The DOI matches its Crossref record; 56 of the 56 references it cites were found in a registry or an index; 21 of the 46 sources its claims cite were checked for support.
Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer Disease Centers, 2005–2010
Open accessAbstract
The neuropathologic examination is considered to provide the gold standard for Alzheimer disease (AD). To determine the accuracy of currently used clinical diagnostic methods, clinical and neuropathologic data from the National Alzheimer's Coordinating Center, which gathers information from the network of National Institute on Aging (NIA)-sponsored Alzheimer Disease Centers (ADCs), were collected as part of the National Alzheimer's Coordinating Center Uniform Data Set (UDS) between 2005 and 2010. A database search initially included all 1198 subjects with at least one UDS clinical assessment and who had died and been autopsied; 279 were excluded as being not demented or because critical data fields were missing. The final subject number was 919. Sensitivity and specificity were determined based on "probable" and "possible" AD levels of clinical confidence and 4 levels of neuropathologic confidence based on varying neuritic plaque densities and Braak neurofibrillary stages. Sensitivity ranged from 70.9% to 87.3%; specificity ranged from 44.3% to 70.8%. Sensitivity was generally increased with more permissive clinical criteria and specificity was increased with more restrictive criteria, whereas the opposite was true for neuropathologic criteria. When a clinical diagnosis was not confirmed by minimum levels of AD histopathology, the most frequent primary neuropathologic diagnoses were tangle-only dementia or argyrophilic grain disease, frontotemporal lobar degeneration, cerebrovascular disease, Lewy body disease and hippocampal sclerosis. When dementia was not clinically diagnosed as AD, 39% of these cases met or exceeded minimum threshold levels of AD histopathology. Neurologists of the NIA-ADCs had higher predictive accuracy when they diagnosed AD in subjects with dementia than when they diagnosed dementing diseases other than AD. The misdiagnosis rate should be considered when estimating subject numbers for AD studies, including clinical trials and epidemiologic studies.
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Claims the paper makes
25 Own result · 11 Partly supported · 10 Own interpretation · 10 No basis given · 8 No full text of the sources · 4 Sources not found · 3 Own method · 1 Supported · 1 Supported so far · 1 Not supported · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“the last diagnostic accuracy studies utilizing a complete ADC dataset were performed in 1998 and 1999 (4, 23)”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Introduction
What the sources say
- Partly supportedcites [4] sourceExperimental — accuracy not yet measured
The Subjects section describes a diagnostic study using patients from 26 Alzheimer's disease centers, and the Results report diagnostic sensitivity and specificity. The Results also say complete information was available for only 2,188 of 3,177 patients. This 1998 paper does not establish that its dataset was complete or that the last such studies were performed in 1998 and 1999. (LLM, conf=0.83)
- Not checked — no full text of the sourcecites [23] 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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Because of 25 possible combinations of CERAD neuritic plaque density and Braak neurofibrillary stage, NIA-Reagan provides instructions for classification of only 3 (32, 38).”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
What the sources say
- Partly supportedcites [32] sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) describes three NIA-Reagan likelihood categories and says off-diagonal plaque–tangle pairings are not clearly addressed. It does not support the count of 25 possible combinations: it describes four CERAD tiers and Braak stages 0–VI. The three categories also cover ranges of Braak stages, rather than just three individual combinations. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [38] 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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“These findings suggest that phenotype is not rigidly linked to etiology and may be moldable to a large extent by an individual's genetic and epigenetic background and/or total environmental exposure.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
What the sources say
- Partly supportedcites [44] sourceExperimental — accuracy not yet measured
The introductory passage following the Abstract conclusion says GRN-associated frontotemporal lobar degeneration is clinically heterogeneous even among relatives with the same mutation, and identifies nonmendelian genetic risk factors. This supports the suggestion that phenotype is not rigidly determined by the causal mutation, but the paper does not establish a large effect of epigenetic background or environmental exposure. Page numbers are unavailable in our copy. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites [45] Larner, 2009, Genotype-phenotype relationships of presenilin-1 mutations in Alzheimer's disease: An update, J Alzheimer Dis source
- Partly supportedcites [46] sourceExperimental — accuracy not yet measured
The Comment section (page unavailable) reports marked clinical heterogeneity among family members likely to share a single disease-causing mutation, supporting the point that this disease’s phenotype is not fixed by its apparent etiology. The paper does not attribute that variation to genetic or epigenetic background or environmental exposure, nor establish how extensively those factors mold phenotype. (LLM, conf=0.86)
- Partly supportedcites [47] Wszolek, 2009, Frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), Orphanet J Rare Dis sourceExperimental — accuracy not yet measured
The Abstract and Genetic counseling sections (pages not supplied) report that the FTDP-17 phenotype can vary even among people with the same mutation, supporting the point that phenotype is not rigidly determined by etiology. Unresolved questions suggests that genetic modifiers and environmental factors may influence its expression, but does not mention epigenetic background, total environmental exposure, or influence 'to a large extent.' (LLM, conf=0.86)
