The DOI matches its Crossref record; 117 of the 119 references it cites were found in a registry or an index; 5 of the 67 sources its claims cite were checked for support.
Clinical diagnosis of Alzheimer’s disease: Recommendations of the International Working Group
Open accessAbstract
In 2018, the National Institute of Aging and the Alzheimer Association proposed a purely biological definition of Alzheimer’s disease (AD) relying on biomarkers. While the intended use of the framework was for research purposes, it has engendered debate and challenges regarding its application in everyday clinical practice. For instance, cognitively unimpaired individuals may have biomarker evidence of both amyloid and tau pathology, but may never develop clinical manifestations in their lifetime. Furthermore, a positive AD pattern may be observed in other brain diseases where AD pathology is present as co‐pathology. In this presentation, the international Working Group (IWG) presents what we consider to be the current limitations of biomarkers in the diagnosis of AD, and on the basis of this evidence we propose recommendations for how biomarkers should and should not be used for diagnosis of AD in a clinical setting. We recommend that AD diagnosis be restricted to the occurrence of positive biomarkers together with specific AD phenotypes, whereas biomarker positive cognitively unimpaired individuals should be considered only at‐risk for progression to AD.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
The International Working Group argues that a purely biological ATN definition of Alzheimer’s disease is not ready for clinical diagnosis and recommends restricting Alzheimer’s disease diagnosis to people with both a specific Alzheimer’s disease clinical phenotype and positive amyloid and tau biomarkers. Biomarker-positive cognitively unimpaired individuals should be considered at-risk for progression, not clinically diagnosed with Alzheimer’s disease.
Key findings
- The IWG recommends a clinical–biological diagnosis: a specific Alzheimer’s disease phenotype plus amyloid-positive and tau-positive biomarker evidence; biomarker-positive cognitively unimpaired people should be classified as at-risk, not as having Alzheimer’s disease.
- A purely biological definition has low predictive accuracy: cognitively unimpaired biomarker-positive individuals often do not progress, and best current estimates of lifetime dementia risk range from 5% to 42%.
- Alzheimer’s pathology is commonly mixed: pure Alzheimer’s disease pathology is found in 3–30% of neuropathological series of people with dementia of the Alzheimer type, and 50–60% of Alzheimer’s-type dementia is estimated to be attributable to copathologies such as α-synucleinopathy, vascular pathology, non-Alzheimer’s tauopathies, and TDP-43 pathology.
- Practical biomarker limitations include artificial thresholds, limited generalisability, and accessibility; Cochrane reviews could not recommend routine CSF or amyloid PET use in clinical practice, plasma biomarkers are not currently recommended, and biomarker investigation in cognitively unimpaired individuals is not recommended.
Methods
- Design: a Personal View and consensus recommendations from the International Working Group, not a primary empirical study.
- Data or sample: no new primary sample is reported; the paper synthesises prior diagnostic frameworks, biomarker literature, neuropathology evidence, Cochrane reviews, and cohort findings.
- Analysis: narrative evidence synthesis leading to expert recommendations, including proposed diagnostic criteria, biomarker measures, and a risk-stratification proposal for cognitively unimpaired biomarker-positive individuals.
Limitations
- The paper states that a purely biological definition risks confusion between Alzheimer’s disease lesions and Alzheimer’s disease, has low predictive accuracy, is complicated by copathologies, and faces uncertain pathogenesis, threshold, generalisability, accessibility, and ethical problems.
- The paper states that current individualised prediction models do not work sufficiently well in cognitively unimpaired people compared with people in the prodromal stage, and that disclosing individual patient-level risk would be premature and is to be avoided.
- Evident from the text: as a Personal View, the recommendations are expert consensus rather than a systematic review or meta-analysis; the proposed risk stratification is a starting point for research and requires validation studies on large cohorts with long follow-up, as the paper itself notes.
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Claims the paper makes
31 Not checked yet · 13 Own interpretation · 2 Partly supported · 1 Supported · 1 No basis given · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“In cognitively unimpaired individuals, self-reported complaints and complaints reported by an informant should be clearly distinguished, because informant complaints indicate that these individuals are at increased risk of progression110 and merit a closer follow-up with regular clinical and neuropsychological evaluations.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > IWG recommendations for clinical diagnosis of Alzheimer’s disease
What the sources say
- Supportedcites [110] Caselli, 2014, Subjective cognitive decline: self and informant comparisons, Alzheimers Dement source
The Methods (section 2.6) state that all participants were cognitively normal at entry. The Results (section 3) report that 9.4% of those with informant-endorsed decline developed MCI, compared with 2.2% of those without it (odds ratio 4.58, p<.05). The Discussion cautions that the number of converters was small. (LLM, conf=0.94)
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- Supported
In the paper
“For instance, cognitively unimpaired individuals can have biomarker evidence of both amyloid β and tau pathology but will often not develop clinical manifestations in their lifetime.”
- Also stated in: § Difficulty in classifying cognitively unimpaired biomarker-positive individuals · hedged
“Cognitively unimpaired individuals with biomarker positivity will not invariably experience subsequent cognitive decline; the best current estimates of lifetime dementia risk range from 5% to 42%.33”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Abstract
What the sources say
- Not checked yetcites [33] Brookmeyer, 2018, Estimation of lifetime risks of Alzheimer's disease dementia using biomarkers for preclinical disease, Alzheimers Dement source
plain- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Difficulty in classifying cognitively unimpaired biomarker-positive individuals · hedged
In the paper
“current individualised prediction models do not work sufficiently well in cognitively unimpaired people compared with people who are in the prodromal stage of Alzheimer’s disease.62”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Difficulty in classifying cognitively unimpaired biomarker-positive individuals
What the sources say
- Not checked yetcites [62] van Maurik, 2019, Personalized risk for clinical progression in cognitively normal subjects-the ABIDE project, Alzheimers Res Ther source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“In 2018, the US National Institute on Aging and the Alzheimer’s Association proposed a purely biological definition of Alzheimer’s disease that relies on biomarkers.”
