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
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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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Matrine exerts its neuroprotective effects by modulating multiple neuronal pathways
Chhabra, S., & Mehan, S. (2023) · Metabolic Brain Disease · doi:10.1007/s11011-023-01214-6 · Cited by 21
Changes of tRNA-Derived Fragments by Alzheimer’s Disease in Cerebrospinal Fluid and Blood Serum
Wu, W., Shen, A., Lee, I., Miranda-Morales, E. G., Spratt, H. M., Pappolla, M. A., Fang, X., & Bao, X. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230412 · Cited by 20
“Identifying prodromal stages of AD remains a major challenge due to the lack of sensitive biomarkers to accurately distinguish early stages of AD from age-related cognitive deficits [8–11].”
Immunotherapy: An emerging treatment option for neurodegenerative diseases
Mukherjee, A., Biswas, S., & Roy, I. (2024) · Drug Discovery Today · doi:10.1016/j.drudis.2024.103974 · Cited by 22
Early detection of Alzheimer’s disease in structural and functional MRI
Maity, R., Sankari, V. M. R., Umapathy, S., Velu, S. R., Alahmadi, T. J., Alhababi, Z. A., & Alkahtani, H. K. (2024) · Frontiers in Medicine · doi:10.3389/fmed.2024.1520878 · Cited by 23
The impact of real-world evidence in implementing and optimizing Alzheimer’s disease care
Hampel, H. J., Li, G., Mielke, M. M., Galvin, J. E., Kivipelto, M., Santarnecchi, E., Babiloni, C., Devanarayan, V., Tkatch, R., Hu, Y. P., et al. (2025) · Med · doi:10.1016/j.medj.2025.100695 · Cited by 20
Tideman, P., Karlsson, L., Strandberg, O. T., Calling, S., Smith, R. A., Midlöv, P., Verghese, P. B., Braunstein, J. B., Mattsson, N., Stomrud, E., et al. (2025) · Nature Medicine · doi:10.1038/s41591-025-03965-4 · Cited by 36
“Biomarker testing in clinical practice is currently only recommended in patients with cognitive impairment 1,3,13,16 .”
InfluentialHansen, N., Juhl, A. L., Grenzer, I. M., et al. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.837376 · Cited by 19
Keshavan, A., O’Shea, F., Chapman, M. D., Hart, M., Lunn, M. P., Paterson, R. W., Rohrer, J. D., Mummery, C. J., Fox, N. C., Zetterberg, H., et al. (2022) · Practical Neurology · doi:10.1136/practneurol-2021-003310 · Cited by 18
Lucena, P. B., Vanherle, S., Lodder, C., de Ravé, M. G., Stancu, I., Lambrichts, I., Vangheluwe, R., Bruffaerts, R., & Dewachter, I. (2022) · Acta Neuropathologica · doi:10.1007/s00401-022-02458-9 · Cited by 22
“Aβ and tau-based CSF biomarkers and PET imaging can identify amyloid and tau pathology in the brain and are used for early diagnosis and even identification of subjects at risk before symptom development [2, 8, 14, 28].”
BackgroundCoregistered transcranial optoacoustic and magnetic resonance angiography of the human brain
Ni, R., Deán‐Ben, X. L., Treyer, V., Gietl, A. F., Höck, C., Klohs, J., Nitsch, R. M., & Razansky, D. (2022) · Optics Letters · doi:10.1364/ol.475578 · Cited by 19
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“A purely biological definition is with a low predictive accuracy for AD and insufficient to definitively predict MCI [6], not readily available in clinical screening as well.”
BackgroundMethodInfluentialIs blood pTau a reliable indicator of the CSF status? A narrative review
Antonioni, A., Raho, E. M., & Lorenzo, F. D. (2023) · Neurological Sciences · doi:10.1007/s10072-023-07258-x · Cited by 20
“While the clinical diagnosis of AD dementia requires the presence of specific symptoms, the neurobiological diagnosis relies on these findings according to the ATN classification, which distinguishes patients according to the presence of amyloid (A), pTau (T) and neurodegeneration (N) [5, 6].”
