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.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Verification
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)
hedgedstates an association- 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.
- 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.
- 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.
- 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.
- 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.
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.
- 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.
- 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.
- 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.
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.
- 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.
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.
- 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.
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.
- 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.
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.
- 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.
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.
- 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.
- 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)
plainstates an association- 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.
- 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.
- 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.
- 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.
- 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
“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.
- 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
“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.
- 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.
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.
- 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.
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.
- 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.
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.
- 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.
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.
- 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.
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.
- 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.
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.
- 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.
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.
- 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.
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.
- 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
“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.
- 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.
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.
- 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
“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.
- 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.
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.
- 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.
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.
- 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.
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.
- 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.
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.
- 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
“In clinical practice, such an extension to earlier thresholds in amyloid or tau biomarkers might lengthen the duration of the asymptomatic stages and decrease the lifetime probability of clinical progression.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Biomarker thresholds
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Overall, evidence for the use of biomarkers in clinical practice remains highly disputed and suffers from a dearth of evidence-based data to recommend biomarker assessments for cognitively unimpaired individuals.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Limitations of a purely biological definition of Alzheimer’s disease > Generalisability and accessibility in clinical practice
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although the definition of Alzheimer’s disease based exclusively on biological markers has gained substantial traction in research settings, emerging studies suggest that the biomarker definition is not ready for application in clinical settings and for diagnosis of individuals without cognitive impairment.”
§ Clinical diagnosis of Alzheimer’s disease: recommendations of the International Working Group > Conclusion
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
A specific clinical phenotype of Alzheimer’s disease can be reliably identified in clinical practice.
“It requires the presence of both a specific clinical phenotype of Alzheimer’s disease (phenotype positive) and biomarker evidence of Alzheimer’s disease pathology (amyloid-positive and tau positive).”
The paper relies on this without support.
Biomarkers are currently unavailable for the pathological changes that underlie the non-Alzheimer’s neurodegenerative diseases often found in people with dementia.
“Unfortunately, biomarkers are currently unavailable for the pathological changes that underlie the non-Alzheimer’s neurodegenerative diseases often found in people with dementia, and disentangling Alzheimer’s disease from other neurodegenerative diseases continues to depend on phenotype or postmortem examination.”
The paper relies on this without support.
In some complex cases, only post-mortem evaluation will provide definitive information about whether Alzheimer's disease is the primary pathology or a copathology.
“In some complex cases, only post-mortem evaluation will provide definitive information.”
The paper relies on this without support.
Biomarker investigations can be limited by the availability, cost, and health-care payment coverage of biomarkers across countries, centres, and clinical situations.
“Biomarker investigations can also be limited by the availability, cost, and health-care payment coverage of biomarkers across countries, centres, and clinical situations.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Disease onset can occur at < 65 (familial early-onset) or > 65 years of age (sporadic late-onset), with the latter afflicting more than 95% of patients [87, 213]”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [87]
Experimental — accuracy not yet measuredIn the citing paper
“In 2021, new recommendations for the clinical diagnosis of AD were proposed by the International working group, highlighting that the diagnosis of AD should be restricted to people who have positive biomarkers together with specific AD phenotypes. Cognitively unimpaired individuals who are only positive to biomarkers should be considered at-risk for progression to AD [10].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [10]
Citations
Cites
McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D., & Stadlan, E. M. (1984) · Neurology · doi:10.1212/wnl.34.7.939 · Cited by 27,915
McKhann, G. M., Knopman, D. S., Chertkow, H., Hyman, B. T., Jack, C. R., Kawas, C. H., Klunk, W. E., Koroshetz, W. J., Manly, J. J., Mayeux, R., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.005 · Cited by 18,657
NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease
Jack, C. R., Bennett, D. A., Blennow, K., Carrillo, M. C., Dunn, B., Haeberlein, S. B., Holtzman, D. M., Jagust, W., Jessen, F., Karlawish, J., et al. (2018) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2018.02.018 · Cited by 10,537
Self-citationAmyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D. (2013) · Neurodegenerative Diseases · doi:10.1159/000337230 · Cited by 10,359
Albert, M. S., DeKosky, S. T., Dickson, D., Dubois, B., Feldman, H. H., Fox, N. C., Gamst, A., Holtzman, D. M., Jagust, W. J., Petersen, R. C., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.008 · Cited by 10,152
Self-citationEuropean Guidelines on cardiovascular disease prevention in clinical practice (version 2012)
Authors/Task Force Members:, Perk, J., De Backer, G., Gohlke, H., Graham, I., Reiner, Ž., Verschuren, M., Albus, C., Benlian, P., Boysen, G., et al. (2012) · European Heart Journal · doi:10.1093/eurheartj/ehs092 · Cited by 8,490
Alzheimer's disease: the amyloid cascade hypothesis
Hardy, J. A., & Higgins, G. A. (1992) · Science · doi:10.1126/science.1566067 · Cited by 7,484
Sperling, R. A., Aisen, P. S., Beckett, L. A., Bennett, D. A., Craft, S., Fagan, A. M., Iwatsubo, T., Jack, C. R., Kaye, J., Montine, T. J., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.003 · Cited by 7,155
Self-citationClassification of primary progressive aphasia and its variants
Gorno-Tempini, M. L., Hillis, A. E., Weintraub, S., Kertesz, A., Mendez, M., Cappa, S. F., Ogar, J. M., Rohrer, J. D., Black, S., Boeve, B. F., et al. (2011) · Neurology · doi:10.1212/wnl.0b013e31821103e6 · Cited by 5,141 · cited 1×
“phenotypes) are: the amnestic syndrome of the hippocampal type 66 (typical), the posterior cortical atrophy variant 67 , and the logopenic variant primary progressive aphasia 68,69 (Supplementary Figure 1).”