- Also stated in: § Introduction · plain
“In 2018, the US National Institute on Aging (NIA) and the Alzheimer’s Association (AA) proposed the amyloid β, tau, neurodegeneration (ATN) research framework for the definition and diagnosis of Alzheimer’s disease (for a glossary of terms, see panel 1).1”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Abstract
What the sources say
- Not checked yetcites [1] Jack, 2018, NIA–AA research framework: toward a biological definition of Alzheimer's disease, Alzheimers Dement source
plain- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Introduction · plain
In the paper
“However, the follow-up of cognitively unimpaired biomarker-positive individuals suggests that the majority of these individuals do not progress over time (panel 2).”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Uncertainty about the pathogenesis model of Alzheimer’s disease
What the sources say
- Not checked yetcites panel 2
hedged- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The relationship between the coexistence of tau and amyloid β pathology on the one hand, and the development of cognitive decline and neurodegeneration on the other hand, remain uncertain at an individual level.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Uncertainty about the pathogenesis model of Alzheimer’s disease
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Several studies (panel 2) indicate that the presence of both tau and amyloid β positivity is insufficient to definitively predict the occurrence of symptoms (mild cognitive impairment or dementia) in individuals without clinical impairment.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Low predictive accuracy
What the sources say
- Not checked yetcites panel 2
hedged- Asserted: passes — The authors put it forward as true.
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In the paper
“Pure Alzheimer’s disease pathology is the exception rather than the rule (found in 3–30% of neuropathological series of people with dementia of the Alzheimer type, depending on age40) at post-mortem examination.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Presence of other pathologies
What the sources say
- Not checked yetcites [40] Robinson, 2018, Neurodegenerative disease concomitant proteinopathies are prevalent, age-related and APOE4-associated, Brain source
plain- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“50–60% of Alzheimer’s-type dementia (dementia defined clinically as Alzheimer’s disease) is estimated to be attributable to these copathologies.40,42–45”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Presence of other pathologies
What the sources say
- Not checked yetcites [40] Robinson, 2018, Neurodegenerative disease concomitant proteinopathies are prevalent, age-related and APOE4-associated, Brain source
- Not checked yetcites [42] Yokota, 2018, Neuropathological comorbidity associated with argyrophilic grain disease, Neuropathology source
- Not checked yetcites [43] Ossenkoppele, 2020, Assessment of demographic, genetic, and imaging variables associated with brain resilience and cognitive resilience to pathological tau in patients with Alzheimer disease, JAMA Neurol source
- Not checked yetcites [44] Karanth, 2020, Prevalence and clinical phenotype of quadruple misfolded proteins in older adults, JAMA Neurol source
- Not checked yetcites [45] Nelson, 2019, Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report, Brain source
hedgedstates a cause- Asserted: passes — The authors put it forward as true.
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In the paper
“Furthermore, a positive Alzheimer’s disease pattern of biomarkers can be observed in other brain diseases in which Alzheimer’s disease pathology is present as a comorbidity.”
- Also stated in: § Presence of other pathologies · hedged
“Another challenge with using a biomarker-only diagnosis of Alzheimer’s disease is that the in-vivo presence of biomarkers of Alzheimer’s disease lesions could certify Alzheimer’s disease as the primary diagnosis, because such lesions are commonly found in people who have other neurodegenerative diseases, most often dementia with Lewy bodies.40”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Abstract
What the sources say
- Not checked yetcites [40] Robinson, 2018, Neurodegenerative disease concomitant proteinopathies are prevalent, age-related and APOE4-associated, Brain source
plainstates an association- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Presence of other pathologies · hedged
- It may state two separate claims as one. 19
- Probably not a substantial claim. 7
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Biomarker thresholds also depend on their intended use (eg, to identify the first signs of amyloid β pathology, or to predict the occurrence of clinical symptoms) and no consensus on the context of use (eg, in asymptomatic vs symptomatic individuals; in people who complain about subjective cognitive decline vs non-complainers) is currently available.1”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Biomarker thresholds
What the sources say
- Partly supportedcites [1] Jack, 2018, NIA–AA research framework: toward a biological definition of Alzheimer's disease, Alzheimers Dement sourceExperimental — accuracy not yet measured
The Implementation section says cut points should fit the research question, giving early detection and high diagnostic certainty as examples. It also says universal biomarker standards have not been established, but does not specifically establish a lack of consensus on thresholds for asymptomatic versus symptomatic people or subjective cognitive decline complainants versus non-complainants. No page numbers were provided for these passages. (LLM, conf=0.83)
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It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The positivity of both amyloid and tau biomarkers is required because an amnestic phenotype with only amyloid positivity is not specific to Alzheimer’s disease and is seen in other neurodegenerative diseases with amyloid copathology (including LATE and dementia with Lewy bodies1,40,41,100) or in patients with cerebral amyloid angiopathy and amnestic vascular cognitive impairment101 (appendix p 2).”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > IWG recommendations for clinical diagnosis of Alzheimer’s disease
What the sources say
- Partly supportedcites [1] Jack, 2018, NIA–AA research framework: toward a biological definition of Alzheimer's disease, Alzheimers Dement sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Partly supportedcites [40] Robinson, 2018, Neurodegenerative disease concomitant proteinopathies are prevalent, age-related and APOE4-associated, Brain sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Partly supportedcites [41] McKeith, 2017, Diagnosis and management of dementia with Lewy bodies: fourth consensus report of the DLB Consortium, Neurology sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plainstates a cause- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Partly supported
None of the sources cited for this claim have been checked yet.
