The DOI matches its Crossref record; 117 of the 119 references it cites were found in a registry or an index; 4 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
32 Not checked yet · 13 Own interpretation · 1 Supported · 1 Partly 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)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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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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- Based: passes — The paper gives a reason why it holds.
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
hedgeddirect- 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
plaincorrelational- 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
“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.
plaindirect- 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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- 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
“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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- Load-bearing: passes — The paper’s conclusions depend on it.
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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
plaindirect- 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
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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
- Not checked yetcites [1] Jack, 2018, NIA–AA research framework: toward a biological definition of Alzheimer's disease, Alzheimers Dement source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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
hedgedcorrelational- 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
plaincorrelational- 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
plainconditional- 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
hedgedcorrelational- 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
“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
plaincorrelational- 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
plaindirect- 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
plaindirect- 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
hedgedconditional- 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
plaincorrelational- 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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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
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- 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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Self-citationClassification of primary progressive aphasia and its variants
Gorno-Tempini, M. L., Hillis, A. E., Weintraub, S., Kertesz, A., Mendez, M., Cappa, S. F., Ogar, J. M., Rohrer, J. D., Black, S., Boeve, B. F., et al. (2011) · Neurology · doi:10.1212/wnl.0b013e31821103e6 · Cited by 5,141 · cited 1×
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BackgroundSelf-citationDiagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB Consortium
McKeith, I. G., Boeve, B. F., Dickson, D. W., Halliday, G., Taylor, J.-P., Weintraub, D., Aarsland, D., Galvin, J., Attems, J., Ballard, C. G., et al. (2017) · Neurology · doi:10.1212/wnl.0000000000004058 · Cited by 4,476
Self-citation
Cited by
Sorted by citations
Items 101–200 of 1,002
Cornuside Is a Potential Agent against Alzheimer’s Disease via Orchestration of Reactive Astrocytes
Shi, J.-Z., Zheng, X.-M., Zhou, Y., Yun, L.-Y., Dong-mei, L., Hao, J.-J., Liu, P., Zhang, W., Xu, J., Yan, Y., et al. (2022) · Nutrients · doi:10.3390/nu14153179 · Cited by 44
“1 trillion dollars is estimated to double by 2030 [3].”
BackgroundArtificial Intelligence Models in the Diagnosis of Adult-Onset Dementia Disorders: A Review
Battineni, G., Chintalapudi, N., Hossain, M. A., Losco, G., Ruocco, C., Sagaro, G. G., Traini, E., Nittari, G., & Amenta, F. (2022) · Bioengineering · doi:10.3390/bioengineering9080370 · Cited by 43
“Around 50 million people were affected by AOCD (dementia) worldwide in 2018, with a cost of approximately one trillion dollars for their care every year [3].”
BackgroundFluid biomarkers for the diagnosis of neurodegenerative diseases
Luebke, M., Parulekar, M. S., & Thomas, F. P. (2023) · Biomarkers in Neuropsychiatry · doi:10.1016/j.bionps.2023.100062 · Cited by 42
Schöll, M., Vrillon, A., Ikeuchi, T., Quevenco, F. C., Iaccarino, L., Vasileva-Metodiev, S. Z., Burnham, S. C., Hendrix, J. A., Epelbaum, S., Zetterberg, H., et al. (2025) · The Journal of Prevention of Alzheimer s Disease · doi:10.1016/j.tjpad.2024.100056 · Cited by 48
Self-citationBernhardt, A. M., Longen, S., Trossbach, S. V., Rossi, M., Weckbecker, D., Schmidt, F., Jäck, A., Katzdobler, S., Fietzek, U. M., Weidinger, E., et al. (2025) · Acta Neuropathologica · doi:10.1007/s00401-025-02853-y · Cited by 42
“The diagnosis of 35 patients with Alzheimer’s disease (AD) was made according to the International Working Group criteria [15].”
Hayato, S., Takenaka, O., Reddy, S. H. S., Landry, I. S., Reyderman, L., Koyama, A., Swanson, C. J., Yasuda, S., & Hussein, Z. (2022) · CPT Pharmacometrics & Systems Pharmacology · doi:10.1002/psp4.12862 · Cited by 41
Vascular risk burden is a key player in the early progression of Alzheimer’s disease
Ferrari‐Souza, J. P., Brum, W. S., Hauschild, L. A., Ros, L. U. D., Ferreira, P. C. L., Bellaver, B., Leffa, D. T., Bieger, A., Tissot, C., Lussier, F. Z., et al. (2021) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2023.12.008 · Cited by 40
Self-citationVillain, N., & Michalon, R. (2024) · European Journal of Neurology · doi:10.1111/ene.16302 · Cited by 43
Self-citationDulewicz, M., Kulczyńska‐Przybik, A., Mroczko, P., Kornhuber, J., Lewczuk, P., & Mroczko, B. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23158598 · Cited by 38
“Some of these criteria are still in research and development for later clinical use (yellow dots in Figure 1) [6,15,18,53,54,57].”