hedgedconditional- 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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Correlation studies between molecular genetics and neuropathology also indicate that for several autosomal dominant dementias, the presenting clinical phenotype may vary widely, from various dementia subtypes to parkinsonism to motor neuron disease-like, even among individuals with the same causative mutation (44-47).”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
What the sources say
- Partly supportedcites [44] sourceExperimental — accuracy not yet measured
The introductory passage following the Abstract conclusion (page unavailable) says GRN-associated frontotemporal lobar degeneration is clinically heterogeneous even among family members with the same mutation. The Results report dementia and parkinsonian diagnoses, but describe motor neuron disease as uncommon and concomitant, not a typical presenting phenotype. This paper addresses GRN-associated disease, so it does not by itself establish the claim across several autosomal dominant dementias. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites [45] Larner, 2009, Genotype-phenotype relationships of presenilin-1 mutations in Alzheimer's disease: An update, J Alzheimer Dis source
- Partly supportedcites [46] sourceExperimental — accuracy not yet measured
The Results (Clinical features) and Comment describe markedly different presentations—including FTD, ALS and Parkinsonism—within one family with autosomal dominant FTD/ALS. But the Genetics section identifies a shared chromosome 9p21 haplotype, not a causative mutation, and the paper does not establish this pattern across several autosomal dominant dementias. (LLM, conf=0.88)
- Partly supportedcites [47] Wszolek, 2009, Frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), Orphanet J Rare Dis sourceExperimental — accuracy not yet measured
The Abstract says FTDP-17 phenotypes vary even within families carrying the same mutation. The Clinical description (Phenotype-genotype correlations; Symptoms and signs) describes dementia-predominant and parkinsonism-predominant presentations and motor neuron dysfunction. The paper addresses FTDP-17, not several autosomal dominant dementias, and does not establish motor neuron disease-like illness as a presenting phenotype. (LLM, conf=0.85)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The new NIA criteria use the same combination of NPs and Braak stage as the minimum lesion density necessary for attributing the cause of dementia to AD (39, 40).”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
What the sources say
- Partly supportedcites [39] sourceExperimental — accuracy not yet measured
The Classification section defines moderate or frequent neuritic plaques and Braak stages III–VI as scores used by the new criteria. But it requires a third measure, Aβ plaque score, to classify AD neuropathologic change; the Reporting section says an intermediate or high overall level, rather than the stated two-measure combination alone, is an adequate explanation of dementia. Our copy provides no page numbers for these passages. (LLM, conf=0.87)
- Partly supportedcites [40] sourceExperimental — accuracy not yet measured
The Classification section says the new criteria use Braak stage and neuritic-plaque score, but also require an Aβ-plaque score as part of the ABC score. The Reporting section says intermediate or high AD neuropathologic change can adequately explain dementia; the passages do not establish moderate or frequent neuritic plaques plus Braak stage III–VI as the minimum sufficient combination. (LLM, conf=0.86)
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.
- Partly supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“When optimizing for sensitivity and specificity, the best result was 70.9% sensitivity and 70.8% specificity. This was achieved when the clinical diagnosis was defined as probable AD and the neuropathological diagnosis as moderate or frequent neuritic plaques with Braak stage III-VI.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Results > Diagnostic Classification Comparison
plaincorrelational- 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 result the paper reports from its own data — 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 median scores for neuritic plaque density and Braak stage were significantly different, with progressively lower scores moving from probable AD through possible AD and not AD groups.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Results > Subject Characteristics
plaincorrelational- 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 result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“here, we found that when non-demented controls were not included, 33% of subjects were not classifiable.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Of these, 107 cases met a minimum histopathological threshold for AD, i.e. neuritic plaque density of moderate or frequent in combination with any Braak neurofibrillary tangle stage between III and VI, inclusive, despite their negative clinical diagnoses.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Results > Analysis of Mismatched Clinical and Neuropathological Diagnoses
plainn = 107- 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 result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Neurologists of the NIA-ADCs had higher predictive accuracy when they diagnosed AD in demented subjects than when they diagnosed dementing diseases other than AD.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Abstract
plaincorrelational- 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. 27
- Probably not a substantial claim. 25
- The quote only partly states this claim. 1
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“However, one study has reported no evident selection bias between autopsied and non-autopsied subjects among an incident community-diagnosed dementia series, suggesting that dementia case composition may not be substantially different in different settings (48).”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
What the sources say
- Disputedcites [48] sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 1 partially supported, 1 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Checked by a reasoning model — may be wrong.
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether 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.
- Disputed
Every source the paper cites for this claim was checked and supports it.