BackgroundSelf-citationDiagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB Consortium
McKeith, I. G., Boeve, B. F., Dickson, D. W., Halliday, G., Taylor, J.-P., Weintraub, D., Aarsland, D., Galvin, J., Attems, J., Ballard, C. G., et al. (2017) · Neurology · doi:10.1212/wnl.0000000000004058 · Cited by 4,476
Self-citation
Cited by
Sorted by citations
Items 901–1,000 of 1,002
Alzheimer’s Disease: Engaging with an Unstable Category
Daly, T. P., & Keuck, L. (2025) · Springer eBooks · doi:10.1007/978-94-024-2252-8_113
Ikanga, J. N., Patel, S. S., Schwinne, M., Obenauf, C., Epenge, E., Gikelekele, G., Tshengele, N., Kavugho, I., Mampunza, S. M. M., Mananga, L., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70735
“2,3 APOE ε 4 also enhances neuroinflammatory responses, alters lipid metabolism, 4–6 and is associated with faster cognitive decline.”
MADF-Net: A Multi-Branch Adaptive Deep Fusion Network for Alzheimer's Disease Prediction
Wang, N., Tian, P., Wu, M.-J., & Zhou, H. (2025) · IEEE Signal Processing Letters · doi:10.1109/lsp.2025.3621339
“Faced with such a severe disease challenge, although there is currently no effective cure for AD, the medical community generally believes that early diagnosis and intervention are key to slowing disease progression and improving patients’ quality of life [5], [6], [7].”
Apolipoprotein E gene allele 4 and amyloid-beta mediate tau-related network breakdown
Nabizadeh, F. (2025) · Brain Communications · doi:10.1093/braincomms/fcaf404
“1,2 As the disease worsens, tau aggregates eventually affect the majority of the cortical regions, extending to the temporal and parietal cortices.”
Language in Alzheimer’s disease
Pistono, A., Tran, T. M., & Lefèbvre, L. (2025) · Oxford University Press eBooks · doi:10.1093/oxfordhb/9780198888482.013.0012
P-TAU205 IS A BIOMARKER LINKED TO TAU-PET ABNORMALITY: A CROSS-SECTIONAL AND LONGITUDINAL STUDYPreprint
Lantero‐Rodriguez, J., Janelidze, S., Palmqvist, S., Braun-Wohlfahrt, L. S., Vávra, J., Bali, D., Dolado, A. O., Mattsson, N., Stomrud, E., Zetterberg, H., et al. (2025) · medRxiv · doi:10.1101/2025.10.21.25338437
Self-citationKammar‐García, A., Peña-González, P., Sigg-Alonso, J., et al. (2025) · Geriatrics · doi:10.3390/geriatrics10060141
Mahdavi, S. A., Maghooli, K., & Farokhi, F. (2025) · Journal of Medical Signals & Sensors · doi:10.4103/jmss.jmss_3_25 · Cited by 2
Longitudinal characteristics of plasma biomarkers in Chinese older adults with Alzheimer’s disease
Li, R., Liu, L., Yang, J., Chai, W., Zhang, M., Wei, M., Wei, Y., Wang, X., Zhang, S., Wang, J., et al. (2025) · Alzheimer s Research & Therapy · doi:10.1186/s13195-025-01882-9 · Cited by 1
Semenkova, A., Piguet, O., Johnen, A., Schroeter, M. L., Godulla, J., Linnemann, C., Baumgartner, M., Otto, M., Felbecker, A., Wezel, S., et al. (2025) · European Journal of Neurology · doi:10.1111/ene.70424
“%) of the 120 ADD patients fulfilled the 2021 International Working Group recommendations for AD [18].”