BackgroundResultInfluentialMohan, M., Mannan, A., Kakkar, C., & Singh, T. G. (2024) · Current Drug Targets · doi:10.2174/0113894501320839240918110656 · Cited by 37
Villavicencio-Tejo, F., Olesen, M. A., Aránguiz, A., & Quintanilla, R. A. (2022) · Antioxidants · doi:10.3390/antiox11030515 · Cited by 40
Contador, J., Vargas‐Martínez, A. M., Sánchez‐Valle, R., Trapero‐Bertran, M., & Lladó, A. (2022) · European Archives of Psychiatry and Clinical Neuroscience · doi:10.1007/s00406-022-01439-z · Cited by 38
“As the different AD clinical phenotypes could also be seen in other neurodegenerative diseases, it has been suggested that the positivity of both, amyloid and tau biomarkers, is necessary to increase the likelihood of AD as the primary diagnosis [31].”
BackgroundWang, X., Yang, H., Liu, C., & Liu, K. (2023) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2023.1194210 · Cited by 36
“CSF Aβ42 is a recommended diagnostic marker for AD (Dubois et al., 2021).”
BackgroundZhao, K., Chen, P., Alexander‐Bloch, A. F., Wei, Y., Dyrba, M., Yang, F., Kang, X., Wang, D., Fan, D., Shan, Y., et al. (2023) · EClinicalMedicine · doi:10.1016/j.eclinm.2023.102276 · Cited by 38
“37 Therefore, IBRAIN might mirror the changes of indiscernible pathological alterations that are indiscernible utilising traditional sMRI diagnostic methodologies.”
BackgroundCognitive Phenotyping and Interpretation of Alzheimer Blood Biomarkers
Bouteloup, V., Villain, N., Vidal, J., González‐Ortiz, F., Yuksekel, I., dos Santos, C. P., Schraen‐Maschke, S., Pellegrin, I., Lehmann, S., Blennow, K., et al. (2025) · JAMA Neurology · doi:10.1001/jamaneurol.2025.0142 · Cited by 40
Self-citationPlasma ATN(I) classification and precision pharmacology in Alzheimer's disease
Imbimbo, B. P., Watling, M., Imbimbo, C., & Nisticò, R. (2023) · Alzheimer's & Dementia · doi:10.1002/alz.13084 · Cited by 34
Snellman, A., Ekblad, L. L., Ashton, N. J., Karikari, T. K., Lantero‐Rodriguez, J., Pietilä, E. A., Koivumäki, M., Helin, S., Karrasch, M., Zetterberg, H., et al. (2023) · Neurobiology of Disease · doi:10.1016/j.nbd.2023.106175 · Cited by 36
“…various biofluid or imaging-based markers: cerebrospinal fluid (CSF) markers are available for measurements of A β 42/40 , total tau (t-tau) and phosphorylated tau (p-tau) and positron emission tomography (PET) for monitoring fibrillar A β and tau deposition in the brain (Dubois et al., 2021).”
BackgroundSelf-citationNovel fluid biomarkers for mild cognitive impairment: A systematic review and meta-analysis
Gaur, A., Rivet, L., Mah, E., Bawa, K. K., Gallagher, D., Herrmann, N., & Lanctôt, K. L. (2023) · Ageing Research Reviews · doi:10.1016/j.arr.2023.102046 · Cited by 37
Roth, S., Burnie, N., Suridjan, I., Yan, J. T., & Carboni, M. (2023) · Journal of Alzheimer s Disease Reports · doi:10.3233/adr230007 · Cited by 32
“This is in line with recent guidelines ([39], and summarized in [40]), which advise a tiered approach: cognitive deficits should be confirmed, and physiological causes for cognitive decline ruled out, before biomarker tests are conducted.”
ResultChen, J., Zhao, X. Y., Zhang, W., Zhang, T., Wu, S., Shao, J., & Shi, F. (2023) · Alzheimer s Research & Therapy · doi:10.1186/s13195-023-01246-1 · Cited by 33
“Introduction Alzheimer’s disease (AD) is the most common neurodegenerative disorder worldwide and is also one of the main health problems affecting elderly people [1].”
BackgroundZhang, S., Zhao, H., Wang, W., Wang, Z., Luo, X., Hramov, A. E., & Kurths, J. (2023) · Neurocomputing · doi:10.1016/j.neucom.2023.126512 · Cited by 35
Measurement of α-synuclein as protein cargo in plasma extracellular vesicles
Gilboa, T., Ter‐Ovanesyan, D., Wang, S., Whiteman, S. T., Kannarkat, G. T., Church, G. M., Chen‐Plotkin, A. S., & Walt, D. R. (2024) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2408949121 · Cited by 38
“Measuring α-synuclein by Simoa, we observed a similar EV - associated peaking pattern in fractions 7 to 12 after the protease protection as we previously observed without PK treatment ( Fig.”