In the paper
“The shortcomings of the NIA-Reagan criteria have been recognized and a revised set of criteria are currently in press (39, 40).”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
What the sources say
- Supportedcites [39] source
The Abstract identifies the NIA-Reagan criteria as the 1997 criteria and says advances in knowledge prompted an update. The “Revised Neuropathologic criteria for Alzheimer’s disease” section explains a limitation of those criteria and presents revised criteria; the Summary states that the committee’s goal was to update them. This supports the substance of the claim, though the paper does not establish the citing document’s time-specific phrase “currently in press.” (LLM, conf=0.90)
- Supportedcites [40] source
The Introduction identifies the 1997 NIA-Reagan guidelines as the criteria being updated and revised, and the Abstract describes major revisions to the previous criteria. The References list the revised neuropathologic guidelines as “in press” (reference 29). Our copy provides no page numbers for these passages. (LLM, conf=0.88)
plain- 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: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In a recent multivariate analysis, approximately two-thirds of the variation in cognitive ability of elderly subjects was accounted for by variation in CERAD neuritic plaque density and Braak stage (41).”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
What the sources say
- Partly supportedcites [41] sourceExperimental — accuracy not yet measured
The Results section (page not provided) says that more than two-thirds of MMSE-score variability in the elderly autopsy cohort was associated with Alzheimer-type pathology, specifically neurofibrillary tangles and neuritic plaques. It does not attribute that figure to CERAD neuritic plaque density and Braak stage as the two measures in the claim; the Discussion describes its findings as compatible with Braak staging. (LLM, conf=0.89)
plaincorrelational- 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: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“There is also relatively close agreement with the last 2 prior assessments of diagnostic accuracy using the total NIA-ADC dataset: Mayeux et al estimated a sensitivity of 93% and a specificity of 55% (4) and Tsuang et al reported a sensitivity of 84% and a specificity of 50% (23).”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
What the sources say
- Supportedcites [4] source
The Results report 93% sensitivity and 55% specificity for the clinical diagnosis of Alzheimer’s disease, matching the figures attributed to Mayeux et al. The Subjects section describes patients referred to 26 Alzheimer’s disease centers. The separate figures attributed to Tsuang et al. are not part of this citation’s claim. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [23] source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether 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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Due to the idiosyncratic assignment of these categories from case to case (32), we instead stratified by all relevant combinations of the deterministic histopathological scores, consisting of the CERAD-defined neuritic plaque density score (29) and the Braak neurofibrillary tangle stage (33).”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Materials and Methods > Analysis Strategy
What the sources say
- Partly supportedcites [32] sourceExperimental — accuracy not yet measured
The Results report relatively low consistency in NIA-Reagan category assignments for cases outside the guidelines, supporting the concern behind the citing authors’ choice. But they also report high consistency for cases that match the guidelines, so the source does not support describing assignments as idiosyncratic across cases generally. The decision to stratify by CERAD and Braak scores is the citing authors’ own method, not a finding attributed to this source. (LLM, conf=0.83)
plaindirect- 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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“because measures of all biomarkers studied to date have considerable overlap with those found other types of dementia (as well the cognitively normal elderly population), it remains difficult to determine whether or not cognitive impairment is due to AD or another more dominant and concurrent process.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Introduction
What the sources say
- Partly supportedcites [1] sourceExperimental — accuracy not yet measured
The section ‘Biomarker abnormalities precede clinical symptoms’ (page not provided) reports amyloid-biomarker abnormalities in 20–40% of cognitively normal elderly people, and ‘AD clinical features and pathological changes’ notes that dementia in older patients often has multiple underlying pathologies. The ‘Biomarkers of neurodegeneration’ section also says CSF tau is not specific to AD. These passages support diagnostic ambiguity, but not the broader assertion that all biomarkers studied have considerable overlap with both other dementias and cognitively normal elderly people. (LLM, conf=0.84)
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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In the revision of the 1997 criteria, combinations of plaque and tangle pathologies considered sufficient to cause dementia and qualify for the neuropathological diagnosis of AD are explicitly stated (40, 41).”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
What the sources say
- Supportedcites [40] source
The Classification section defines an ABC score combining amyloid plaques, neurofibrillary tangles, and neuritic plaques. The Reporting section states that, in individuals with cognitive impairment, intermediate or high levels are an adequate explanation for dementia and warrant a final diagnosis of Alzheimer’s disease. (LLM, conf=0.90)
- Could not verifycites [41] sourceExperimental — accuracy not yet measured
The Neuropathology section describes how the study counted plaques and tangles, but does not state what combinations qualify for an AD diagnosis or are sufficient to cause dementia. Searches for the 1997 criteria, their revision, and diagnostic thresholds found no passage addressing that claim in our copy; the other relevant matches were in the References section. (LLM, conf=0.72)
plain- 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: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“New clinical diagnostic consensus criteria have now been finalized under the auspices of the NIA and Alzheimer's Association (52), with novel features including recognition of a preclinical stage of AD and the incorporation of imaging and laboratory-based cerebrospinal fluid biomarkers.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
What the sources say
- Partly supportedcites [52] 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.