In the paper
“Most of all, this binary threshold does not reflect the reality of amyloid β and tau pathology, which is continuous and present at a minimal extent in almost all people older than 70 years,17 with important discrepancies between pathology burden and clinical symptoms at intermediate extents (panel 2).”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Biomarker thresholds
What the sources say
- Not checked yetcites [17] Braak, 2011, Stages of the pathologic process in Alzheimer disease: age categories from 1 to 100 years, J Neuropathol Exp Neurol source
- Not checked yetcites panel 2
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The clear-cut separation between negative and positive patients in relation to a given biomarker is somewhat artificial and differs between sites and studies.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Biomarker thresholds
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, amyloid β and tau biomarkers are not sufficient to confidently predict progression to prodromal Alzheimer’s disease or Alzheimer’s disease dementia, or to define a person’s position on the Alzheimer’s disease continuum, without clinical input.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Uncertainty about the pathogenesis model of Alzheimer’s disease
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Cognitively unimpaired individuals with biomarker positivity will not invariably experience subsequent cognitive decline; the best current estimates of lifetime dementia risk range from 5% to 42%.33”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Difficulty in classifying cognitively unimpaired biomarker-positive individuals
What the sources say
- Not checked yetcites [33] Brookmeyer, 2018, Estimation of lifetime risks of Alzheimer's disease dementia using biomarkers for preclinical disease, Alzheimers Dement source
hedged- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“For physicians, Alzheimer’s disease equates with Alzheimer’s disease neuropathological changes, whereas for patients, Alzheimer’s disease equates with dementia, dependency, and death.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Ethical concerns
What the sources say
- Not checked yetcites [12] Frisoni, 2019, Re-aligning scientific and lay narratives of Alzheimer's disease, Lancet Neurol source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“CSF investigation is prioritised because it provides simultaneous information on the two types of biomarkers (amyloid β and tau) and is less expensive than amyloid PET, tau PET, or both.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > IWG recommendations for clinical diagnosis of Alzheimer’s disease
plainstates a cause- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may state two separate claims as one.
In the paper
“However, this increased sensitivity in the detection of cognitive decline comes at the expense of a reduced specificity, and numerous other causes than neurodegeneration or Alzheimer’s disease can be responsible for the observed changes, such as metabolic disorders, psychiatric disorders, or sleep apnoea.72”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Biomarker thresholds
What the sources say
- Not checked yetcites [72] Chipi, 2019, Biomarker-based signature of alzheimer's disease in pre-MCI individuals, Brain Sci source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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In the paper
“In both situations, pathophysiological Alzheimer’s disease biomarkers can be positive.111”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > IWG recommendations for clinical diagnosis of Alzheimer’s disease
What the sources say
- Not checked yetcites [111] Niemantsverdriet, 2018, Added diagnostic value of cerebrospinal fluid biomarkers for differential dementia diagnosis in an autopsy-confirmed cohort, J Alzheimers Dis source
hedgedstates an association- Asserted: passes — The authors put it forward as true.
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In the paper
“As shown in panel 2, the effect of biomarker positivity on clinical progression remains weak to moderate and was established using selected volunteers from research cohorts.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Generalisability and accessibility in clinical practice
What the sources say
- Not checked yetcites panel 2
plainstates an association- Asserted: passes — The authors put it forward as true.
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In the paper
“This deep difference in use and understanding of the term can adversely affect the therapeutic alliance.12”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Ethical concerns
What the sources say
- Not checked yetcites [12] Frisoni, 2019, Re-aligning scientific and lay narratives of Alzheimer's disease, Lancet Neurol source
plainstates a possible cause- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“The current in-vivo detection of tau positivity using 18F-flortaucipir PET seems to correspond only to widespread tau pathology in the brain (ie, Braak stages ≥IV),69 whereas CSF phosphorylated tau elevation can reflect earlier stages of tauopathy.70”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Biomarker thresholds
What the sources say
- Not checked yetcites [69] Fleisher, 2020, Positron emission tomography imaging with [18F]flortaucipir and postmortem assessment of Alzheimer disease neuropathologic changes, JAMA Neurol source
- Not checked yetcites [70] Mattsson-Carlgren, 2020, Aβ deposition is associated with increases in soluble and phosphorylated tau that precede a positive tau PET in Alzheimer's disease, Sci Adv source
hedgedstates an association- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“If a person decides to receive the results and the results are positive, they should be counselled that they are at risk for subsequent clinical progression to prodromal Alzheimer’s disease or Alzheimer’s disease dementia, but are not clinically diagnosed as having Alzheimer’s disease.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > IWG recommendations for clinical diagnosis of Alzheimer’s disease
plainstates an association- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
In the paper
“As underscored by the Cochrane reviews, the prognostic value of a diagnosis based on biomarkers remains limited, first because there is a high variability of decline rate among individuals with biomarker-positive Alzheimer’s disease,79 and second because non-Alzheimer’s disease neurodegenerative diseases contribute to cognitive decline.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Generalisability and accessibility in clinical practice
What the sources say
- Not checked yetcites [79] Jang, 2019, Prediction of fast decline in amyloid positive mild cognitive impairment patients using multimodal biomarkers, Neuroimage Clin source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In symptomatic patients, the identification of the specific clinical phenotype (interfering or not with independence in everyday activities) is a major step in diagnosis, because it expresses the brain dysfunction that the biomarkers are signalling.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Difficulty in classifying cognitively unimpaired biomarker-positive individuals
plainstates a cause- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“Subjective cognitive decline might be a risk factor of clinical progression,24 but the ability of subjective cognitive decline to predict progression to objective cognitive decline (ie, mild cognitive decline, or dementia, or both) remains low (OR 1·5–3·081).”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Generalisability and accessibility in clinical practice
What the sources say
- Not checked yetcites [24] Ebenau, 2020, ATN classification and clinical progression in subjective cognitive decline: the SCIENCe project, Neurology source
- Not checked yetcites [81] Slot, 2019, Subjective cognitive decline and rates of incident Alzheimer's disease and non-Alzheimer's disease dementia, Alzheimers Dement source
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“However, an isolated amnestic syndrome of the hippocampal type with only tau biomarker positivity can occur in primary age-related tauopathy37,38 or in atypical presentations of mixed 3 repeat or 4 repeat tau frontotemporal lobar degeneration100,102 (appendix p 2).”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > IWG recommendations for clinical diagnosis of Alzheimer’s disease
What the sources say
- Not checked yetcites [37] Toledo, 2015, Alzheimer's disease cerebrospinal fluid biomarker in cognitively normal subjects, Brain source
- Not checked yetcites [38] Bell, 2019, Neuropathologic, genetic, and longitudinal cognitive profiles in primary age-related tauopathy (PART) and Alzheimer's disease, Alzheimers Dement source
- Not checked yetcites [100] Villain, 2019, Alzheimer's disease including focal presentations, Semin Neurol source
plainstates an association- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Subjective memory complaints and subjective cognitive decline, if isolated and not supported by objective cognitive impairment, are not specific enough to be considered part of the Alzheimer’s disease phenotype.109”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > IWG recommendations for clinical diagnosis of Alzheimer’s disease
What the sources say
- Not checked yetcites [109] Jessen, 2020, Prediction of dementia of Alzheimer type by different types of subjective cognitive decline, Alzheimers Dement source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“individuals included in such longitudinal cohorts are usually recruited by advertisement and do not represent the variety of individuals to whom the biomarker investigations would be applied in clinical practice.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Generalisability and accessibility in clinical practice
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In clinical practice, such an extension to earlier thresholds in amyloid or tau biomarkers might lengthen the duration of the asymptomatic stages and decrease the lifetime probability of clinical progression.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Biomarker thresholds
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Overall, evidence for the use of biomarkers in clinical practice remains highly disputed and suffers from a dearth of evidence-based data to recommend biomarker assessments for cognitively unimpaired individuals.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Generalisability and accessibility in clinical practice
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although the definition of Alzheimer’s disease based exclusively on biological markers has gained substantial traction in research settings, emerging studies suggest that the biomarker definition is not ready for application in clinical settings and for diagnosis of individuals without cognitive impairment.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Conclusion
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
A specific clinical phenotype of Alzheimer’s disease can be reliably identified in clinical practice.