Tackling Stereochemistry in Drug Molecules with Vibrational Optical Activity
Bogaerts, J., Aerts, R., Vermeyen, T., Johannessen, C., Herrebout, W., & Batista, J. M. (2021) · Pharmaceuticals · doi:10.3390/ph14090877 · Cited by 33
Evaluation of clinical benefits of treatments for Alzheimer's disease
Liu, K. Y., Walsh, S., Brayne, C., Merrick, R., Richard, E., & Howard, R. (2023) · The Lancet Healthy Longevity · doi:10.1016/s2666-7568(23)00193-9 · Cited by 31
Bermejo‐Pareja, F., & del Ser, T. (2024) · Journal of Clinical Medicine · doi:10.3390/jcm13020536 · Cited by 39
Viral Infections, Are They a Trigger and Risk Factor of Alzheimer’s Disease?
Rippee‐Brooks, M. D., Wu, W., Dong, J., Pappolla, M. A., Fang, X., & Bao, X. (2024) · Pathogens · doi:10.3390/pathogens13030240 · Cited by 31
“…hyper-phosphorylated tau (hyper-p-tau), although the presence of A β and Tau cannot completely conclude AD, as there are cognitively unimpaired individuals who can have biomarker evidence of both A β and Tau pathology but will often not develop clinical manifestations in their lifetime [5].”
BackgroundDei, A., Micheli, M. M., Aldigeri, R., Gardini, S., Pellegrini, F. F., Perini, M., Messa, G., Antonini, M., Spigoni, V., Cinquegrani, G., et al. (2024) · Journal of Endocrinological Investigation · doi:10.1007/s40618-024-02320-7 · Cited by 41
“This overt clinical phase of AD is preceded by a variably long—up to several decades—preclinical phase, namely mild cognitive impairment (MCI), a cognitive stage between expected cognitive impairment of normal aging and the early stage of a more serious decline [3].”
BackgroundShue, F., White, L. J., Hendrix, R. D., Ulrich, J. D., Henson, R. L., Knight, W., Martens, Y. A., Wang, N., Roy, B., Starling, S. C., et al. (2024) · Science Advances · doi:10.1126/sciadv.adk3674 · Cited by 33
“Clinical AD diagnosis accuracy using medical history, neuropsychological testing, neuroimaging, and/or fluid biomarkers has improved substantially ( 9 ).”
Agnello, L., Gambino, C. M., Ciaccio, A. M., Masucci, A., Vassallo, R., Tamburello, M., Scazzone, C., Sasso, B. L., & Ciaccio, M. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25084323 · Cited by 38
“Additionally, some authors showed that NfLs are significantly increased in FTD patients than in other NDs, such as AD and PD, opening the possibility to use them for differential diagnosis [39].”
BackgroundZhang, W., Smith, N. S., Zhou, Y., McGee, C. M., Bartoli, M., Fu, S., Chen, J., Domena, J. B., Joji, A., Burr, H., et al. (2024) · Acta Biomaterialia · doi:10.1016/j.actbio.2024.06.001 · Cited by 34
Dyer, A. H., Dolphin, H., O’Connor, A., Morrison, L., Sedgwick, G., Young, C., Killeen, E., Gallagher, C., McFeely, A., Connolly, E., et al. (2024) · Alzheimer s Research & Therapy · doi:10.1186/s13195-024-01555-z · Cited by 39
“The increasing availability of Alzheimer Disease (AD) biomarkers has led to a paradigm shift towards the conceptualisation of AD as a clinical-biological diagnosis rather than one based on clinical phenotype alone [1, 2].”
BackgroundHaraldsen, I., Hatlestad‐Hall, C., Marra, C., Renvall, H., Maestú, F., Acosta-Hernández, J., Alfonsín, S., Andersson, V., Anand, A., Ayllón, V., et al. (2024) · Frontiers in Neurorobotics · doi:10.3389/fnbot.2023.1289406 · Cited by 34
New horizons in the diagnosis and management of Alzheimer’s Disease in older adults
Dolphin, H., Dyer, A. H., Morrison, L., Shenkin, S. D., Welsh, T. J., & Kennelly, S. (2024) · Age and Ageing · doi:10.1093/ageing/afae005 · Cited by 33
“However as brains age, there are often multiple factors causing neurodegeneration and cell death [17] with amyloid and tau pathology only two of multiple pathological causes of cognitive impairment [6].”