Yang, Y., Chen, W., Lin, Z., Wu, Y., Li, Y., & Xia, X. (2024) · BMC Complementary Medicine and Therapies · doi:10.1186/s12906-024-04403-7 · Cited by 19
“More than 50 million people worldwide currently live with AD, and this number is expected to exceed 152 million by 2050 [2].”
BackgroundTargeting lncRNA NEAT1 Hampers Alzheimer’s Disease Progression
Li, Y., Fan, H., Ni, M., Zhang, W., Fang, F., Sun, J., Lyu, P., & Ma, P. (2023) · Neuroscience · doi:10.1016/j.neuroscience.2023.02.016 · Cited by 19
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“, 11, 12 Some ThepresentationandprogressionpatternsofADarevariabledueto a multifactorial integration of environment, aging, senescence, genetic factors, cognitive reserve and resilience, and the gradual failure of adaptive and compensatory biological mechanisms.”
Self-citationVasileva-Metodiev, S. Z., Spargo, D. J., Klein, E., Quevenco, F., Cotton, S. E., Sánchez‐Juan, P., Niimi, Y., & Fowler, N. R. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251322978 · Cited by 20
“68”
Advances in biosensors for diagnosis of Alzheimer's and Parkinson's diseases
Negahdary, M., Sakthinathan, I., Mirsadoughi, E., Ligler, F. S., Coté, G. L., Forster, R. J., & Mabbott, S. B. (2025) · Biosensors and Bioelectronics · doi:10.1016/j.bios.2025.117535 · Cited by 19
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Early Diagnosis of Alzheimer’s Disease: Moving Toward a Blood-Based Biomarkers Era
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“Although blood-based biomarkers (ie, Aβ, p-tau) are still not recommended in clinical practice which need to be further standardized and validated.(7) The”
BackgroundSerum neurofilament light chain and cognition decline in US elderly: A cross‐sectional study
Liu, X., Chen, J., Meng, C., Zhou, L., & Liu, Y. (2023) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.51929 · Cited by 17
“…protein molecules found in cerebrospinal fluid, such as tau protein and amyloid-b 42 filaments, have been extensively studied as potential biological markers for early diagnosis of AD 14 , their screening value in the general population is severely restricted by their intrusiveness and high cost.”
BackgroundSymptoms and conventional treatments of Alzheimer's disease
Chorawala, M. R., Shah, A. C., Pandya, A. J., Kothari, N. R., & Prajapati, B. G. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-13205-6.00009-1 · Cited by 20
Metals, Nanoparticles, Particulate Matter, and Cognitive Decline
Calderón‐Garcidueñas, L., Chávez-Franco, D. A., Luévano-Castro, S. C., Escobedo, E. H. M., Hernández-Castillo, A., Carlos, E., Franco-Ortíz, A., Castro-Romero, S. P., Cortés-Flores, M., Crespo-Cortés, C. N., et al. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2021.794071 · Cited by 18
Objective Criteria for Subtle Cognitive Decline in Aging and Preclinical Alzheimer Disease
Thomas, K. R., & Edmonds, E. C. (2025) · Neurology · doi:10.1212/wnl.0000000000213536 · Cited by 20
Cerami, C., Boccardi, M., Meli, C., Panzavolta, A., Funghi, G., Festari, C., Cappa, S. F., Chatzikostopoulos, T., Chicherio, C., Clarens, M. F., et al. (2025) · Journal of Neuropsychology · doi:10.1111/jnp.12431 · Cited by 18
“Clinical neuropsychological examination alone has shown little accuracy to identify the underlying pathology responsible for NCDs (Beach et al., 2012; Bertoux et al., 2020), while biomarkers can exclude or confirm an aetiology (Dubois et al., 2021; Frisoni et al., 2024).”