Shin, J., Brady, E. S., Chen, C., Lauderdale, K., Agrawal, A., Zhang, Y., Jiang, X., Nambiar, P., Herbert, J., Mallen, D. D., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.11.11.687887
“AD develops over decades before any cognitive symptoms with progressive Aβ accumulation as the strongest pathological risk factor 6-12 , and APOE4-driven hippocampal hyperactivity 18-21 as the strongest functional risk factor predisposing individuals to subsequent Aβ accumulation 55 and memory…”
InfluentialSoleimani‐Meigooni, D. N., & Rabinovici, G. D. (2025) · Cambridge University Press eBooks · doi:10.1017/9781108985055.006
Self-citationMild Cognitive Impairment across the Dementias
Petersen, R. C. (2025) · Cambridge University Press eBooks · doi:10.1017/9781108985055.014
AIE Probes for Neurological Sensing
Ahmad, H., Farhan, A., Chen, X., Yu, C., Yan, Y., Mazhar, M., Muhammad, S., & Guo, B. (2025) · Royal Society of Chemistry eBooks · doi:10.1039/9781837676453-00072
The Potential of Exhaled Breath Analysis for Alzheimer’s Disease Monitoring (mini review)
Patsiris, S., Exarchos, T., & Vlamos, P. (2025) · Advances in experimental medicine and biology · doi:10.1007/978-3-032-03398-7_15
Screening and In Vivo Validation of Key Genes Involved in Myelin Damage in Alzheimer’s Disease
Li, H.-T., Zhang, J.-W., Li, B.-W., Wu, H., Ge, J., Wu, D., Zhao, Q., & Wang, Y. (2025) · Molecular Neurobiology · doi:10.1007/s12035-025-05427-x
“Alzheimer’s disease (AD), the most common type of dementia, shows typical clinical features, such as amnestic memory impairment, language degradation, and visuospatial deficits [1].”
Elngar, A. A., Ibrahim, A. M., Helmy, B. E.-D., & Farid, O. (2025) · International Conference on Business Analytics for Technology and Security (ICBATS) · doi:10.1109/icbats66542.2025.11258348
“Memory impairment frequently manifests as an early indicator, with individuals commonly experiencing difficulties in recalling dates, appointments, or discussions that transpired just moments prior [15].”
Chen, C., Song, Y., Feng, S., et al. (2025) · SSRN Electronic Journal · doi:10.2139/ssrn.5901188
Exploring neuroprotective effects of Chuanzhitongluo capsule on an alzheimer’s disease rat model
Sun, Y., Shao, M., Du, L., Gan, Y., Guan, Y., Cheng, G., Li, S., Jin, H., Li, B., Zhang, G., et al. (2025) · Metabolic Brain Disease · doi:10.1007/s11011-025-01772-x · Cited by 1
“Cognitive deficits and neuron losses are hallmarks of AD (Tönnies and Trushina 2017), and multiple factors contribute to AD’s pathogenesis (Dubois et al. 2021).”