BackgroundInfluentialInfluence of Different Diagnostic Criteria on Alzheimer Disease Clinical Research
Bieger, A., Brum, W. S., Borelli, W. V., Therriault, J., Bastiani, M. A. D., Moreira, A. G., Benedet, A. L., Ferrari‐Souza, J. P., da Costa, J. C., Souza, D. O., et al. (2024) · Neurology · doi:10.1212/wnl.0000000000209753 · Cited by 35
Self-citationSacchi, L., D’Agata, F., Campisi, C., Arcaro, M., Carandini, T., Örzsik, B., Maschio, V. P. D., Fenoglio, C., Pietroboni, A. M., Ghezzi, L., et al. (2024) · Human Brain Mapping · doi:10.1002/hbm.26805 · Cited by 33
Advanced nano delivery system for stem cell therapy for Alzheimer's disease
Pan, Y., Li, L., Cao, N., Liao, J., Chen, H., & Zhang, M. (2024) · Biomaterials · doi:10.1016/j.biomaterials.2024.122852 · Cited by 33
Bernhardt, A. M., Tiedt, S., Teupser, D., Dichgans, M., Meyer, B., Gempt, J., Kuhn, P., Simons, M., Palleis, C., Weidinger, E., et al. (2023) · EBioMedicine · doi:10.1016/j.ebiom.2023.104456 · Cited by 32
Zaman, M., Fu, Y., Chen, P., Sun, H., Yang, S., Wu, Z., Wang, Z., Poudel, S., Serrano, G. E., Beach, T. G., et al. (2023) · Molecular & Cellular Proteomics · doi:10.1016/j.mcpro.2023.100608 · Cited by 29
“The most common clinical manifestations of AD include irreversible memory loss, progressive cognitive decline, and impaired reasoning accompanied by loss of functional autonomy (5).”
BackgroundApplication of biomarker-derived fluorescent probes for the detection of Alzheimer's disease
Ding, H., Li, Z., Luo, K., Gong, Q., & Tian, X. (2023) · TrAC Trends in Analytical Chemistry · doi:10.1016/j.trac.2023.117369 · Cited by 30
Magnetic Resonance Imaging in Animal Models of Alzheimer’s Disease Amyloidosis
Ni, R. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms222312768 · Cited by 34
“Recent advances in diagnostic imaging have provided insights into the time course of AD pathology, including Aβ, tau, and neuroinflammation, in patients and in animal disease models [4,5].”
BackgroundMethodChen, C., Ma, X., Wei, J., Shakir, N., Zhang, J. K., Zhang, L., Nehme, A., Cui, Y., Ferguson, D., Bai, F., et al. (2022) · Translational Psychiatry · doi:10.1038/s41398-022-02132-4 · Cited by 32
Blood based biomarkers for movement disorders
Morris, H. R. (2022) · Acta Neurologica Scandinavica · doi:10.1111/ane.13700 · Cited by 29
Calderón‐Garcidueñas, L., Hernández-Luna, J., Aiello-Mora, M., Brito-Aguilar, R., Evelson, P., Villarreal-Ríos, R., Torres‐Jardón, R., Ayala, A., & Mukherjee, P. S. (2023) · Biomolecules · doi:10.3390/biom13060927 · Cited by 28
Dumas, A., Destrebecq, F., Esposito, G., Suchoňová, D., & Frederiksen, K. S. (2023) · Aging Brain · doi:10.1016/j.nbas.2023.100093 · Cited by 31
“They have, in particular, made recommendations for the use in clinical practice of blood biomarkers for amyloid β and tau pathology [32].”
BackgroundKrálová, K., Kráľ, M., Vrtělka, O., & Setnička, V. (2023) · Spectrochimica Acta Part A Molecular and Biomolecular Spectroscopy · doi:10.1016/j.saa.2023.123392 · Cited by 30
Li, Y., Fan, H., Ni, M., Zhang, W., Fang, F., Sun, J., Lyu, P., & Ma, P. (2021) · Neuroscience · doi:10.1016/j.neuroscience.2021.11.001 · Cited by 30
Recent Developments in Positron Emission Tomography Tracers for Proteinopathies Imaging in Dementia
Ni, R., & Nitsch, R. M. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.751897 · Cited by 30
Mechanistic Insight into the Inhibition of Choline Acetyltransferase by Proton Pump Inhibitors
Baidya, A. T. K., Das, B., Devi, B., Långström, B., Ågren, H., Darreh‐Shori, T., & Kumar, R. (2023) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.2c00738 · Cited by 32
Clinical utility of cerebrospinal fluid biomarkers measured by LUMIPULSE ® system
Nojima, H., Itō, S., Kushida, A., Abe, A., Motsuchi, W., Verbel, D., Vandijck, M. L. J., Jannes, G., Vandenbroucke, I., & Aoyagi, K. (2022) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.51681 · Cited by 30
“Therefore, IWG suggested that a comprehensive diagnosis combining clinical symptoms and other factors including biomarkers would be important.(41) Recently, it has been reported that racial differences are present in some biomarkers of AD.”