Self-citationSomatic Mutations and Alzheimer’s Disease
Downey, J., Lam, J. C. K., Li, V. O. K., & Gozes, I. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220643 · Cited by 18
Management of patients with cognitive impairment
Parfenov, V. A. (2023) · Neurology neuropsychiatry Psychosomatics · doi:10.14412/2074-2711-2023-1-97-102 · Cited by 22
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“Spatial cognitive impairment can lead to many diseases, such as Alzheimer’s disease [1].”
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“However, a comprehensive evaluation of AD should still require both the presence of cognitive symptoms and a specific biomarker profile [19].”
BackgroundUpdate on Nonhuman Primate Models of Brain Disease and Related Research Tools
Qiao, N., Ma, L., Zhang, Y., & Wang, L. (2023) · Biomedicines · doi:10.3390/biomedicines11092516 · Cited by 18
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“Consequently, individuals who test positive for these biomarkers, yet do not exhibit cognitive impairment, should be classified as at risk rather than definitively diagnosed with AD [46].”
BackgroundAlzheimer's disease: diagnosis and treatment, errors in patient management
Parfenov, V. A., Гришина, Д. А., & Tyurina, A. Y. (2024) · Neurology neuropsychiatry Psychosomatics · doi:10.14412/2074-2711-2024-2-95-100 · Cited by 17
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Alzheimer’s disease transcriptional landscape in ex vivo human microglia
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“Despite its prevalence, AD remains difficult to differentiate from other forms of dementia during life, especially in its advanced stages 2 .”
Jin, Z., Lu, Y., Tang, H., & Cui, H. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70472 · Cited by 24
Lorenzo, R. D., Zecca, C., Chimienti, G., Latronico, T., Liuzzi, G. M., Pesce, V., Dell’Abate, M. T., Borlizzi, F., Giugno, A., Urso, D., et al. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26167792 · Cited by 18
The changing definition of Alzheimer's disease
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“This finding suggests that over 50% of our progressor group may be at risk for Alzheimer’s disease due to elevated amyloid followed by the development of subtle cognitive symptoms.(38) Further, we found a statistically significant interaction be-”
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Identifying healthy individuals with Alzheimer’s disease neuroimaging phenotypes in the UK Biobank
Azevedo, T., Bethlehem, R. A. I., Whiteside, D. J., Swaddiwudhipong, N., Rowe, J. B., Lió, P., Rittman, T., Initiative, T. A. D. N., Silbert, L. C., Lind, B., et al. (2023) · Communications Medicine · doi:10.1038/s43856-023-00313-w · Cited by 17
“The challenge of identifying disease at the earliest possible point has led to proposed criteria for at-risk or presymptomatic Alzheimer ’ s disease that rely on biomarker evidence rather than clinical syndrome 11 .”
Self-citationGagliardi, G. P., Rodriguez‐Vieitez, E., Montal, V., Sepulcre, J., Diez, I. P., Lois, C., Hanseeuw, B. J., Schultz, A. P., Properzi, M. J., Papp, K. V., et al. (2023) · Communications Medicine · doi:10.1038/s43856-023-00324-7 · Cited by 16
Wang, S., Kang, D. W., Um, Y. H., Kim, S., Lee, C. U., & Lim, H. K. (2023) · Biomolecules · doi:10.3390/biom13091336 · Cited by 19
“Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by a gradual and long-term decline in cognitive function [1].”
BackgroundWang, Y., Zhang, Y., & Yu, E. (2023) · Clinical Neurology and Neurosurgery · doi:10.1016/j.clineuro.2023.108071 · Cited by 16
“…2021, the International Working Group on AD made the recommendation the current diagnosis of Alzheimer ’ s disease requires both positive biomarkers and symptoms of cognitive impairment, and that the A/T(N) research framework should be used as the clinical diagnosis model of AD in the future [70].”