Huszár, Z., Engh, M. A., Pavlekovics, M., Sato, T., Steenkamp, Y., Hanseeuw, B. J., Terebessy, T., Molnár, Z., Hegyi, P., & Csukly, G. (2024) · Figshare · doi:10.6084/m9.figshare.26705691
Wang, X., Shi, Z., Qiu, Y., Sun, D., & Zhou, H. (2024) · Figshare · doi:10.6084/m9.figshare.26719356
Yang, Y., Chen, W., Lin, Z., Wu, Y., Li, Y., & Xia, X. (2024) · Figshare · doi:10.6084/m9.figshare.25546929
Wang, X., Li, F., Tian, J., Gao, Q., & Zhu, H. (2024) · Figshare · doi:10.6084/m9.figshare.26626129
Lu, J., Ma, X., Zhang, H., Xiao, Z., Li, M., Wu, J., Ju, Z., Chen, L., Zheng, L., Ge, J., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26600593
Gonzalez, A. S., John, A., Brotherhood, E., Camic, P. M., McKee‐Jackson, R., Melville, M., Sullivan, M. P., Tudor-Edwards, R., Windle, G., Crutch, S. J., et al. (2023) · Figshare · doi:10.6084/m9.figshare.24295614
Hou, X.-H., Suckling, J., Shen, X.-N., Liu, Y., Zuo, C.-T., Huang, Y.-Y., Li, H.-Q., Wang, H.-F., Tan, C., Cui, M., et al. (2023) · Figshare · doi:10.6084/m9.figshare.24465132
Hendriksen, H. M. A., van Gils, A. M., van Harten, A. C., et al. (2023) · Figshare · doi:10.6084/m9.figshare.23896107
Gonzalez, A. S., John, A., Brotherhood, E., Camic, P. M., McKee‐Jackson, R., Melville, M., Sullivan, M. P., Tudor-Edwards, R., Windle, G., Crutch, S. J., et al. (2024) · Figshare · doi:10.6084/m9.figshare.24295749
Hendriksen, H. M. A., van Gils, A. M., van Harten, A. C., et al. (2023) · Figshare · doi:10.6084/m9.figshare.23896104
Nihashi, T., Sakurai, K., Kato, T., Kimura, Y., Ito, K., Nakamura, A., & Terasawa, T. (2024) · Figshare · doi:10.6084/m9.figshare.25341266
Marcatori biologici delle malattie neurodegenerative
Vrillon, A., Aveneau, C., & Paquet, C. (2025) · EMC - Neurologia · doi:10.1016/s1634-7072(25)51074-7
Dobrynina, L. A., Gadzhieva, Z. S., Shamtieva, K. V., Kremneva, E. I., Volik, A. V., Akhmetshina, Y. I., Zabitova, M. R., & Kalashnikova, L. A. (2025) · Almanac of Clinical Medicine · doi:10.18786/2072-0505-2025-53-023
Neurocognitive assessment in Alzheimer's disease clinical research
Moelter, S. T. (2025) · Elsevier eBooks · doi:10.1016/b978-0-443-30008-0.00004-1
Subjective cognitive impairment as a manifestation of Alzheimer's disease or emotional disorders
Гришина, Д. А., Борисовна, Л. А., & А., М. Е. (2025) · Neurology neuropsychiatry Psychosomatics · doi:10.14412/2074-2711-2025-6-99-105
Language Domains in Alzheimer’s Disease: State of the Art and Future Directions
de Souza, G. B., & Beber, B. C. (2025) · PAJAR - Pan-American Journal of Aging Research · doi:10.15448/2357-9641.2025.1.48722
Zhou, J., Chen, W., Song, J., Yu, D., Shi, C., Luo, H., & Huang, S. (2025) · Neurological Sciences · doi:10.1007/s10072-025-08667-w
“In contrast, LOAD is primarily linked to aging and the APOE ε4 allele [ 11 ].”
Bayesian-Optimized Eye Movement Event Detection for Assisted Alzheimer’s Diagnosis
Wang, X., Nie, Y., Zhao, J., et al. (2026) · Lecture notes in electrical engineering · doi:10.1007/978-981-95-4049-5_15
Kara, F., & Kantarci, K. (2025) · Springer eBooks · doi:10.1007/978-3-031-95878-6_9
Ray, T. (2026) · The Journal for Nurse Practitioners · doi:10.1016/j.nurpra.2025.105673
Giuffrè, G. M., Battisti, F., Tudor, A. M., Lenkowicz, J., Avitabile, A., Rosati, A. M., Martellacci, N., Patarnello, S., Torelli, F., Cesario, A., et al. (2026) · Journal of Alzheimer s Disease · doi:10.1177/13872877251411461
“8,9 Moreover, the fi rst disease-modifying treatments (DMT) targeting the core pathology of AD have received regulatory approval in several countries, based on evidence demonstrating their ef fi cacy in reducing amyloid burden and slowing clinical progression.”