BackgroundHead-to-head comparison of plasma and PET imaging ATN markers in subjects with cognitive complaints
Lu, J., Ma, X., Zhang, H., Xiao, Z., Li, M., Wu, J., Ju, Z., Chen, L., Zheng, L., Ge, J., et al. (2023) · Translational Neurodegeneration · doi:10.1186/s40035-023-00365-x · Cited by 28
“Meanwhile, the assessment of relationship between ATN biomarkers and cognitive symptoms (C) is important given that a clinical-biological rather than a purely biological diagnosis of AD is recommended in clinical settings [7].”
BackgroundLi, R., Wang, X., & Yu, H. Q. (2023) · Findings of the Association for Computational Linguistics: EMNLP (Findings of EMNLP) · doi:10.18653/v1/2023.findings-emnlp.474 · Cited by 37
“In particular, combing the gold and bronze dataset, which is generated by LLMs only, outperform the model trained only on the gold or gold+silver dataset for some categories.”
MethodHuszár, Z., Engh, M. A., Pavlekovics, M., Sato, T., Steenkamp, Y., Hanseeuw, B. J., Terebessy, T., Molnár, Z., Hegyi, P., & Csukly, G. (2024) · Alzheimer s Research & Therapy · doi:10.1186/s13195-024-01455-2 · Cited by 30
“The International Working Group (IWG) [5] emphasizes that diagnosis should align with clinical symptoms.”
BackgroundLiu, D., Baranova, A. V., & Zhang, F. (2024) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2024.148 · Cited by 27
“Reliance on a set of clinical symptoms or a single biomarker is insufficient for an AD diagnosis (9, 10).”
Calderón‐Garcidueñas, L., Hernández-Luna, J., Mukherjee, P. S., Styner, M. A., Chávez-Franco, D. A., Luévano-Castro, S. C., Crespo-Cortés, C. N., Stommel, E. W., & Torres‐Jardón, R. (2022) · Toxics · doi:10.3390/toxics10040156 · Cited by 28
Shared pathophysiology: Understanding stroke and Alzheimer’s disease
Sriram, S., Mehkri, Y., Quintin, S. S., & Lucke-Wold, B. P. (2022) · Clinical Neurology and Neurosurgery · doi:10.1016/j.clineuro.2022.107306 · Cited by 29
Rye, I., Vik, A., Kociński, M., Lundervold, A. S., & Lundervold, A. J. (2022) · Scientific Reports · doi:10.1038/s41598-022-18805-5 · Cited by 31
Source space connectomics of neurodegeneration: One-metric approach does not fit all
Prado, P., Moguilner, S., Mejía, J. A., Sainz‐Ballesteros, A., Otero, M., Birba, A., Santamaría‐García, H. A., Legaz, A., Fittipaldi, S., Cruzat, J., et al. (2023) · Neurobiology of Disease · doi:10.1016/j.nbd.2023.106047 · Cited by 27
“Introduction Alzheimer’s disease (AD) and behavioral variant frontotemporal dementia (bvFTD) are neurodegenerative conditions urgently calling for affordable, scalable, cross-cultural, and physio-pathological plausible biomarkers accompanying diagnosis and characterization (Dubois et al., 2021; Jagust, 2021; Parra et…”
BackgroundBerger, M., Ryu, D., Reese, M. A., McGuigan, S., Evered, L. A., Price, C. C., Scott, D. A., Westover, M. B., Eckenhoff, R. G., Bonanni, L., et al. (2023) · Neurotherapeutics · doi:10.1007/s13311-023-01401-4 · Cited by 28
Baiardi, S., Hansson, O., Levin, J., & Parchi, P. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14039 · Cited by 27
“103,104 The leading current approach is based on the A/T/(N) system, which provides a binary classification of biomarker results for the three pathological processes: “A” refers to biomarkers that measure A β deposition, “T” to those that assess p-tau accumulation, and “N” to those that assess…”
BackgroundTaha, H. B. (2025) · npj Dementia · doi:10.1038/s44400-024-00002-y · Cited by 31
Biel, D., Luan, Y., Brendel, M., Hager, P., Dewenter, A., Moscoso, A., Svaldi, D. O., Higgins, I. A., Pontecorvo, M. J., Roemer, S. N., et al. (2022) · Alzheimer s Research & Therapy · doi:10.1186/s13195-022-01105-5 · Cited by 34
“While neuroimaging and fluid biomarkers of Aβ and tau are routinely established for AD diagnosis [2, 3], reliable prognosis of cognitive decline remains a critical challenge, which is further complicated by the considerable heterogeneity in symptom manifestation and disease progression [4–6].”