plainconditional- 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: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. 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
“Amyloid staging may be of immediate clinical diagnostic utility when used to guide amyloid imaging as the progression of amyloid plaques beyond the cortex appears to be a useful marker of higher Braak tangle stage and of the presence of dementia (49, 50).”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
What the sources say
- Not checked — no full text of the sourcecites [49] Thal, 2002, Phases of A beta-deposition in the human brain and its relevance for the development of AD, Neurology source
- Partly supportedcites [50] Beach, 2012, Striatal amyloid plaque density predicts Braak neurofibrillary stage and clinicopathological Alzheimer's disease: Implications for amyloid imaging, J Alzheimer Dis 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.
hedgedconditional- 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: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A result the paper reports from its own data — 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 most frequent primary neuropathological diagnoses in these cases were frontotemporal lobar degeneration (60 cases), followed by Lewy body disease (39 cases), Creutzfeldt-Jakob disease (20 cases) and progressive supranuclear palsy (18 cases).”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Results > Analysis of Mismatched Clinical and Neuropathological Diagnoses
plainn = 164- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether 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 result the paper reports from its own data — 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 mean age of the “not AD” group was significantly lower than that of the probable or possible AD groups (72.8, 81.2 and 83.2 years, respectively).”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Results > Subject Characteristics
plaincorrelational- 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: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Sensitivity ranged from 70.9% to 87.3%; specificity ranged from 44.3% to 70.8%.”
- Also stated in: § Diagnostic Classification Comparison · plain
“Sensitivity ranged from 70.9% to 87.3% and specificity ranged from 44.3% to 70.8%.”
- Also stated in: § Discussion · plain
“We found that sensitivity for AD diagnosis ranged from 70.9% to 87.3% whereas specificity ranged from 44.3% to 70.8%.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Abstract
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.
- Also stated in: § Diagnostic Classification Comparison · plain
A result the paper reports from its own data — 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 PPV for the clinical diagnosis of AD ranged from 46.0% to 83.3%, with the best result achieved when the clinical diagnosis was defined by probable AD and the neuropathological diagnosis as moderate or frequent neuritic plaques with Braak stage III-VI (the prevalence of subjects at or above this histopathological threshold was 67.2%).”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Results > Diagnostic Classification Comparison
plaincorrelational- 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 result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“For the set of minimum neuropathological criteria that are perhaps most commonly used to define AD (i.e. CERAD neuritic plaque density of ‘moderate” or “frequent” and Braak stage III-VI), the sensitivity and specificity of the clinical diagnosis of “probable AD” were each approximately 71%, whereas for “combined “probable” and possible AD” sensitivity was about 83% with specificity about 55%.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
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 result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Sensitivity was generally increased with more permissive clinical criteria and specificity was increased with more restrictive criteria, whereas the opposite was true for neuropathological criteria.”
- Also stated in: § Diagnostic Classification Comparison · plain
“In general, sensitivity was increased with more permissive clinical criteria and specificity was increased with more restrictive clinical criteria, whereas the opposite was true for neuropathological criteria.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Abstract
plaindirect- 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.
- Also stated in: § Diagnostic Classification Comparison · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Of the 526 subjects diagnosed as clinically probable AD, 438 were confirmed as neuropathological AD, as defined above, and 88 did not meet neuropathological criteria.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Results > Analysis of Mismatched Clinical and Neuropathological Diagnoses
plainn = 526- 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 result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A small number of cases received primary neuropathological diagnoses of progressive supranuclear palsy (3 cases), corticobasal degeneration (2 cases) and neuroaxonal dystrophy/Hallervorden-Spatz-like disease (2 cases); there were several other miscellaneous neuropathological diagnoses (1 case each) (Table 4).”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Results > Analysis of Mismatched Clinical and Neuropathological Diagnoses
plainn = 3- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether 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 result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“When a clinical diagnosis was not confirmed by minimum levels of AD histopathology, the most frequent primary neuropathological diagnoses were tangle-only dementia or argyrophilic grain disease, frontotemporal lobar degeneration, cerebrovascular”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Abstract
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.
The quote only partly states this claim.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Many cases had contributing neuropathological diagnoses in addition to their primary diagnosis; the most frequent contributing diagnoses were similar to the most frequent primary diagnoses.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Results > Analysis of Mismatched Clinical and Neuropathological Diagnoses
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether 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 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
“While not formally analyzed here, we did note a high rate of multiple neuropathological diagnoses in demented subjects whereas clinicians rarely assign more than one diagnosis.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether 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.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The excluded subjects significantly differed from the 919 included subjects in terms of age, gender distribution and AD-related histopathological scores, but not in the mean interval last clinical assessment and death.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Results > Subject Characteristics
plainn = 919- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether 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 claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“there have been several changes in neuropathological diagnostic criteria, including the “Khachaturian criteria” of 1985 (27), the “Tierney” criteria of 1988 (28), The Consortium to Establish a Registry for Alzheimer's Disease (CERAD) criteria in 1991 (29), and the National Institute on Aging (NIA)-Reagan criteria in 1997 (30).”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Introduction
What the sources say
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.