Proteins as Candidates for the Neurodegeneration Biomarkers
Бокша, И. С., Prokhorova, T. A., Savushkina, O. K., Терешкина, Е. Б., Vorobyeva, E. A., & Burbaeva, G. S. (2025) · Neurochemical Journal · doi:10.1134/s1819712425700631
Hüppi, R. M., Langer, N., Vieira, B. H., & Initiative, T. F. L. D. N. (2026) · medRxiv · doi:10.64898/2026.01.13.26343927
Diagnosis of Alzheimer’s Disease Using Biological Markers in Corticobasal Syndrome
Гришина, Д. А., Grinyuk, V. V., Nodel, M. R., et al. (2026) · Neuroscience and Behavioral Physiology · doi:10.1007/s11055-026-01950-z
Subjective cognition trajectories, Alzheimer biomarkers, and incident mild cognitive impairmentPreprint
Kuhn, E., Kleineidam, L., Stark, M., et al. (2026) · medRxiv · doi:10.64898/2026.01.27.26344715
Medial temporal lobe atrophy is associated with age and pathologies, especially small vessel disease
van Westen, D., Stomrud, E., Lorenzini, L., Palmqvist, S., Barkhof, F., Hansson, O., & Spotorno, N. (2026) · Scientific Reports · doi:10.1038/s41598-025-33602-6
Sánchez-Mendoza, A. V., Vázquez‐García, R. A., Castaño, V., Torres-Ramos, M., Solano, A. H. J., Camarillo-López, R. H., & Rosales‐Hernández, M. C. (2026) · ACS Omega · doi:10.1021/acsomega.5c07481
Early detection of Alzheimer’s disease: Progress, challenges, and future outlook
Albayrak, A. (2026) · Disiplinlerarası Yenilik Araştırmaları Dergisi · doi:10.56723/dyad.1737746
McNaughton, E. P., Shen, K., Wang, J., Roenningen, A. E., Wiesman, A. I., Flores-Alonso, S. I., Bhatti, P., McIntosh, A. R., & Kent, B. A. (2026) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2026.02.001
Conti, M., Teghil, A., Schettino, M., D’Antonio, F., Monti, M. S., Talarico, G., Bruno, G., Vita, A. D., Alessandri, G., Guariglia, C., et al. (2026) · Journal of Clinical and Experimental Neuropsychology · doi:10.1080/13803395.2026.2637509
“Early diagnosis has become a central point for primary interventions (Devi, 2023), and there is growing interest in preclinical stages of AD, with the purpose of defining clinical and biomarker profiles (Dubois et al., 2021; Jack et al., 2018).”
Zhu, T., Cai, L., Hu, L., Yang, D., Li, M., Quan, F., Lu, C., Liu, S., & Cui, J. (2026) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2026.1752516
“The World Alzheimer Report 2021 highlighted that MCI, which can be stable or even reversible, represents a critical window for the secondary prevention of dementia (Dubois et al., 2021).”
Ribeiro, I. C., Gonçalves, B. C., Aventurato, Í. K., da Silva, M. C. R., Rizzi, L., Rochetti, A. L. G., Fernandes, G. B. P., Cendes, F., & Balthazar, M. L. F. (2026) · Arquivos de Neuro-Psiquiatria · doi:10.1055/s-0046-1817040
A Collaborative AI Framework for Rare Event Modelling in Early Alzheimer's Detection
Roy, M., Vasudeva, S., Patnaik, A., et al. (2026) · Advances in computational intelligence and robotics book series · doi:10.4018/979-8-3373-5906-9.ch013
Dautricourt, S. (2021) · theses.fr (ABES) · doi:10.70675/63472a25z31eaz4ebczaebdzd8d2e061b4b8
Yuan, M., Gu, C., Nguyen, T. T. T., Xu, L., Chen, X., Sun, J., Zhong, L., Zheng, Y., Zhang, L., Lu, Q., et al. (2026) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2026.121644
Alzheimer’s disease : epistemology, ethics, innovation
Daly, T. P. (2021) · theses.fr (ABES) · doi:10.70675/6e99838az7dd4z402fz98fdzeca072d3ad13
Behl, C. (2026) · Springer eBooks · doi:10.1007/978-3-662-72210-7_1
Wiechmann, D., Kerz, E., Albrecht, M., Qiao, Y., Pinho, J., Reetz, K., & Costa, A. S. (2026) · Frontiers in Neurology · doi:10.3389/fneur.2026.1780783 · Cited by 1
Role of Biomarker in Treating Alzheimer's Disease
Anand, P., Kumar, D., Gupta, S., Tiwari, J., & Singh, S. N. (2026) · BENTHAM SCIENCE PUBLISHERS eBooks · doi:10.2174/9798898814953126010006
Belviranlı, M., Okudan, N., & Sezer, T. (2026) · Metabolic Brain Disease · doi:10.1007/s11011-026-01857-1
Dementias and Mild Cognitive Impairment in Adults
Boscarino, J. J., Maietta, J. E., Schoenberg, M. R., & Duff, K. M. (2026) · Springer eBooks · doi:10.1007/978-3-032-07777-6_15
Clinical recognition memory testing in older adults should move beyond accuracy alone
Kuruvilla, M. V. (2026) · Frontiers in Psychology · doi:10.3389/fpsyg.2026.1764573
Ugwah-Oguejiofor, C. J., Okechukwu, P. N., Mathias, S. N., Ofokansi, M. N., & Janakiraman, A. K. (2026) · Studies in natural products chemistry · doi:10.1016/b978-0-443-49144-3.00007-1
Alzheimer’s disease: Diagnostic criteria and their evolution
Vorobev, S. V., Emelin, А. Y., Yanishevskiy, S. N., & Tantasheva, A. M. (2026) · S S Korsakov Journal of Neurology and Psychiatry · doi:10.17116/jnevro202612604229
Cognitive health of Moscow residents 55 years and older: Epidemiological data
Belousov, V. V., Gureeva, Y. S., Tairova, R. T., et al. (2026) · S S Korsakov Journal of Neurology and Psychiatry · doi:10.17116/jnevro20261260425
Gebril, N. M., Elettreby, A. M., Younis, A. H., Moawad, M. H. E. D., Hafez, A. M., Elsayed, T. G., Abdelrahman, K. M., & El-Kot, S. M. (2026) · Molecular Neurobiology · doi:10.1007/s12035-026-05864-2
“The revised criteria highlight the importance of confirming pathology using established biomarkers (PET or CSF), while recognizing the growing role of plasma biomarkers in screening, risk stratification, and clinical trial recruitment [9, 59, 64, 65].”