BackgroundBeyond the amyloid cascade: An update of Alzheimer's disease pathophysiology
Gouilly, D., Rafiq, M., Nogueira, L., Salabert, A., Payoux, P., Péran, P., & Pariente, J. (2023) · Revue Neurologique · doi:10.1016/j.neurol.2022.12.006 · Cited by 31
Relevance of Minor Neuropsychological Deficits in Patients With Subjective Cognitive Decline
Stark, M., Wolfsgruber, S., Kleineidam, L., Frommann, I., Altenstein, S., Bartels, C., Brosseron, F., Büerger, K., Burow, L., Butryn, M., et al. (2023) · Neurology · doi:10.1212/wnl.0000000000207844 · Cited by 28
“33 In this perspective, SCD in patients without MCI is not considered su ffi ciently speci fi c or predictive for future impairment to be classi fi ed as such an AD-de fi ning clinical phenotype.”
BackgroundWyman‐Chick, K. A., Choudhury, P., Bayram, E., Ruiz, C. A., Matar, E., Chiu, S., Ferreira, D., Hamilton, C. A., Donaghy, P. C., Rodriguez‐Porcel, F. E., et al. (2024) · Neurology and Therapy · doi:10.1007/s40120-024-00620-x · Cited by 30
“More recently, the amyloid/tau/neurodegen‑ eration (ATN) framework has been utilised in research settings to identify neuropathological changes in prodromal and overt AD [64, 65].”
BackgroundZheng, H., Xiong, X., & Zhang, X. (2024) · Brain Sciences · doi:10.3390/brainsci14060565 · Cited by 31
Vogelgsang, J. S., Hansen, N., Stark, M., Wagner, M., Klafki, H., Morgado, B., Jahn‐Brodmann, A., Schott, B. H., Esselmann, H., Bauer, C., et al. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.13909 · Cited by 24
“4 Most recently, the National Institute on Aging–Alzheimer’s Association (NIA-AA) presented a draft of revised clinical guidelines for AD, defining AD purely by amyloid positivity (AP) measured by PET, cerebrospinal fluid (CSF), or plasma amyloid biomarker.”
BackgroundSelf-citationAltered T-cell reactivity in the early stages of Alzheimer's disease
Rickenbach, C., Mallone, A., Häusle, L., Frei, L., Seiter, S., Sparano, C., Kirabali, T., Blennow, K., Zetterberg, H., Ferretti, M. T., et al. (2025) · Brain · doi:10.1093/brain/awaf167 · Cited by 27
“11 As particularly the preclinical phase of AD is not well understood, its in-depth characterization would allow improving biomarkers and potentially preventive therapeutic strategies before the onset of symptoms.”
Self-citationTondo, G., Boccalini, C., Vanoli, E. G., Presotto, L., Muscio, C., Ciullo, V., Banaj, N., Piras, F., Filippini, G., Tiraboschi, P., et al. (2022) · Neurology · doi:10.1212/wnl.0000000000200351 · Cited by 28
Self-citationUrbano, T., Chiari, A., Malagoli, C., Cherubini, A., Bedin, R., Costanzini, S., Teggi, S., Maffeis, G., Vinceti, M., & Filippini, T. (2023) · Environmental Research · doi:10.1016/j.envres.2023.115425 · Cited by 25
FDG‐PET markers of heterogeneity and different risk of progression in amnestic MCI
Caminiti, S., Francesco, S. D., Tondo, G., Galli, A., Redolfi, A., & Perani, D. (2023) · Alzheimer's & Dementia · doi:10.1002/alz.13385 · Cited by 27
“…atrophy significantly contributed to a more severe hypometabolism in left PCC ( t = 6.74; MNI coordinates = –4, –30, 32; P < 0.001), left hippocampus ( t = 7.36; MNI coordinates = –28, 12, –26; P < 0.001), and right middle cingulate cortex ( t = 6.54; MNI coordinates = 6, –22, 32; P < 0.001).”
InfluentialSteroid hormones: risk and resilience in women’s Alzheimer disease
Calvo, N., & Einstein, G. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1159435 · Cited by 27
Devi, G. (2023) · Handbook of clinical neurology · doi:10.1016/b978-0-323-98817-9.00015-6 · Cited by 27
“A combined clinical biomarker approach seems to be the most valid, as a solely biomarker-based approach has significant issues (Dubois et al., 2021).”