“It requires the presence of both a specific clinical phenotype of Alzheimer’s disease (phenotype positive) and biomarker evidence of Alzheimer’s disease pathology (amyloid-positive and tau positive).”
The paper relies on this without support.
Biomarkers are currently unavailable for the pathological changes that underlie the non-Alzheimer’s neurodegenerative diseases often found in people with dementia.
“Unfortunately, biomarkers are currently unavailable for the pathological changes that underlie the non-Alzheimer’s neurodegenerative diseases often found in people with dementia, and disentangling Alzheimer’s disease from other neurodegenerative diseases continues to depend on phenotype or postmortem examination.”
The paper relies on this without support.
In some complex cases, only post-mortem evaluation will provide definitive information about whether Alzheimer's disease is the primary pathology or a copathology.
“In some complex cases, only post-mortem evaluation will provide definitive information.”
The paper relies on this without support.
Biomarker investigations can be limited by the availability, cost, and health-care payment coverage of biomarkers across countries, centres, and clinical situations.
“Biomarker investigations can also be limited by the availability, cost, and health-care payment coverage of biomarkers across countries, centres, and clinical situations.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Disease onset can occur at < 65 (familial early-onset) or > 65 years of age (sporadic late-onset), with the latter afflicting more than 95% of patients [87, 213]”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [87]
Experimental — accuracy not yet measuredIn the citing paper
“In 2021, new recommendations for the clinical diagnosis of AD were proposed by the International working group, highlighting that the diagnosis of AD should be restricted to people who have positive biomarkers together with specific AD phenotypes. Cognitively unimpaired individuals who are only positive to biomarkers should be considered at-risk for progression to AD [10].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [10]
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A Multiform Heterogeneity Framework for Alzheimer’s Disease Based on Multimodal Neuroimaging
Zhao, K., Chen, P., Wang, D., Zhou, R., Ma, G., & Liu, Y. (2024) · Biological Psychiatry · doi:10.1016/j.biopsych.2024.12.009 · Cited by 6
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“…criteria for diagnosis and staging of AD for research purposes now include the use of biomarkers in the diagnosis of AD [59], and International Working Group recommendations include the appropriate use of biomarkers in the context of other evaluations for AD diagnosis in a clinical setting [60,61].”
Roh, H. W., Chang, Y. Y., Kim, K. Y., Jeon, S. Y., Wang, S., Kim, E., Bae, J. N., & Ryu, S. (2026) · Psychiatry Investigation · doi:10.30773/pi.2025.0400 · Cited by 8
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“The decrease in the 18F-FDG uptake on PET in the temporoparietal cortex is included as a sensitive determinant among the diagnostic biomarkers in recently established criteria and guidelines for AD [46].”
BackgroundA Functional Assessment Tool to Distinguish Controls From Alzheimer’s Disease in Lima, Peru
Custodio, N., Montesinos, R., Chambergo‐Michilot, D., Herrera‐Pérez, E., Pintado‐Caipa, M., Wendy Seminario, G., Cuenca, J., Mesia, L., Failoc‐Rojas, V. E., & Diaz, M. M. (2022) · American Journal of Alzheimer s Disease & Other Dementias® · doi:10.1177/15333175221104354 · Cited by 10
“One of the most debilitating features of AD is the functional impairment that occurs as the disease progresses, impeding ability to maintain work, social or family obligations reflected in a decline of activities of daily living (ADLs) and functional performance.(1) Mild cognitive impairment (MCI), a pre-cursor to AD,…”
BackgroundInfluentialChen, H., Yao, X., Chen, L., Shang, S., Luo, X., Wang, X., Xia, W., & Zhang, H. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.892374 · Cited by 8
“Patients with AD suffer from prominent memory loss as well as various behavioral and psychiatric dysfunctions (Dubois et al., 2021).”
BackgroundUncovering the distinct macro-scale anatomy of dysexecutive and behavioural degenerative diseases
Corriveau‐Lecavalier, N., Barnard, L. R., Botha, H., Graff‐Radford, J., Ramanan, V. K., Lee, J., Dicks, E., Rademakers, R., Boeve, B. F., Machulda, M. M., et al. (2023) · Brain · doi:10.1093/brain/awad356 · Cited by 10
“25,27 There have been recent efforts to resolve this ambiguity.”
Vaishnav, N., Gonzalez, R., Karunungan, K. L., Tyler, A. M., Zheng, W., & Arias, J. J. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-230067 · Cited by 8
“The International Working Group’s 2021 statement on the topic recommends that the diagnosis of “Alzheimer’s disease” be limited to those who have both posi-tivebiomarkers and specificADphenotypes,whereas asymptomatic patients be described as “at-risk” for progression to AD [4].”