Gut Dysbiosis in Alzheimer’s Disease: Insights from the Microbiome
Kiran, N. S., Yashaswini, C., Chatterjee, A., & Prajapati, B. G. (2026) · Springer eBooks · doi:10.1007/978-981-95-7494-0_11
WWOX in brain development and disease: Molecular mechanisms and therapeutic opportunities
Obeid, M., Wang, J., Abudiab, B., Akkawi, R., & Aqeilan, R. I. (2026) · Neurobiology of Disease · doi:10.1016/j.nbd.2026.107446 · Cited by 1
Biomarkers in preclinical and early Alzheimer’s disease in China: a scoping review
Peng, G., Yang, Y., Wang, Y., Chandekar, S. A., & Yu, J. (2026) · The Journal of Prevention of Alzheimer s Disease · doi:10.1016/j.tjpad.2026.100599 · Cited by 1
“Early diagnosis and intervention are critical to slowing disease progression, preserving cognitive function, and reducing the socioeconomic burdens associated with AD [4].”
Yang, Y., Jia, L., Xu, J., Wu, J., Huang, H., Yang, H., Qi, Z., Wang, Y., Yu, H., & Wang, S. (2026) · Cell Death Discovery · doi:10.1038/s41420-026-03159-y
“Given the trend of population aging, this prevalence is projected to triple by 2050 [4].”
Xie, Q., Tan, Z.-L., Wang, Y.-J., & Chen, H.-X. (2026) · Clinical Neurology and Neuroscience · doi:10.11648/j.cnn.20261002.11
Zhong, R., Chen, Z.-Q., Li, S.-F., & Jiang, J. (2026) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2026.121918
Diagnosis of Alzheimer’s disease in asymptomatic individuals: a historical perspective
Nitríni, R. (2026) · Dementia & Neuropsychologia · doi:10.1590/1980-5764-dn-2026-0487
Subjective cognition trajectories, Alzheimer biomarkers, and incident mild cognitive impairment
Kuhn, E., Kleineidam, L., Stark, M., Peters, O., Hellmann‐Regen, J., Preis, L., Gref, D., Priller, J., Spruth, E. J., Gemenetzi, M., et al. (2026) · The Journal of Prevention of Alzheimer s Disease · doi:10.1016/j.tjpad.2026.100609
“These findings, consistent with recent evidence from the SCIENCe cohort [17], support short-term SP-based change as a dynamic “ SCD-plus ” feature and highlight its potential value for early risk stratification in aging populations [1,8,9,51].”