Amyloid PET disclosure in subjective cognitive decline: Patient experiences over time
Hendriksen, H. M. A., de Rijke, T. J., Fruijtier, A. D., van de Giessen, E., van Harten, A. C., van Leeuwenstijn‐Koopman, M. S. S. A., van der Schaar, J., Trieu, C., Visser, D., Smets, E. M. A., et al. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14148 · Cited by 17
Mulumba, J., Duan, R., Luo, B., Wu, J., Sulaiman, M., Wang, F., & Yang, Y. (2025) · Exploration of neuroscience · doi:10.37349/en.2025.100675 · Cited by 23
Manera, V., Rovini, E., & Wais, P. E. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1149886 · Cited by 19
“For instance, biomarkers of amyloid β pathology (low CSF Aβ42 or increased CSF Aβ40–Aβ42 ratio; increased tracer retention in amyloid PET) and biomarkers of tau pathology (increased phosphorylated tau in CSF; increased tracer retention in tau PET) can characterize AD pathology before the appearance of clinical symptom…”
BackgroundKegyes-Brassai, A. C., Pierson-Bartel, R., Bolla, G., Kamondi, A., & Horvath, A. A. (2024) · GeroScience · doi:10.1007/s11357-024-01357-z · Cited by 15
“Since amyloid misfolding starts decades before the first onset of cognitive symptoms [10], these findings suggest the utility of sleep macrostructure as screening or diagnostic markers [11].”
The effect of Lewy body (co-)pathology on the clinical and imaging phenotype of amnestic patients
Silva‐Rodríguez, J., Labrador‐Espinosa, M. Á., Zhang, L., Castro‐Labrador, S., López‐González, F. J., Moscoso, A., Sánchez‐Juan, P., Schöll, M., & Grothe, M. J. (2025) · Brain · doi:10.1093/brain/awaf037 · Cited by 16
“2,3 By contrast, Lewy body (LB) pathology, composed of misfolded α -synuclein, is typically associated to a distinct dementia syndrome characterized by a relatively more dysexecutive cognitive profile and a higher prevalence of neuropsychiatric abnormalities, such as hallucinations.”
Kuhn, E., Klinger, H. M., Amariglio, R. E., Wagner, M., Jessen, F., Düzel, E., Heneka, M. T., Chételat, G., Rentz, D. M., Sperling, R. A., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.14307 · Cited by 16
Imaging and Fluid Biomarkers of Alzheimer Disease: Complementation Rather Than Competition
Drzezga, A. E., & Barthel, H. (2025) · Journal of Nuclear Medicine · doi:10.2967/jnumed.125.270152 · Cited by 18
Bucci, M., Almkvist, O., Blūma, M., Ashton, N. J., Savitcheva, I., Chiotis, K., Molfetta, G. D., Blennow, K., Zetterberg, H., & Nordberg, A. K. (2025) · Journal of Neurochemistry · doi:10.1111/jnc.70182 · Cited by 15
“Future research should aim to replicate these findings in larger and more diverse populations and explore the added value of combining neuropsychological tests with advanced neuroimaging and multimodal biomarker approaches (Dubois et al. 2021).”
Self-citationMattsson, N., Palmqvist, S., Horie, K., Barthélemy, N. R., Salvadó, G., Binette, A. P., Tideman, P., Morris, J. C., Benzinger, T. L. S., Perrin, R. J., et al. (2026) · The Lancet Neurology · doi:10.1016/s1474-4422(26)00029-3 · Cited by 16
Wang, S., Zheng, K., Kong, W., Huang, R., Liu, L., Wen, G., & Yu, Y. (2022) · Briefings in Bioinformatics · doi:10.1093/bib/bbac515 · Cited by 15
Nester, C. O., Qin, J., Wang, C., Katz, M. J., Lipton, R. B., & Rabin, L. A. (2022) · Archives of Clinical Neuropsychology · doi:10.1093/arclin/acac102 · Cited by 16
Attitudes of Neurologists Toward the Use of Biomarkers in the Diagnosis of Early Alzheimer’s Disease
Fortea, J., García-Arcelay, E., Terrancle, Á., Gálvez, B., Díez-Carreras, V., Rebollo, P., Mauriño, J., & García‐Ribas, G. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-221160 · Cited by 16
“The International Working Group for New Research Criteria (IWG) recommends that biomarker diagnosis should be conducted in patients with specific AD phenotypes in line with 2011 NIA-AA criteria [5, 6].”