Exploring the Genetic Heterogeneity of Alzheimer’s Disease: Evidence for Genetic Subtypes
Elman, J. A., Schork, N. J., Rangan, A. V., & Initiative, F. T. A. D. N. (2024) · Journal of Alzheimer’s Disease · doi:10.3233/jad-231252 · Cited by 9
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“Furthermore, in recent years, neuropsychological assessment, together with the analysis of new biomarkers, has been essential for a better characterization of MCI and establishing its prognosis (Bondi et al., 2014; Dubois et al., 2021; Edmonds et al., 2016; Graves et al., 2020).”
BackgroundAre we ready to use anti-amyloid therapy in Alzheimer's disease?
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“Despite excessive investigations, the pathology and treatment of AD is not fully understood (Anstey et al., 2019; Breijyeh & Karaman, 2020; Dubois et al., 2021; Livingston et al., 2020; Weller & Budson, 2018).”
BackgroundSchwinne, M., Alonso, Á., Roberts, B. R., Hickle, S. D., Verberk, I. M. W., Epenge, E., Gikelekele, G., Tshengele, N., Kavugho, I., Mampunza, S. M. M., et al. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-230976 · Cited by 8
“However, AD is diagnosed based on clinical symptoms of dementia along with a distinct biomarker profile or PET scan [5].”
Khastehband, S., Dabbaghi, K. G., Khosravirad, Z., Jamalnia, S., GhorbaniNia, R., Mahmoudikohani, F., & Zakeri, H. (2023) · Galen Medical Journal · doi:10.31661/gmj.v12i.3061 · Cited by 9
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Linking gut microbiota dysbiosis to molecular pathways in Alzheimer’s disease
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“…the participants are cognitively unimpaired (with or without amyloid or tau biomarkers); the prodromal stage includes the early symptomatic phenotype (e.g., MCI), and the AD dementia stage refers to the phase where severe cognitive symptoms are present which affect social and daily activities [19].”
BackgroundBarnes, C. A., Permenter, M. R., Vogt, J. A., Chen, K., & Beach, T. G. (2024) · The Journal of Comparative Neurology · doi:10.1002/cne.25670 · Cited by 8
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“The development and adoption of this imaging biomarker align with the growing understanding of and advancements in the diagnostic landscape of AD [7,8].”
InfluentialSun, W., Ye, S., Wang, Y., Chen, H., Che, P., Chen, J., & Zhang, N. (2025) · Brain Communications · doi:10.1093/braincomms/fcaf094 · Cited by 8
“Alzheimer’s disease patients had to meet the diagnostic criteria of the IWG-2, 22 presenting with early and prominent episodic memory impairment and a positive result on 11 C-labeled Pittsburgh compound B (PiB) PET.”
Mao, M., Komes, D., Zhao, S., Pjanović, R., Wang, D., & Wang, Y. (2025) · The Innovation Medicine · doi:10.59717/j.xinn-med.2025.100121 · Cited by 8
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“Kinematic data were recorded by using the MPU-6500 Six-Axis (Gyro + Accelerometer) MEMS Motion Tracking devices embedded in the controller, in the tracker and in the headset, in conjunction with the precise spatial tracking provided by the base station.”
Advancements and challenges in using AI for biomarker detection in early Alzheimer’s disease
Beheshti, I., Albensi, B. C., Freitas, A. A., & Ghafourian, T. (2025) · Drug Discovery Today · doi:10.1016/j.drudis.2025.104415 · Cited by 9
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How to use neuroimaging biomarkers in the diagnosis framework of neurodegenerative diseases?
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“Further recommendations from the International Working Group have emphasized the need for a clinical-biological diagnosis of AD, which requires betaamyloid and tau biomarker positivity along with a clinical phenotype typically observed in AD [9].”
BackgroundGonzalez, A. S., John, A., Brotherhood, E., Camic, P. M., McKee‐Jackson, R., Melville, M., Sullivan, M. P., Edwards, R. T., Windle, G., Crutch, S. J., et al. (2023) · Pilot and Feasibility Studies · doi:10.1186/s40814-023-01403-1 · Cited by 7
“Most of the people presenting with young-onset dementia and some people with later onset dementia develop non-memoryled dementias such as the atypical forms of Alzheimer’s disease (AD) [3, 4] or frontotemporal dementia (FTD) [5].”
BackgroundDombrowski, W., Mims, A. D., Kremer, I. N., Desandes, P. C., Rodrigo‐Herrero, S., Epps, F. R., Snow, T., Gutierrez, M., Nasta, A., Epperly, M., et al. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-231491 · Cited by 6
Kiselica, A. M., Atkins, K. J., Han, S. D., Díaz-Orueta, U., Gogniat, M. A., Blanco‐Campal, A., Hermann, G., Neuropsychologists, C., & Duff, K. M. (2024) · Journal of Alzheimer s Disease · doi:10.1177/13872877241292089 · Cited by 7
“22 Such a system applied to the AD population may allay concerns with inappropriate disclosures, inaccurate descriptions of healthy patients as diseased, stigmatization associated with the disease label,andpatientconfusionsurroundingthelackofa1:1relation-ship between biomarker positivity and…”
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“However, conventional diagnostic methods for AD, such as neuroimaging and cerebrospinal fluid (CSF) biomarker analysis, often lack the capability for pre-symptomatic detection [2].”
The Outcome of Patients with Amyloid-Negative Amnestic Mild Cognitive Impairment
Cardoso, S., Silva, D., Alves, L., Guerreiro, M., & de Mendonça, A. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-215465 · Cited by 7
“Different diagnostic criteria with slight differences were advanced, namely prodromal AD [6–8] and mild cognitive impairment (MCI) due to AD [9], that rely on biomarkers reflect-ing pathological alterations of the AD continuum, namely the presence of amyloid in the brain [10], detected by measuring…”
How can secondary dementia prevention trials of Alzheimer's disease be clinically meaningful?