Cutting-edge Strategies for Overcoming Therapeutic Barriers in Alzheimer's Disease
Inamdar, A., Gurupadayya, B., Halagali, P., Nandakumar, S., Pathak, R., Singh, H., & Sharma, H. (2024) · Current Pharmaceutical Design · doi:10.2174/0113816128344571241018154506 · Cited by 33
Anterior-temporal network hyperconnectivity is key to Alzheimer’s disease: from ageing to dementia
Chauveau, L., Landeau, B., Dautricourt, S., Turpin, A., Delarue, M., Hébert, O., Sayette, V. D. L., Chételat, G., & de Florès, R. (2025) · Brain · doi:10.1093/brain/awaf008 · Cited by 31
Interpretable brain disease classification and relevance-guided deep learning
Tinauer, C., Heber, S., Pirpamer, L., Damulina, A., Schmidt, R., Stollberger, R., Ropele, S., & Langkammer, C. (2022) · Scientific Reports · doi:10.1038/s41598-022-24541-7 · Cited by 26
“Recently revised diagnosis criteria for AD are clinical-biological and require both clinical phenotype and biomarker evidence (A β or tau) of AD 5 .”
BackgroundDevi, G. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1213968 · Cited by 29
“Further refinements led to the two current definitions for AD—the American radiologist-led purely biomarker-based amyloid, tau, and neurodegeneration (ATN) on neuroimaging definition proposed in 2018 and the 2021 European neurologist-led IWG definition that requires functional impairment in addition to biomarkers (Jac…”
BackgroundInsights into the pathological basis of dementia from population‐based neuropathology studies
Wharton, S. B., Simpson, J. E., Ince, P. G., Richardson, C. D., Merrick, R. L., Matthews, F. E., Brayne, C., & CFAS (2023) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12923 · Cited by 27
“Indeed, a biological definition of AD for research purposes, the ATN system based on Aβ, tau and neurodegenerative biomarkers, has been proposed by the National Institute on Ageing and Alzheimer’s Association (NIA-AA), which defines AD by the presence of pathological markers,(129) and which has provoked debate into it…”
BackgroundHu, Y., Niu, L., Chen, Y., Yang, H., Qiu, X., Jiang, F., Liu, C., Cai, H., & Le, W. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70314 · Cited by 31
The Brain’s Glymphatic System: Drawing New Perspectives in Neuroscience
Ciurea, A. V., Mohan, A. G., Covache-Busuioc, R.-A., Costin, H. P., & Saceleanu, V. M. (2023) · Brain Sciences · doi:10.3390/brainsci13071005 · Cited by 27
“Clearance of Aβ and tau proteins into cerebrospinal fluid (CSF) serves as the basis for measurement purposes as clinical biomarkers of AD [26,27].”
BackgroundCerebrovascular and Alzheimer’s disease biomarkers in dementia with Lewy bodies and other dementias
Rennie, A., Ekman, U., Shams, S., Rydén, L., Samuelsson, J., Zettergren, A., Kern, S., Oppedal, K., Blanc, F., Hort, J., et al. (2024) · Brain Communications · doi:10.1093/braincomms/fcae290 · Cited by 21
Afrin, M. R., Upadhyaya, P. G., Hashim, A., Bhattacharya, K., Chanu, N. R., Das, D., Khanal, P., & Deka, S. (2025) · Ageing Research Reviews · doi:10.1016/j.arr.2025.102736 · Cited by 27
Terrabuio, E., Pietronigro, E. C., Bani, A., Bianca, V. D., Laudanna, C., Rossi, B., Finotti, G., Santos-Lima, B., Zenaro, E., Turano, E., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-62405-6 · Cited by 33
“In APP / A β and tau pathologies have a synergistic effect in AD and diagnosis requires the presence of both hallmarks 18 – 20 .”
Chen, Y., Liu, Z., Gong, P., Zhang, H., Chen, Y., Yao, S., Li, W., Zhang, Y., & Yu, Y. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23169041 · Cited by 25
“Alzheimer’s disease (AD) is a chronic neurodegenerative disorder characterized by progressive memory loss and cognitive impairment [1].”
BackgroundPrognostic and Predictive Factors in Early Alzheimer’s Disease: A Systematic Review
Garcia, M. J., Leadley, R. M., Ross, J., Bozeat, S., Redhead, G., Hansson, O., Iwatsubo, T., Villain, N., & Cummings, J. L. (2024) · Journal of Alzheimer s Disease Reports · doi:10.3233/adr-230045 · Cited by 53
“…suggest diagnosis of AD should include A (cid:2) biomarkers (CSF or positron emission tomography) and tau marker biomarkers (CSF or positron emission tomography), typically this more robust diagnosis has not been used in many of the retrospective studies or historical registries [48].”
BackgroundSelf-citationThe Early Diagnosis of Alzheimer’s Disease: A Patient-Centred Conversation with the Care Team
Nasreddine, Z. S., Garibotto, V., Kyaga, S., & Padovani, A. (2022) · Neurology and Therapy · doi:10.1007/s40120-022-00428-7 · Cited by 31
“with amyloid PET [57]; furthermore, these biomarker assays are associated with lower costs than PET [18].”