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
“The neuropathological examination is considered to provide the gold standard for Alzheimer disease (AD).”
- Also stated in: § Introduction · boosted
“it is generally accepted that histological examination is the best indicator of AD diagnosis.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Abstract
boosted- 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.
- Also stated in: § Introduction · boosted
In the paper
“For the neuropathological diagnosis of AD, the NIA-Reagan criteria (30) are the most current guidelines”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Materials and Methods > Analysis Strategy
What the sources say
- Not checked — no full text of the sourcecites [30] source
plain- 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: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
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
“In most studies, sensitivity is relatively high while specificity is low and many studies have reported only sensitivity or positive predictive value, which has led to a false impression that the clinical diagnosis of AD is extremely accurate.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
plaindirect- 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: fails — The paper may give no reason why it holds.
Probably not a substantial claim. 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
“For example, with an estimated response rate to a trial medication of 50%, a 20% misdiagnosis rate would lower the actual response rate to 40% (if non-AD dementia subjects do not respond to the medication), which would require an approximate doubling of subject recruitment to maintain statistical power.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
hedgeddirect- 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 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
“While the clinical diagnosis of AD often is validated by neuropathological examination, a clinical diagnosis of a non-AD dementia is often not verified by neuropathology.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
plain- 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
“it is important, for current research and clinical usage, to obtain more appropriate figures.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Introduction
plain- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check 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 be too vague to check against evidence.
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
“Because many studies have reported only sensitivity or positive predictive value, a general impression has arisen that the clinical diagnosis of AD is extremely accurate.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Introduction
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check 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 be too vague to check against evidence.
In the paper
“The data analyzed in this study have been collected as part of the NACC Uniform Data Set (UDS) since 2005 (31) and thus represent the most current research practices.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Introduction
What the sources say
- Not checked — no full text of the sourcecites [31] 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.
It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The 3 groups did not significantly differ in the mean interval between last clinical assessment and death.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Results > Subject Characteristics
plain- 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: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Sensitivity estimates have ranged between 41% and 100% (median of 87%), while specificity has ranged between 37% and 100% (median of 58%).”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Introduction
What the sources say
- Not matchedcites 2-25
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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.
- Not matched
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
“Thus, a large fraction of subjects are not classifiable by NIA-Reagan criteria and the neuropathologist is left to make an arbitrary assignment.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
plaindirect- 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.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The gender distribution was generally skewed towards more males but did not significantly differ among groups.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Results > Subject Characteristics
plain- 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: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. 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
“These, however, do not give entirely specific guidelines for making the diagnosis, but rather set probability levels, given threshold levels of histopathological severity (CERAD neuritic plaque density and Braak neurofibrillary stage) for when dementia may be due to AD.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
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.
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
“However, even a modest level of diagnostic misclassification could have a significant effect on clinical trial calculations for minimum subject number and thus should be considered in clinical trial planning.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
hedgedconditional- 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
“In a recent examination of NACC data, Nelson et al estimated that 18% of subjects with dementia fell outside of the NIA-Reagan guidelines (34);”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
What the sources say
- Not checked — no full text of the sourcecites [34] source
hedged- 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: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
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
“It is likely that, just as some subjects with 90% coronary artery stenosis suffer myocardial infarctions and some do not, individual subjects will vary in their ability to withstand a given lesion density (perhaps due to “cognitive reserve”), differences in genetic background or differences in environmental exposures.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check 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 be too vague to check against evidence. 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
“For selecting subjects for clinical trials, the relatively high sensitivity is somewhat reassuring because it means that a relatively small percentage of non-AD subjects will be included in clinical trials.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
hedgeddirect- 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: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no 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
“Because ADCs are tertiary referral centers, diagnostic accuracy rates may differ from those that may be achieved in secondary or primary care settings.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
hedgedconditional- 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: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Rests on an assumption: Patients with a more complex clinical syndrome are more likely to be referred to a tertiary care center.
- Rests on an assumption: The greater level of neurological expertise at tertiary care centers contributes to more accurate diagnoses.
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
“Thus there are “low,” “intermediate” and “high” probability designations for classifying autopsy subjects although definitive recommendations on which of these 3 levels should be attained to justify the conclusion that dementia is due primarily to AD have not been defined.”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
plain- 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: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Although neuropathological consensus criteria for AD have changed several times over the last 3 decades, the clinical criteria have remained virtually unchanged since the NINCDS-ADRDA-sponsored criteria published in 1984 (6).”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
What the sources say
- Not checked — no full text of the sourcecites [6] McKeel, 2004, Neuropathologic criteria for diagnosing Alzheimer disease in persons with pure dementia of Alzheimer type, J Neuropathol Exp Neurol source
plain- 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: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“AD has generally been attributed to be the neuropathological cause in between 65% and 75% of dementia cases (42, 43).”
§ Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer's Disease Centers, 2005–2010 > Discussion
What the sources say
plaindirect- 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: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
Biopsy has long been contraindicated for AD due to a high risk/benefit ratio.
“For many disorders this is possible during life through biopsy but biopsy has long been contraindicated for AD due to a high risk/benefit ratio.”
The paper relies on this without support.
The consensus of expert opinion has required that the clinically documented presence of dementia be part of the definition of AD.
“Indeed, until the present time the consensus of expert opinion has required that the clinically documented presence of dementia be part of the definition of AD.”
The paper relies on this without support.
It has been the common practice for both clinical and neuropathological diagnostic definitions of AD to require the presence of dementia.
“Subjects without dementia were excluded because it has been the common practice for both clinical and neuropathological diagnostic definitions of AD to require the presence of dementia.”
The paper relies on this without support.
Non-demented subjects are not generally classified as AD.
“Therefore, non-demented subjects are not generally classified as AD.”
The paper relies on this without support.
The available body of knowledge does not allow neuropathologists to be dogmatic about exactly how much plaque and tangle pathology is necessary to cause dementia.
“We feel that our approach here has been cautious as the available body of knowledge does not allow neuropathologists to be dogmatic about exactly how much plaque and tangle pathology is necessary to cause dementia.”
The paper relies on this without support.
The clinical methods for diagnosing AD have not changed substantially since the introduction of NINDS-ADRDA criteria in 1984.
“whereas the clinical methods for diagnosing AD have not changed substantially since the introduction of the National Institute of Neurological Disorders and Stroke-Alzheimer's Disease and Related Disorders Association (NINDS-ADRDA) criteria in 1984 (26)”
The paper relies on this without support.
A large fraction of cognitively unimpaired elderly possesses sparse neuritic plaques and/or Braak stages 0-II.
“Lowering the lesion density threshold further (e.g. allowing sparse neuritic plaques and/or Braak stages 0-II) seemed counterintuitive because a large fraction of cognitively unimpaired elderly possesses such attributes.”
The paper relies on this without support.
Patients with a more complex clinical syndrome are more likely to be referred to a tertiary care center.
“For example, patients with a more complex clinical syndrome are more likely to be referred to a tertiary care center.”
The paper relies on this without support.
The greater level of neurological expertise at tertiary care centers contributes to more accurate diagnoses.
“On the other hand, the greater level of neurological expertise at these centers would presumably contribute to more accurate diagnoses.”
The paper relies on this without support.
Large reported autopsy series are only done in tertiary care settings.
“Because large reported autopsy series are only done in tertiary care settings, it is not possible to know for certain whether such differences exist.”
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 source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“while physicians struggle with accurate and reliable diagnostics even when multimodality is present, as proven by histopathological correlation42.”
From Fusion of medical imaging and electronic health records using deep learning: a systematic review and implementation guidelines (2020) · cites this paper as [42]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“common causes of dementias outside of AD such as vascular dementia (VD), Lewy body dementia (LBD), and frontotemporal dementia (FTD) widen the differential diagnosis of neurodegenerative conditions and contribute to variability in diagnostic sensitivity and specificity12.”
From Multimodal deep learning for Alzheimer's disease dementia assessment (2022) · cites this paper as [12]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Beach et al (6) found that sensitivity ranged from 70.9% to 87.3% and specificity from 44.3% to 70.8%.”
From Concordance of Clinical Alzheimer Diagnosis and Neuropathological Features at Autopsy (2020) · cites this paper as [6]
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 · cited 3×
“For the clinical diagnosis of AD, NINDSADRDA criteria (26) were stratified by considering ‘‘probable AD’’ alone as well as ‘‘probable’’ plus ‘‘possible AD.”
MethodInfluentialNeuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123 · cited 1×
“’’ Because of the idiosyncratic assignment of these categories from case to case (32), we instead stratified all relevant combinations of the deterministic histopathologic scores, consisting of the CERAD-defined neuritic plaque density score (29) and the Braak neurofibrillary tangle stage (33).”
BackgroundSperling, 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 · cited 1×
“New clinical diagnostic consensus criteria have now been finalized under the auspices of the NIA and Alzheimer’s Association (52), with novel features including recognition of a preclinical stage of AD and the incorporation of imaging and laboratory-based cerebrospinal fluid biomarkers.”
BackgroundMirra, S. S., Heyman, A., McKeel, D., Sumi, S. M., Crain, B. J., Brownlee, L. M., Vogel, F. S., Hughes, J. P., Belle, G. V., Berg, L., et al. (1991) · Neurology · doi:10.1212/wnl.41.4.479 · Cited by 4,961 · cited 2×
“’’ Because of the idiosyncratic assignment of these categories from case to case (32), we instead stratified all relevant combinations of the deterministic histopathologic scores, consisting of the CERAD-defined neuritic plaque density score (29) and the Braak neurofibrillary tangle stage (33).”
BackgroundHypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade
Jack, C. R., Knopman, D. S., Jagust, W. J., Shaw, L. M., Aisen, P. S., Weiner, M. W., Petersen, R. C., & Trojanowski, J. Q. (2010) · The Lancet Neurology · doi:10.1016/s1474-4422(09)70299-6 · Cited by 4,806 · cited 1×
“The emergence of new biomarkers may have a major impact on clinical diagnostic practice (1); however, because measures of all biomarkers studied to date have considerable overlap with those found in other types of dementia (as well the cognitively normal elderly population), it remains difficult to determine whether c…”
BackgroundPhases of Aβ-deposition in the human brain and its relevance for the development of AD
Thal, D. R., Rüb, U., Orantes, M., & Braak, H. (2002) · Neurology · doi:10.1212/wnl.58.12.1791 · Cited by 3,490 · cited 1×
“Amyloid staging may be of immediate clinical diagnostic utility when used to guide amyloid imaging as the progression of amyloid plaques beyond the cortex appears to be a useful marker of higher Braak tangle stage and of the presence of dementia (49, 50).”
BackgroundHyman, B. T., Phelps, C. H., Beach, T. G., Bigio, E. H., Cairns, N. J., Carrillo, M. C., Dickson, D. W., Duyckaerts, C., Frosch, M. P., Masliah, E., et al. (2012) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.10.007 · Cited by 3,092
Self-citationMontine, T. J., Phelps, C. H., Beach, T. G., Bigio, E. H., Cairns, N. J., Dickson, D. W., Duyckaerts, C., Frosch, M. P., Masliah, E., Mirra, S. S., et al. (2012) · Acta Neuropathologica · doi:10.1007/s00401-011-0910-3 · Cited by 2,894 · cited 3×
“The new NIA criteria use this same combination of NPs and Braak stage as the minimum lesion density necessary for attributing the cause of dementia to AD (39, 40).”
BackgroundMethodSelf-citationDiagnosis of Alzheimer's Disease
Khachaturian, Z. S. (1985) · Archives of Neurology · doi:10.1001/archneur.1985.04060100083029 · Cited by 2,499
Practice parameter: Management of dementia (an evidence-based review) [RETIRED]
Doody, R. S., Stevens, J. E., Beck, C., Dubinsky, R., Kaye, J. A., Gwyther, L. P., Mohs, R. C., Thal, L. J., Whitehouse, P. J., DeKosky, S. T., et al. (2001) · Neurology · doi:10.1212/wnl.56.9.1154 · Cited by 1,708
Cited by
Sorted by citations
Items 501–600 of 1,108
Rosén, C., Farahmand, B. Y., Skillbäck, T. B., Nägga, K., Mattsson, N., Kilander, L., Religa, D., Wimo, A. B., Blennow, K., Winblad, B. G., et al. (2015) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2015.04.007 · Cited by 20
“8%, depending on the clinical and neuropathologic criteria used [24].”
BackgroundUsefulness of Dual-Point Amyloid PET Scans in Appropriate Use Criteria: A Multicenter Study
Segovia, F., Gómez-Río, M. M., Sánchez-Vañó, R., Górriz, J. M., Ramı́rez, J., Triviño‐Ibáñez, E. M., Pardo, C. C., Martinez-Lozano, M. D., & Sopena‐Novales, P. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180232 · Cited by 19
“…and inclusion of the results of tested procedures in the final clinical diagnosis; 2) the shortcomings of clinical assessment, even using highly restricted criteria [40, 41]; and 3) the absence of a group of healthy controls or of patients with other known diseases or in different stages of AD.”
Reho, P., Kalia, V., Jackson, G. L., Wang, F., Eiten, E., Brennan, K. J. M., Brickman, A. M., Mayeux, R. P., Miller, G. W., Vardarajan, B. N., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70050 · Cited by 22
NeuroNet-AD: A Multimodal Deep Learning Framework for Multiclass Alzheimer’s Disease Diagnosis
Rahman, S., Rahman, M. M., Bhatt, S., Sundararajan, R., & Faezipour, M. (2025) · Bioengineering · doi:10.3390/bioengineering12101107 · Cited by 24
“However, early diagnosis of AD is challenging as studies show that the misdiagnosis rates of probable AD are above 16% [12].”
Fagan, A. M. (2014) · Advances in Geriatrics · doi:10.1155/2014/302712 · Cited by 21
“This biomarker accuracy, while good, is not better than current clinical accuracies, at least in specialized dementia centers and clinics [8].”