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Catatonia in patients with dementia: A descriptive study of clinical profiles and treatment response
Ramognino, V., Fovet, T., Horn, M., Lebouvier, T., & Amad, A. (2024) · Asian Journal of Psychiatry · doi:10.1016/j.ajp.2024.104033 · Cited by 8
Magnetic Resonance Imaging in Animal Models of Alzheimer’s Disease AmyloidosisPreprint
Ni, R. (2021) · Preprints.org · doi:10.20944/preprints202110.0231.v1 · Cited by 7
Miotto, E. C., Brucki, S. M. D., Cerqueira, C. T., Bazán, P. R., Silva, G. A. A., Martin, M. D. G. M., Squarzoni, P., Faria, D. D. P., Coutinho, A. M., Buchpiguel, C. A., et al. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220100 · Cited by 7
“A recently published recommendation of the International Working Group in 2021 on the AD diagnosis included its application to people who have positive biomarkers together with specific AD phenotypes, whereas biomarker-positive cognitively unimpaired individuals could be considered at-risk for progression to AD dement…”
BackgroundUltra-Early Screening of Cognitive Decline Due to Alzheimer’s Pathology
Wei, P. (2023) · Biomedicines · doi:10.3390/biomedicines11051423 · Cited by 8
“However, both the 2018 NIA-AA research framework [3] and the 2021 recommendations of the International Working Group [8] emphasize that the pathology of Alzheimer’s disease is defined by A β and tau biomarkers and the pathogenesis of Alzheimer’s disease is a continuous progression process ranging…”
BackgroundMethodGenes related to neurotransmitter receptors as potential biomarkers for Alzheimer's disease
Chen, W., Zhang, T., & Zhang, H. (2024) · Neuroscience Letters · doi:10.1016/j.neulet.2024.137816 · Cited by 7
Blood-based biomarkers of Alzheimer’s disease—A guideline for clinical use
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Functional cognitive disorder: Beyond pseudodementia
Marín‐Medina, D. S., Arenas-Vargas, P. A., Velásquez-Duque, M. D. P., & Bagnati, P. (2024) · Neurology Perspectives · doi:10.1016/j.neurop.2024.100179 · Cited by 6
Zhan, S., Wang, J., Dong, J., Ji, X., Huang, L. T., Zhang, Q., Xu, D., Peng, L., Wang, X., Zhang, Y., et al. (2025) · Asian Journal of Psychiatry · doi:10.1016/j.ajp.2025.104532 · Cited by 6
Unequal disease burdens: exploring the intersection of gender, health and disease dynamics in China
Yang, X., Li, R., Liu, J., Shu, J., Chen, H., Dong, M., Lv, J., Yuan, Y., Song, Q., Guo, L., et al. (2025) · BMC Public Health · doi:10.1186/s12889-025-23354-3 · Cited by 7
Advancements in the investigation of the mechanisms underlying cognitive aging
Zou, H., Zhang, S., Cui, X., Xu, H., Zhou, Z., Cheng, D., Han, Y., Tang, Y., Dong, A., & Dong, X. (2025) · Biogerontology · doi:10.1007/s10522-025-10300-4 · Cited by 8
“This observation has prompted the scientific community to advocate for a multidimensional assessment framework, integrating behavioral, neuroimaging, and molecular marker data to differentiate between normal aging and preclinical pathological states (Dubois et al. 2021).”
Rossem, D. V., Allemeersch, G., de Barros, N. P., Temmerman, J., Desmet, M., Ringoot, I., Ribbens, A., Michiels, V., Mey, J. D., Baeken, C., et al. (2025) · Scientific Reports · doi:10.1038/s41598-025-12975-8 · Cited by 7
Lei, H., Chen, X., Ruan, L., Liu, X., Ye, F., Li, K., Cheng, W., Yu, B., Di, C., & Di, C. (2025) · Ageing Research Reviews · doi:10.1016/j.arr.2025.102927 · Cited by 7
Sharma, A., & Singh, T. G. (2025) · Brain Research · doi:10.1016/j.brainres.2025.150047 · Cited by 7
From clinical phenotype to proteinopathy: molecular neuroimaging in neurodegenerative dementias
Studart‐Neto, A., & Coutinho, A. M. (2022) · Arquivos de Neuro-Psiquiatria · doi:10.1590/0004-282x-anp-2022-s138 · Cited by 6
Chen, C., Wang, K., & Hou, X. (2022) · Optics Express · doi:10.1364/oe.474043 · Cited by 6
Cerebrospinal fluid biomarkers in psychiatric autoimmune encephalitis: a retrospective cohort study
Hansen, N., Juhl, A. L., Grenzer, I. M., Teegen, B., Wiltfang, J., & Fitzner, D. (2023) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2023.1165153 · Cited by 6
Garcia, D. L., & Gollan, T. H. (2024) · Neuropsychology · doi:10.1037/neu0000943 · Cited by 6
Moschopoulos, C. D., Stanitsa, E., Protopapas, K., Kavatha, D., Papageorgiou, S. G., Antoniadou, A., & Papadopoulos, A. (2024) · Life · doi:10.3390/life14040508 · Cited by 6
“Amyloid and tau PET is considered to be a sensitive and specific neuroimaging biomarker for AD, with recent criteria proposing that amyloid-and tau-positive PET suffice for an AD diagnosis [128,129].”
BackgroundChang, H., Huang, C., Huang, S., Hsu, S., Lin, K., Ho, T., Wu, H., & Chang, C. (2024) · Psychiatry and Clinical Neurosciences · doi:10.1111/pcn.13680 · Cited by 7
Yu, M., Shen, Z., Zhang, S., Zhang, Y., Zhao, H., & Zhang, L. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e33761 · Cited by 6
“Individuals with the disease usually experience a relentless decline in memory and cognition to an extent that sufficiently interferes with daily life [2].”
Clinical significance of plasma candidate biomarkers of Alzheimer’s Disease
Lewczuk, P., Łukaszewicz‐Zając, M., Kornhuber, J., & Mroczko, B. (2024) · Neurologia i Neurochirurgia Polska · doi:10.5603/pjnns.100675 · Cited by 7
Seligmann, B. E., Camiolo, S., Hernandez, M., Yeakley, J. M., Sahagian, G. A., & McComb, J. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-240174 · Cited by 7
“4 This series of tests requires access to a medical specialist and numerous laboratory visits.”