BackgroundKarthivashan, G., & Kar, S. (2023) · Journal of Nanobiotechnology · doi:10.1186/s12951-023-01957-5 · Cited by 15
“Historically, AD has been diagnosed based on symptomatology, with definitive diagnosis relies on post-mortem examination [3].”
BackgroundTau as a diagnostic instrument in clinical trials to predict amyloid in Alzheimer's disease
Shcherbinin, S., Morris, A., Higgins, I. A., Tunali, I., Lu, M., Deveau, C., Southekal, S. S., Kotari, V., Evans, C. D., Arora, A., et al. (2023) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1002/trc2.12415 · Cited by 15
“2 Similarly, the International Working Group 3 defines the diagnosis of AD as clinical– biological, requiring the presence of clinical phenotype in addition to amyloid and tau positivity.”
Bakhtiari, A., Benedek, K., Law, I. G., Fagerlund, B., Mortensen, E. L., Osler, M., Lauritzen, M., Larsson, H. B. W., & Vestergaard, M. B. (2023) · GeroScience · doi:10.1007/s11357-023-01031-w · Cited by 17
“Although A β deposition alone is insufficient to diagnose AD, A β -positive individuals without cognitive impairment are regarded as asymptomatic at risk [4].”
BackgroundBian, X., Wang, Q., Wang, Y., & Lou, S. (2024) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2023.1305208 · Cited by 15
Lattice 123 pattern for automated Alzheimer’s detection using EEG signal
Doğan, Ş., Barua, P. D., Bayğın, M., Tuncer, T., Tan, R., Ciaccio, E. J., Fujita, H., Devi, A., & Acharya, U. R. (2024) · Cognitive Neurodynamics · doi:10.1007/s11571-024-10104-1 · Cited by 16
Bringas, S., Duque, R., Lage, C., & Montaña, J. L. (2024) · IEEE Journal of Biomedical and Health Informatics · doi:10.1109/jbhi.2024.3392354 · Cited by 18
“AD can lead to a significant impairment in these people’s physical functions and a loss of independence in basic activities of daily living (use of the bathroom, dressing, etc.) [2].”
BackgroundNow and future: Strategies for diagnosis, prevention and therapies for Alzheimer’s disease
Shi, J., Touchon, J., Middleton, L. T., Boada, M., Vassar, R. J., Vellas, B. J., & Shen, Y. (2024) · 中国科学通报：英文版 · doi:10.1016/j.scib.2024.09.042 · Cited by 16
Pecher, H., Storch, M., Beyer, F., Witte, A. V., Baasner, C.-F., Schönknecht, P. O. D., & Weise, C. M. (2024) · NeuroImage Clinical · doi:10.1016/j.nicl.2024.103687 · Cited by 18
“Of note, ADNI used a clinical approach for diagnosis (McKhann et al. 1984; Petersen et al. 2010), yet current diagnostic consensus guidelines highlight the necessity of fluid or imaging biomarker positivity to accurately diagnose AD (Dubois et al. 2021).”
Salivary Metabolomics in the Diagnosis and Monitoring of Neurodegenerative Dementia
Hyvärinen, E., Solje, E., Vepsäläinen, J. J., Kullaa, A. M., & Tynkkynen, T. (2023) · Metabolites · doi:10.3390/metabo13020233 · Cited by 16
“In cognitively asymptomatic individuals with positive biomarkers for AD, the lifetime dementia risk is estimated to be from 5% to 42% [7].”