Mindt, M. R., Savin, M. J., Guzman, V., Arentoft, A., Barragan, E. V., Cubbellotti, S., Heuer, H. W., Germano, K. K., Rosen, H. J., Cho, S. J., et al. (2026) · medRxiv · doi:10.64898/2026.06.01.26354636
Self-citationSubjective cognitive impairment in patients with cerebral microangiopathy
Добрынина, Л. А., Byrochkina, A. A., Витальевна, Ш. К., Geints, A. A., Гаджиева, З. Ш., Kremneva, E. I., Gnedovskaya, E. V., & Kalashnikova, L. A. (2026) · S S Korsakov Journal of Neurology and Psychiatry · doi:10.17116/jnevro202612605163
A review on thymoquinone: a promising therapeutic molecule in Alzheimer's
Kaur, S. D., SINGH, V. A., Kaurav, H., Nangare, S., & Vihal, S. (2026) · Nutritional Neuroscience · doi:10.1080/1028415x.2026.2682949
Soriano-Herrador, C., Úbeda‐Bañón, I., Villanueva‐Anguita, P., Montesinos-Vinader, J. L., Saiz‐Sánchez, D., Astillero‐Lopez, V., Alberdi-Velez, P., Fernández‐Irigoyen, J., Lachén‐Montes, M., Santamaría, E., et al. (2026) · Research Square · doi:10.21203/rs.3.rs-9823502/v1
López‐Martos, D., Suárez‐Calvet, M., Salvadó, G., Cacciaglia, R., Shekari, M., González‐Escalante, A., Horta‐Barba, A., Palma‐Gudiel, H., Milà‐Alomà, M., Brugulat‐Serrat, A., et al. (2026) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2026.06.006
Self-citationHsiao, J. K. (2026) · JAMA · doi:10.1001/jama.2026.10969
Wang, P.-J., Yang, X., Ji, L., Shi, J., Cai, X., Sun, P., Liu, H.-X., Jiang, F., & Yang, F. (2026) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2026.1858299
“(1) CFTO-LOAD group: (i) Chinese Han ethnicity, aged ≥ 65 years; (ii) first-time outpatient visit to the neurology/psychiatry clinic with no prior exposure to anti-dementia medications, cholinesterase inhibitors, N-methyl-D-aspartate receptor antagonists, or any other psychotropic drugs; (iii) diagnosis of probable AD…”
Ji, H., Wang, H., Zhao, Z., et al. (2026) · Biomedical Signal Processing and Control · doi:10.1016/j.bspc.2026.110929
Liang, J., Gao, Y., Li, Y., Yuan, M., Yan, F.-X., Qu, S., Liu, L., & Ma, X. Y. (2026) · Research Square · doi:10.21203/rs.3.rs-9862612/v1
Predicting the risk of neurodegenerative diseases based on clinical microsignals
Bondarenko, Y. D., & Kauk, O. I. (2026) · Ukrainian Neurosurgical Journal · doi:10.25305/unj.341180
“Despite significant progress in studying the molecular and neuroimaging mechanisms of neurodegeneration, clinical diagnosis is still based mainly on established syndromes, when the pathological process has already led to a substantial loss of neuronal networks [3, 4].”
Retina-derived Quantitative Biomarkers of Brain HealthPreprint
Ma, T., Yan, T., Sun, J., Wu, N., Xu, M., Zhang, R., Zeng, N., Sun, Q., Hui, Y., Wu, Y., et al. (2026) · medRxiv · doi:10.64898/2026.07.05.26357344
Defining and Measuring Cognitive Decline and Clinical Relevance
Kurz, C., NEWHOUSE, P. A., Wyman‐Chick, K. A., Galvin, J. E., Lautenschlager, N. T., & Sabbagh, M. N. (2026) · Neurology and Therapy · doi:10.1007/s40120-026-00996-y
“Overreli‑ ance on biological definitions can disconnect diagnosis from clinically meaningful outcomes, such as functional decline, patient experience, care partner burden, and real‑world impact [2].”
InfluentialSelf-citationDoganyigit, B., Schurr, T. A., Hofer, A., Schütz, S., & Defrancesco, M. (2026) · Journal of Alzheimer s Disease · doi:10.1177/13872877261468789
“3 However, clinical phenotypes, particularly in atypical variants, can sometimes overlap.”
Jiang, S., Zhang, L., Ji, X., et al. (2026) · European journal of medical research · doi:10.1186/s40001-026-04878-9
“…for epilepsy, analogous to the Aβ/tau paradigm in Alzheimer’s disease: CRYAB reflects neuroinflammatory processes, while NfL quantifies neuronal injury, mirroring how Aβ and tau enhance diagnostics by simultaneously assessing disease triggers (Aβ) and neurodegenerative sequelae (tau) [37].”
Villain, M., Beauchêne, D., Mével-Becker, M., et al. (2026) · American Journal of Speech-Language Pathology · doi:10.1044/2026_ajslp-24-00133
Self-citationThe mechanisms and management of fecal incontinence in geriatric neurological diseases
Sakakibara, R. (2026) · Clinical Autonomic Research · doi:10.1007/s10286-026-01232-1
Suffian, M., Mammone, N., Ieracitano, C., et al. (2026) · Frontiers in Neurology · doi:10.3389/fneur.2026.1851752
Scouarnec, L. L., Bouteloup, V., Daly, T. P., Planche, V., Chêne, G., Dufouil, C., for the MEMENTO Study Group, Michèle Allard, A., Amroun, S., Andrade, K. S., et al. (2026) · npj Dementia · doi:10.1038/s44400-026-00128-1
“Taken together, these fi ndings support the International WorkingGroup(IWG)approach,whichrecommendsaclinico-biological de fi nition of AD that combines biomarker evidence with clinical symptoms for risk strati fi cation and early intervention 25 .”