BackgroundJia, F., Han, W., Gao, S., Huang, J., Zhao, W., Lu, Z., Zhao, W., Li, Z., Wang, Z., & Guo, Y. (2024) · Frontiers in Molecular Biosciences · doi:10.3389/fmolb.2024.1478611 · Cited by 7
Studart‐Neto, A., Barbosa, B. J. A. P., Coutinho, A. M., de Souza, L. C., Schilling, L. P., da Silva, M. N. M., Castilhos, R. M., Bertolucci, P. H. F., Borelli, W. V., Gomes, H. R., et al. (2024) · Dementia & Neuropsychologia · doi:10.1590/1980-5764-dn-2024-c001 · Cited by 11
Cerebrospinal-fluid Orexin-A levels in different neurocognitive disorders: a comparison study
Lozano-Tovar, S., Cremascoli, R., Nuccetelli, M., Sancesario, G., Cattaldo, S., Prina, E., Verde, F., Cappelli, S., Bernardini, S., Mercuri, N. B., et al. (2025) · Neurological Sciences · doi:10.1007/s10072-025-08148-0 · Cited by 7
“Patients with AD met the criteria for AD diagnosis according to recently published clinical criteria [21].”
Saracino, D., & Ber, I. L. (2022) · Revue Neurologique · doi:10.1016/j.neurol.2022.03.007 · Cited by 7
Waseem, W., Anwar, F., Saleem, U., Ahmad, B., Zafar, R., Anwar, A., Jan, M. S., Rashid, U., Sadiq, A., & Ismail, T. (2022) · ACS Omega · doi:10.1021/acsomega.2c03058 · Cited by 7
Autocorrection if→of function words in reading aloud: A novel marker of Alzheimer’s risk.
Gollan, T. H., Stasenko, A., Li, C., Smirnov, D. S., Galasko, D. R., & Salmon, D. P. (2022) · Neuropsychology · doi:10.1037/neu0000829 · Cited by 7
Self-citationWang, L., Hu, Z., Chen, H., Sheng, X., Qin, R., Shao, P., Yang, Z., Yao, W., Zhao, H., Xu, Y., et al. (2023) · Brain Sciences · doi:10.3390/brainsci13020339 · Cited by 6
“This characteristic presents as a typical manifestation of the disease in its early stages [7,8].”
BackgroundHigh-resolution omics of vascular ageing and inflammatory pathways in neurodegeneration
Kwok, A. J., Lu, J., Huang, J., Ip, B. Y. M., Mok, V., Lai, H. M., & Ko, H. (2023) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2023.06.005 · Cited by 6
Translating NIA‐AA criteria into usual practice: Report from the ReDeMa Project
Sánchez‐Soblechero, A., Berbel, Á., Villarejo‐Galende, A., Palmí-Cortés, I., Vieira, A., Gil‐Moreno, M. J., Fernández, C., Martín-Montes, A., Carreras, M. T., Fernández, Y., et al. (2024) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1002/trc2.12451 · Cited by 5
“10 These core biomarkers have replaced the neuropathological study in the research setting, 11,12 but there is no consensus about their use in clinical practice.”
BackgroundDunn, T., Howlett, S. E., Stanojevic, S., Shehzad, A., Stanley, J., & Rockwood, K. J. (2021) · Journal of Medical Internet Research · doi:10.2196/29219 · Cited by 6
“Along these lines, the lack of correlation between clinical manifestations of the disease and biomarker positivity has motivated the reconsideration of a purely biological definition of AD, suggesting that the disease designation be restricted to people who combine biomarker positivity with specific AD phenotypes [25].”
BackgroundMozersky, J. T., AGREED, O. B. O., Roberts, J. S., Rumbaugh, M. C., Chhatwal, J. P., Wijsman, E. M., Galasko, D. R., & Blacker, D. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220113 · Cited by 6
Self-citationTaking the A Train? Limited Consistency of Aβ42 and the Aβ42/40 Ratio in the AT(N) Classification
Gouilly, D., Tisserand, C., Nogueira, L., Saint‐Lary, L., Rousseau, V., Bénaiteau, M., Rafiq, M., Carlier, J., Milongo-Rigal, E., Pagès, J., et al. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210236 · Cited by 6
EWA-DB, Slovak Database of Speech Affected by Neurodegenerative DiseasesPreprint
Rusko, M., Sabo, R., Trnka, M., Zimmermann, A., Malaschitz, R., Ružický, E., Brandoburová, P., Kevická, V., & Škorvánek, M. (2023) · medRxiv · doi:10.1101/2023.10.13.23296810 · Cited by 7
“…disease (PD), are the two most common neurodegenerative diseases, which have been historically diagnosed based on their clinical symptoms, however, additional diagnostic tools such as imaging or biological markers are being increasingly implemented in their clinical diagnostic criteria 1, 2 .”
BackgroundItkyal, V. S., Abrol, A., LaGrow, T. J., et al. (2023) · Research Square · doi:10.21203/rs.3.rs-3740218/v1 · Cited by 6
“Given that Alzheimer's disease affects a signi�cant portion of the global population, early and precise AD diagnosis is imperative to facilitate timely interventions and enhance patient well-being (Cummings et al., 2022; Dubois et al., 2021; L.-K. Huang et al., 2020).”
BackgroundAmyloid‐β but not tau accumulation is strongly associated with longitudinal cognitive decline
Wang, W., Huang, J., Qian, S., Zheng, Y., Yu, X., Jiang, T., Ai, R., Hou, J., Ma, E., Cai, J., et al. (2024) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.14860 · Cited by 5
Cámara‐Calmaestra, R., Martínez‐Amat, A., Aibar‐Almazán, A., Hita‐Contreras, F., de Miguel‐Hernando, N., Rodríguez‐Almagro, D., Jiménez‐García, J. D., & Achalandabaso‐Ochoa, A. (2024) · Physiotherapy · doi:10.1016/j.physio.2024.101440 · Cited by 13
Using cerebrospinal fluid biomarkers to diagnose Alzheimer’s disease: an Australian perspective
Eratne, D., Collins, S. J., Nestor, P. J., Pond, D. C., Velakoulis, D., Yates, M. W., & Masters, C. L. (2024) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2024.1488494 · Cited by 6
Parfenov, V. A., Гришина, Д. А., Борисовна, Л. А., Zakharov, V. V., Shevtsova, K. V., & Chervyakova, Y. I. (2025) · Neurology neuropsychiatry Psychosomatics · doi:10.14412/2074-2711-2025-1-4-9 · Cited by 5
Hemispheric asymmetry in neurodegenerative diseases
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Self-citationCuní‐López, C., Stewart, R., Okano, S., Redlich, G. L., Appleby, M. W., White, A. R., & Quek, H. (2025) · Scientific Reports · doi:10.1038/s41598-025-92593-6 · Cited by 5
“S8; Supplementary datasets 3 and 4 ).”