BackgroundHeyer, S., Simon, M., Doyen, M., Mortada, A., Roch, V., Jeanbert, E., Thilly, N., Malaplate, C., Kearney-Schwartz, A., Jonveaux, T., et al. (2024) · Alzheimer's Research & Therapy · doi:10.1186/s13195-024-01535-3 · Cited by 14
“Currently, postmortem autopsy remains the only way to confirm a diagnosis of a neurodegenerative disease [2, 7].”
Jiao, Y., Han, W., Zhang, L., Wang, M., Lyu, Z., Su, Y., Wang, Z., Wang, L., Wang, J., Xu, P., et al. (2025) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2025.111368 · Cited by 14
“In contrast, no significant perfusion impairment was detected in the mildly impaired A β + MCI 1 and A β + MCI 2 groups, except for a mild decreasing trend in hippocampal perfusion (Lin et al., 2016).”
InfluentialSoriano-Herrador, C., Úbeda‐Bañón, I., Villanueva‐Anguita, P., Saiz‐Sánchez, D., Astillero‐Lopez, V., Martı́nez-Marcos, A., & Flores‐Cuadrado, A. (2025) · Neurobiology of Disease · doi:10.1016/j.nbd.2025.106971 · Cited by 15
“In fact, the diagnosis of AD should include people who are positive for biomarkers and who have specific disease phenotypes (Dubois et al., 2021).”
Benussi, A., Agosta, F., Alfano, A. R., Antico, A., Bellelli, G., Bonanni, L., Bottini, G., Bozzali, M., Brignoli, O., Bruno, G., et al. (2025) · Neurological Sciences · doi:10.1007/s10072-025-08576-y · Cited by 17
CSF biomarker concordance with amyloid PET in Phase 3 studies of aducanumab
Nisenbaum, L., Martone, R. L., Chen, T., Rajagovindan, R., Dent, G. W., Beaver, J. D., Rubel, C. E., Racine, A. M., He, P., Harrison, K., et al. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.12919 · Cited by 16
Filippi, M., Cecchetti, G., Cagnin, A., Marra, C., Nobili, F. M., Parnetti, L., & Agosta, F. (2023) · Journal of Neurology · doi:10.1007/s00415-023-11642-0 · Cited by 15
“Moreover, a biological diagnosis is crucial in case of atypical phenotypes (posterior cortical atrophy, logopenic variant of primary progressive aphasia, behavioral/dysexecutive variant, corticobasal syndrome) to assure the demonstration of an AD underlying pathology [15].”
BackgroundInfluentialJessen, F., Bohr, L., Kruse, C., & Dodel, R. C. (2023) · Der Nervenarzt · doi:10.1007/s00115-023-01492-6 · Cited by 14
“Während über viele Jahrzehnte die Alzheimer-Krankheit gleichgesetzt wurde mit der syndromal-definierten AlzheimerDemenz, wurde in den letzten Jahren ein biologisches Krankheits- und Diagnostikverständnis entwickelt [6].”
BackgroundGuo, X., Zhang, X., Tang, P., Li, C., & Li, R. (2023) · Age and Ageing · doi:10.1093/ageing/afad112 · Cited by 15
Li, J., Li, X., Chen, F., Li, W., Chen, J., & Zhang, B. (2023) · Reviews in the Neurosciences · doi:10.1515/revneuro-2023-0098 · Cited by 15
Wang, J., Shi, L. D., Zhu, X., Tang, Q., Wu, M., Li, B., Liu, W., & Jin, Y. (2024) · Talanta · doi:10.1016/j.talanta.2024.125656 · Cited by 14
Chen, Y., Zhang, M., Yang, C., Gao, M., Yan, Y., Deng, C., & Sun, N. (2024) · Analytical Chemistry · doi:10.1021/acs.analchem.3c05868 · Cited by 14
Chu, H., Huang, C., Guan, Y., Xie, F., Chen, M., & Guo, Q. (2024) · Clinical Nutrition · doi:10.1016/j.clnu.2024.05.024 · Cited by 16
Huang, K., Hsiao, I., Huang, C., Huang, C., Chang, H., Huang, S., Lin, K., Ma, M.-C., Huang, C., & Chang, C. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.14297 · Cited by 13
Marco, M. D., Blackburn, D. J., & Venneri, A. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.678588 · Cited by 15
Aducanumab: What about the Patient?