Self-citationCretin, B., Philippi, N., Bousiges, O., et al. (2026) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2026.1786247
“Concurrent diagnoses such as hydrocephalus, contusion, deep brain hemorrhage, large territorial or thalamic stroke sequelae were excluded (Dubois et al., 2021).”
Influential
Metadata
- Authors
- Dubois, B., Villain, N., Frisoni, G. B., Rabinovici, G. D., Sabbagh, M., Cappa, S., Bejanin, A., Bombois, S., Epelbaum, S., Teichmann, M., Habert, M.-O., Nordberg, A., Blennow, K., Galasko, D., Stern, Y., Rowe, C. C., Salloway, S., Schneider, L. S., Cummings, J. L., & Feldman, H. H.
- Affiliations
- Sorbonne Université (FR)
- University of Geneva (CH)
- University of California, San Francisco (US)
- Cleveland Clinic (US)
- Istituto Universitario di Studi Superiori di Pavia (IT)
- Universitat Autònoma de Barcelona (ES)
- Inserm (FR)
- Institut national de recherche en sciences et technologies du numérique (FR)
- Centre National de la Recherche Scientifique (FR)
- Karolinska University Hospital (SE)
- Sahlgrenska University Hospital (SE)
- University of California San Diego (US)
- Columbia University (US)
- The University of Melbourne (AU)
- Brown University (US)
- University of Southern California (US)
- Corresponding author
- Dubois, Bruno
- ORCID
- Dubois, Bruno
- Villain, Nicolas
- Frisoni, Giovanni B
- Rabinovici, Gil D
- Cappa, Stefano
- Bejanin, Alexandre
- Bombois, Stéphanie
- Epelbaum, Stéphane
- Teichmann, Marc
- Habert, Marie-Odile
- Nordberg, Agneta
- Blennow, Kaj
- Galasko, Douglas
- Stern, Yaakov
- Rowe, Christopher C
- Salloway, Stephen
- Schneider, Lon S
- Cummings, Jeffrey L
- Feldman, Howard H
- Venue
- The Lancet Neurology
- Publisher
- Elsevier BV
- Published
- 2021-06
- Volume
- 20
- Issue
- 6
- Pages
- 484-496
- ISSN
- 1474-4422 (ISSN-L)
- PMC
- PMC8339877
- OpenAlex
- W3159530258
- Semantic Scholar
- dc5f525087f24d7c6a95d667de138557d460fc7e
- Cited by
- 1,051
- References
- 119
- Citations by year
- 2026: 146 · 2025: 272 · 2024: 237 · 2023: 209 · 2022: 153 · 2021: 33
- FWCI
- 28.16
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (am, 171 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- The Lancet Neurology (acceptedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion, other-oa)
- HAL (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Oskar-Bordeaux (Universite de Bordeaux) (submittedVersion)
- Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
- Funders
- National Institutes of Health
- Merck
- Rainwater Charitable Foundation
- U.S. Department of Defense
- Novartis
- National Health and Medical Research Council
- National Institute on Aging
- Roche
- Eisai
- National Institute of General Medical Sciences
- Medtronic
- Adamas Pharmaceuticals
- Johnson and Johnson
- UCB Pharma
- Abbott Laboratories
- American College of Radiology
- Alzheimer's Drug Discovery Foundation
- ACADIA Pharmaceuticals
- Eli Lilly and Company
- Avid Radiopharmaceuticals
- Genentech
- Merz Pharmaceuticals
- Biogen
- Sorbonne Université
- Alzheimer's Association
- GE Healthcare
- National Institute of Neurological Disorders and Stroke
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Oncology › Cancer-related cognitive impairment studies
- Keywords
- Alzheimer's disease, diagnosis, biomarkers, amyloid-beta, tau pathology, NIA-AA criteria, cognitively unimpaired individuals, prodromal Alzheimer's disease, at-risk individuals, comorbidities, diagnostic recommendations
- MeSH terms
- Alzheimer Disease, Humans, Phenotype, Biomarkers, Amyloid beta-Peptides, tau Proteins, Disease Progression, Cognitive Dysfunction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