Radiomics of PET Using Neural Networks for Prediction of Alzheimer's Disease Diagnosis
Zhang, Y., Steingrimsson, J. A., Ambekar, A., Oh, H., Eloyan, A., & Initiative, A. D. N. (2025) · Statistics in Medicine · doi:10.1002/sim.70128 · Cited by 5
Wu‐Chung, E. L., Kennedy, K. M., Medina, L. D., Schulz, P. E., Oswald, F. L., Heijnen, C. J., Leal, S. L., Denny, B. T., & Fagundes, C. P. (2025) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2025.06.027 · Cited by 6
Liu, Y., Chen, S., Li, S., Pei, Z., Fan, S., & Guo, Y. (2025) · Journal of Alzheimer s Disease Reports · doi:10.1177/25424823251362444 · Cited by 6
Air pollution as a key risk factor for alzheimer’s disease: A comprehensive review
Zhu, X., Guo, C., Zhang, Y., & Wei, Y. (2025) · Environmental Technology & Innovation · doi:10.1016/j.eti.2025.104555 · Cited by 6
Hyperspectral retinal imaging to detect Alzheimer’s disease in a memory clinic setting
Dallora, A. L., Alexander, J., Palesetti, P. P., Guénot, D., Selvander, M., Berglund, J. S., & Behrens, A. (2025) · Alzheimer s Research & Therapy · doi:10.1186/s13195-025-01887-4 · Cited by 9
“Efforts to improve the diagnosis and management of dementia focus on enhancing the accuracy of clinical diagnoses through advanced neuroimaging and blood biomarkers [2, 3, 9].”
Brain and retina in Alzheimer's disease: Pathological intersections and estimates from imaging
Banihashemi, M. A., Krance, S. H., Ji, P. X., Koo, M., Ottoy, J., Swartz, R. H., Kertes, P. J., Hudson, C., Goubran, M., & Black, S. E. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70884 · Cited by 7
Maintaining and regaining episodic memory in Alzheimer disease: a circuit-based perspective
Düzel, E., & Kreutz, M. R. (2026) · Nature Reviews Neurology · doi:10.1038/s41582-026-01189-9 · Cited by 8
Vera, D. M., Enache, D., Tambaro, S., Abuhashish, E., Rosell‐Valle, C., Winblad, B. G., de Fonseca, F. R., Bereczki, E., & Nilsson, P. (2022) · Brain Communications · doi:10.1093/braincomms/fcad001 · Cited by 5
“Currently, biomarkers, specifically CSF markers, can be used primarily as a research tool and optionally by physicians to identify at-risk patients for developing Alzheimer’s disease, with some patient stratification strategies considering their progression recently issued.(10) The amyloid, tau and neurodegeneration (…”
Case report: Anti-ARHGAP26 autoantibodies in atypical dementia with Lewy bodies
Hansen, N., Rentzsch, K., Hirschel, S., et al. (2023) · Frontiers in Dementia · doi:10.3389/frdem.2023.1227823 · Cited by 5
Marín-Marín, L., Lagranja, J. R., Ávila, C., & Costumero, V. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-230929 · Cited by 5
“However, this perspective has been challenged by other researchers who pro-pose that an AD diagnosis should be restricted to individuals exhibiting both biomarkers and an AD phenotype [3].”
Wertman, E. (2024) · Journal of Clinical Medicine · doi:10.3390/jcm13144202 · Cited by 6
“These models are associated with biomolecular constructs [17,422,423] and overlook factors contributing to SLODP [418].”
BackgroundMethodInfluentialChen, A. M., Gajdošík, M., Ahmed, W., Ahn, S., Babb, J. S., Blessing, E., Boutajangout, A., de Leon, M. J., Debure, L., Gaggi, N. L., et al. (2024) · NeuroImage · doi:10.1016/j.neuroimage.2024.120742 · Cited by 5
“…most individuals are diagnosed only after exhibiting objective cognitive impairment ( e.g. , memory loss and deficits in executive function) (Dubois et al., 2021), despite there being histologic (Price et al., 2009), structural (Petrone et al., 2019), and functional (Veitch et al., 2019;…”
BackgroundFocus groups on digital cognitive assessment in the context of Alzheimer's disease
van der Landen, S. M., van den Berg, R. L., Keijzer, M. J., van Liere, M. N., de Boer, C., Visser, L. N. C., van der Flier, W. M., Rhodius‐Meester, H. F. M., & Sikkes, S. A. M. (2025) · Digital Health · doi:10.1177/20552076251318903 · Cited by 5
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“Bieger (Bieger et al., 2024) compared AD diagnosis in the ADNI cohort according to NIA-AA 2011 (McKhann et al., 2011), NIA-AA 2018 (Jack et al., 2018), IWG-2 2016 (Dubois et al., 2016), and IWG-3 2021 criteria (Dubois et al., 2021).”
Yoon, H., Lee, N., Um, Y. H., & Choi, W. H. (2025) · Diagnostics · doi:10.3390/diagnostics15131599 · Cited by 5
“The deposition of β -amyloid (A β ) plaques in the brain is recognized as a significant pathological hallmark of AD [2].”
The Diagnostic Value of a Short Memory Test: The TNI-93
Foucard, C., Palisson, J., Belin, C., Bereaux, C., Dumurgier, J., Paquet, C., Degos, B., Bouaziz-Amar, É., Maillet, D., Houot, M., et al. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210546 · Cited by 5
Ren, S., Hu, J., Huang, L., Li, J., Jiang, D., Hua, F., Guan, Y., Guo, Q., Xie, F., & Huang, Q. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220527 · Cited by 5
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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