BackgroundInfluentialRaikes, A. C., Hernandez, G. D., Matthews, D. C., Lukic, A. S., Law, M., Shi, Y., Schneider, L. S. S., & Brinton, R. D. (2022) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1002/trc2.12258 · Cited by 21
Self-citationCabreira, V., McWhirter, L., & Carson, A. J. (2023) · Neurologic Clinics · doi:10.1016/j.ncl.2023.02.004 · Cited by 21
Zhang, N., Nao, J., & Dong, X. (2023) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.3c06672 · Cited by 23
Research Progress on the Pathogenesis, Diagnosis, and Drug Therapy of Alzheimer’s Disease
Yang, Y., & Qiu, L. (2024) · Brain Sciences · doi:10.3390/brainsci14060590 · Cited by 22
Screening for early Alzheimer’s disease: enhancing diagnosis with linguistic features and biomarkers
Chou, C., Chang, C.-T., Chang, Y., Lee, C., Chuang, Y., Chiu, Y., Liang, W.-L., Fan, Y.-M., & Liu, Y. (2024) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2024.1451326 · Cited by 25
Ni, R. (2021) · Pharmaceuticals · doi:10.3390/ph14111179 · Cited by 18
Babiloni, C. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220582 · Cited by 21
“In this line of reasoning, it was 64 proposed that the diagnosis of AD should be based 65 not only on brain amyloidosis and tauopathy but also 66 on the presence of progressing clinical phenotypic 67 manifestations compatible with AD [3].”
BackgroundInfluentialTogher, Z., Dolphin, H., Russell, C., Ryan, M., Kennelly, S., & O’Dowd, S. (2022) · International Journal of Geriatric Psychiatry · doi:10.1002/gps.5789 · Cited by 21
“Whilst previously considered a clinical diagnosis, in the last number of years, development and increasing availability of in‐vivo AD biomarkers has led to it being considered more a clinico‐biological diagnosis, based on both biomarkers and clinical phenotype.(3)”
BackgroundAstrocyte Signature in Alzheimer’s Disease Continuum through a Multi-PET Tracer Imaging Perspective
Fontana, I. C., Scarpa, M., Malarte, M., Rocha, F. M., Ausellé‐Bosch, S., Blūma, M., Bucci, M., Chiotis, K., Kumar, A., & Nordberg, A. K. (2023) · Cells · doi:10.3390/cells12111469 · Cited by 22
Self-citationCerebrospinal fluid microRNAs as potential biomarkers in Alzheimer’s disease
Eddin, A. N., Hamsho, K., Adi, G., Al-Rimawi, M., Alfuwais, M., Rab, S. A., AlKattan, K. M., & Yaqinuddin, A. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1210191 · Cited by 26
“The current modalities used to diagnose AD fall into three categories: clinical neuropsychological criteria, radiological imaging, and biochemical tests (Dubois et al., 2021).”
MethodHendriksen, H. M. A., van Gils, A. M., van Harten, A. C., Hartmann, T., Mangialasche, F., Kamondi, A., Kivipelto, M., Rhodius‐Meester, H. F. M., Smets, E. M. A., van der Flier, W. M., et al. (2023) · Alzheimer s Research & Therapy · doi:10.1186/s13195-023-01276-9 · Cited by 21
“AD has shifted from a disease that could only be clinically described and/or diagnosed post-mortem, to a disease in which neuropathological changes can be identified antemortem [30, 31].”
BackgroundLerch, O., Ferreira, D., Stomrud, E., van Westen, D., Tideman, P., Palmqvist, S., Mattsson, N., Hort, J., Hansson, O., & Westman, E. (2024) · Alzheimer s Research & Therapy · doi:10.1186/s13195-024-01517-5 · Cited by 24
“…current clinical diagnostic algorithm doesn’t recommend routine evaluation of pathophysiological biomarkers in cognitively unimpaired individuals [10], for research purposes, the framework separately evaluating individual biomarkers regardless of clinical syndrome, the “ATN framework”, has been…”
BackgroundAgah, E., Mojtabavi, H., Behkar, A., Heidari, A., Ajdari, A., Shaka, Z., Mousavi, S. V., Firoozeh, N., Tafakhori, A., & Rezaei, N. (2024) · Journal of Translational Medicine · doi:10.1186/s12967-024-05767-7 · Cited by 28
“Total tau (t-tau) and p-tau, along with amyloid beta peptide 42 (Abeta-42) are well-known biomarkers for Alzheimer’s disease (AD) [17].”
BackgroundMitochondrial pathway polygenic risk scores are associated with Alzheimer's Disease
Paliwal, D., McInerney, T. W., Pa, J., Swerdlow, R. H., Easteal, S., Andrews, S. J., & Initiative, F. T. A. D. N. (2020) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2021.08.005 · Cited by 21
Villain, N., Planche, V., & Lévy, R. (2022) · Revue Neurologique · doi:10.1016/j.neurol.2022.08.002 · Cited by 24
Self-citation
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
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