addition, in [36].”
Resolution of the Expert Council on the problem of early diagnosis of Alzheimer's disease
Bogolepova, A. N., Васенина, Е. Е., Васильевна, В. Н., Vorobyеv, S. V., Si, G., Emelin, А. Y., Zakharov, V. V., Illarioshkin, S. N., Kosivtsova, O. V., Kostyuk, G. P., et al. (2024) · Neurology neuropsychiatry Psychosomatics · doi:10.14412/2074-2711-2024-5-111-119 · Cited by 3
Reducing confusion surrounding expert conceptions of Alzheimer's and dementia: A practical analysis
Daly, T. P., & Mastroleo, I. (2024) · Journal of Neuropsychology · doi:10.1111/jnp.12398 · Cited by 3
“…is what leads them to reject this definition because of its low immediate clinical relevance and potential harm to patients (e.g. anxiety, overtreatment; Dubois et al., 2021; Villain & Planche, 2024) and public health (e.g. spending scarce resources ineffectively, avoiding population harm).”
Rajaee, A., Petramfar, P., Ansari, R., Asadi, S., Vazin, A., & Zarshenas, M. M. (2024) · Journal of Herbal Medicine · doi:10.1016/j.hermed.2024.100975 · Cited by 3
Time to align sensitive cognitive assessment with protein biomarkers in Alzheimer's disease
Vonk, J. M. J. (2025) · Journal of Neuropsychology · doi:10.1111/jnp.12413 · Cited by 3
“…Working Group (IWG) advocates for an integrative clinical-biological approach, emphasizing that the diagnosis of Alzheimer's disease should not rely solely on protein biomarkers but must also incorporate phenotypic expression such as objective cognitive impairment (Dubois et al., 2021, 2024).”
Brain morphology mediating the effects of common genetic risk variants on Alzheimer’s disease
Breddels, E. M., Snihirova, Y., Pishva, E., Gülöksüz, S., Blokland, G. A. M., Luykx, J. J., Andreassen, O. A., Linden, D. E. J., van der Meer, D., & Initiative, A. D. N. (2025) · Journal of Alzheimer s Disease Reports · doi:10.1177/25424823251328300 · Cited by 3
“10 In addition, common genetic variants found by genome-wide association studies (GWAS) 11 – 13 had only small effect sizes and, even combined, explained only a small fraction of the heritability of LOAD.”
Mild cognitive impairment due to cerebrovascular disease and Alzheimer’s
Parfenov, V. A., Гришина, Д. А., Борисовна, Л. А., et al. (2025) · Neurology neuropsychiatry Psychosomatics · doi:10.14412/2074-2711-2025-3-77-83 · Cited by 3
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.
A language model drew the claims from the paper on 2026-10-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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