Petersen, R. C. (2021) · Annals of Neurology · doi:10.1002/ana.26181 · Cited by 14
“Although not universally accepted at this point, other views incorporating clinical features with biomarkers for amyloid and tau have been proposed.(6) Although not in complete agreement, both positions highlight the importance of biomarkers for amyloid and tau in defining the disease.”
BackgroundSaunders, S., Ritchie, C. W., Russ, T. C., Terrera, G. M., & Milne, R. (2022) · BMC Geriatrics · doi:10.1186/s12877-021-02693-x · Cited by 16
“Since the late 1990s, MCI has been defined in formal diagnostic criteria and is now commonly referred to as MCI due to Alzheimer’s disease as per the NIA-AA guidelines [7, 8].”
BackgroundGozdas, E., Hinkley, L. M., Fingerhut, H., Dacorro, L., Gu, M., Sacchet, M. D., Hurd, R. E., & Hosseini, S. M. H. (2022) · NeuroImage Clinical · doi:10.1016/j.nicl.2022.103159 · Cited by 15
“Amyloid beta (A β ) and tau imaging can be used to detect the preclinical pathology of AD using an advanced molecular imaging method, positron emission tomography (PET) (Dubois et al., 2021; Maschio and Ni, 2022).”
Amyloid-β PET Classification on Cognitive Aging Stages Using the Centiloid Scale
de Souza, G. S., Andrade, M. A., Borelli, W. V., Schilling, L. P., Matushita, C. S., Portuguez, M. W., da Costa, J. C., & da Silva, A. M. M. (2021) · Molecular Imaging and Biology · doi:10.1007/s11307-021-01660-7 · Cited by 16
“Moreover, although pre-clinical evaluation of Aβ positivity is not recommended by the IWG [11], we believe that individuals who have an early Aβ deposition without a clinical diagnosis might benefit from early therapy and prevention strategies.”
BackgroundMethodInfluentialLecanemab approval in EU: what should we be ready for?– the EANM perspective
Yakushev, I. Y., Verger, A., Brendel, M., et al. (2025) · European Journal of Nuclear Medicine and Molecular Imaging · doi:10.1007/s00259-025-07066-9 · Cited by 13
Chen, X., Song, W., Zhang, H., Xu, Y., Yi, B., & Zhou, Q. (2025) · Chemical Engineering Journal · doi:10.1016/j.cej.2025.159756 · Cited by 13
Chronic kidney disease and dementia: an epidemiological perspective
Ikram, M. A. (2025) · Nature Reviews Nephrology · doi:10.1038/s41581-025-00967-w · Cited by 19
Universal Artificial Urinary Biomarker Probe Enabled by an Aptamer–DNAzyme–Nanozyme Construct
Xiao, Y., Wong, J. H., Gao, N., Barron, A. M., Stanley, C. V., Than, A., Zheng, L., Ling, T., Li, D., & Chen, P. (2025) · Nano Letters · doi:10.1021/acs.nanolett.5c02356 · Cited by 15
Sticker-and-spacer model for amyloid beta condensation and fibrillation
Connor, J. P., Quinn, S. D., & Schaefer, C. (2022) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2022.962526 · Cited by 15
“Amyloid deposition does not correlate with neuronal loss (Kametani and Hasegawa, 2018) and amyloid burden can be identified in cognitively unimpaired individuals (Arenaza-Urquijo and Vemuri, 2018; Dubois et al., 2021).”
BackgroundBunnik, E. M., Smedinga, M., Milne, R., Georges, J., Richard, E., & Schermer, M. (2022) · Ethics & Human Research · doi:10.1002/eahr.500146 · Cited by 14
A framework for addressing Alzheimer's disease: Without a frame, the work has no aim
BALL, D. E., Mattke, S., Frank, L. B., Murray, J. F., Noritake, R., MacLeod, T., Benham‐Hermetz, S., Kurzman, A., & Ferrell, P. B. (2022) · Alzheimer s & Dementia · doi:10.1002/alz.12869 · Cited by 12
A multimodal fusion method for Alzheimer’s disease based on DCT convolutional sparse representation
Zhang, G., Nie, X., Liu, B., Yuan, H., Li, J., Sun, W., & Huang, S. (2023) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.1100812 · Cited by 15
“In clinical, AD is characterized by general dementia such as cognitive decline and memory loss (Dubois et al., 2021).”
BackgroundAhmad, I., Singh, R., Pal, S., Prajapati, S., Sachan, N., Laiq, Y., & Husain, H. (2023) · Applied Biochemistry and Biotechnology · doi:10.1007/s12010-023-04340-0 · Cited by 16
“In addition to that, formation of neurofibrillary and neuritic plaques is correlated with pervasive oxidative stress and damage [22, 52].”
BackgroundChen, Q., Chen, F., Long, C., Zhu, Y., Jiang, Y., Zhu, Z., Lu, J., Zhang, X., Nedelská, Z., Hort, J., et al. (2023) · Alzheimer s Research & Therapy · doi:10.1186/s13195-023-01233-6 · Cited by 13
“Introduction Alzheimer’s disease (AD) is a major global concern [1].”
BackgroundZhang, J., Xia, J., Liu, X., & Olichney, J. (2023) · Brain Sciences · doi:10.3390/brainsci13050770 · Cited by 15
The “when” matters: Evidence from memory markers in the clinical continuum of Alzheimer’s disease.
Forno, G., Parra, M. A., Thumala, D., Villagra, R., Cerda, M., Pedro Zitko, M., Ibáñez, A. M., Lillo, P., & Slachevsky, A. (2023) · Neuropsychology · doi:10.1037/neu0000891 · Cited by 13
Precision medicine in neurodegeneration: the IHI-PROMINENT project
Tate, A., Suárez‐Calvet, M., Ekelund, M., Eriksson, S., Eriksdotter, M., van der Flier, W. M., Georges, J., Kivipelto, M., Kramberger, M. G., Lindgren, P., et al. (2023) · Frontiers in Neurology · doi:10.3389/fneur.2023.1175922 · Cited by 13
Zhang, Q., Fan, C., Wang, L., Li, T., Wang, M., Han, Y., Jiang, J., Initiative, A. F. T. A. D. N., Weiner, M. W., Aisen, P. S. S., et al. (2023) · GeroScience · doi:10.1007/s11357-023-00897-0 · Cited by 15
Self-citationMai, Y., Cao, Z., Zhao, L., Yu, Q., Xu, J., Liu, W., Liu, B., Tang, J., Luo, Y., Liao, W., et al. (2023) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.14492 · Cited by 12
“7,8 The early stages are the best time for AD treatment, but the heterogeneity of MCI and AD leads to significant diagnostic challenges.”
Robillard, J. M., Masellis, M., Martin, S. E., Khachaturian, A. S., & Dixon, R. A. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-230359 · Cited by 14
Atypical clinical variants of Alzheimer’s disease: are they really atypical?
Whitwell, J. L. (2024) · Frontiers in Neuroscience · doi:10.3389/fnins.2024.1352822 · Cited by 15
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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