BackgroundSoria-Lopez, J. A., Huisa, B. N., Edland, S. D., Litvan, I., Peavy, G. M., Salmon, D. P., Hansen, L. A., Galasko, D. R., Brewer, J. B., González, H. M., et al. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180789 · Cited by 19
“Specificity of the clinical diagnosis of AD, however, was lower than reported for English-speaking Whites [1–3 , 5 ].”
Magnin, É. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-201207 · Cited by 22
Salivary Proteomics Reveals Significant Changes in Relation to Alzheimer’s Disease and Aging
Contini, C., Serrao, S., Manconi, B., Olianas, A., Iavarone, F., Bizzarro, A., Masullo, C., Castagnola, M., Messana, I., Diaz, G., et al. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220246 · Cited by 19
“The 79.8% accuracy in the classification of elderly subjects with and without AD was relatively higher than that reported for clinical diagnostic methods [73], but lower than that obtained using ultrasensitive assays of biomarkers, namely A (cid”
InfluentialSarto, J., Esteller, D., Guillén, N., Falgàs, N., Borrego‐Écija, S., Massons, M., Fernández‐Villullas, G., González, Y., Tort‐Merino, A., Bosch, B., et al. (2025) · Journal of Neurology · doi:10.1007/s00415-025-12897-5 · Cited by 23
“To increase diagnostic certainty, current diagnostic criteria for AD include the use of specific biomarkers (biochemical in cerebrospinal fluid [CSF] and amyloid and tau positron emission tomography [PET]) [4–7].”
The Relationship between Amyloid Deposition, Neurodegeneration, and Cognitive Decline in Dementia
Vandenberghe, R. R. (2014) · Current Neurology and Neuroscience Reports · doi:10.1007/s11910-014-0498-9 · Cited by 21
“Until a few years ago clinicians may have been relatively confident about the positive predictive value of their clinical diagnoses of amnestic MCI or clinically probable AD for the presence of neuritic amyloid plaque, nevertheless 10-40% of such cases actually do not have increased amyloid burden [8, 9, 11, 10, 12].”
BackgroundUtility of CSF biomarkers in psychiatric disorders: a national multicentre prospective study
Paquet, C., Magnin, É., Wallon, D., Troussière, A., Dumurgier, J., Jager, A., Bellivier, F., Bouaziz-Amar, É., Blanc, F., Beaufils, É., et al. (2016) · Alzheimer s Research & Therapy · doi:10.1186/s13195-016-0192-z · Cited by 19
“logical studies [10, 11], positron emission tomography (PET) amyloid imaging [9, 12] and cerebrospinal fluid”
BackgroundDelvaux, E., Mastroeni, D., Nolz, J., Chow, N., Sabbagh, M. N., Caselli, R. J., Reiman, E. M., Marshall, F. J., & Coleman, P. D. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.05.012 · Cited by 19
“When the disease is already clinically diagnosed, comparison of clinical and neuropathologic diagnosis of AD showed specificity ranging from 44% to 70% with sensitivity ranging between 71% and 87% (Beach et al., 2012).”
BackgroundÁlvarez, I., Aguilar, M., González, J. M., Ysamat, M., Lorenzo‐Bosquet, C., Alonso, Á., Tartari, J. P., Romero, S. P. Z., Díez-Fairén, M., Cárcel, M., et al. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-170753 · Cited by 19
“Ourdiagnosisaccuracy wassimilartothatfoundinpreviousstudies[26].”
Positron emission tomography–guided magnetic resonance spectroscopy in Alzheimer disease
Sheikh‐Bahaei, N., Sajjadi, S. A., Manavaki, R., McLean, M. A., O'Brien, J. T., & Gillard, J. H. (2018) · Annals of Neurology · doi:10.1002/ana.25202 · Cited by 20
“Moreover, we found mI/Cr increases in MCI compared to HC, with no significant difference between MCI and AD.”
BackgroundInfluentialAlzheimer’s disease is getting easier to spot
Dolgin, E. (2018) · Nature · doi:10.1038/d41586-018-05721-w · Cited by 19
Lao, P. J., Brickman, A. M., & Initiative, A. D. N. (2018) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1016/j.dadm.2018.08.007 · Cited by 18
“AD, with sensitivity and specificity ranging between 71%–87% and 44%–71%, respectively [8,9].”
Luzi, F., Savickas, V., Taddei, C., Hader, S., Singh, N., Gee, A. D., & Bongarzone, S. (2020) · Future Medicinal Chemistry · doi:10.4155/fmc-2019-0329 · Cited by 17
Associations of APOE e2 genotype with cerebrovascular pathology: a postmortem study of 1275 brains
Goldberg, T. E., Huey, E. D., & Devanand, D. P. (2021) · Journal of Neurology, Neurosurgery & Psychiatry · doi:10.1136/jnnp-2020-323746 · Cited by 19
Setbacks in Alzheimer research demand new strategies, not surrender
Jobke, B., McBride, T. C., Nevin, L. M., Peiperl, L., Ross, A. J., Stone, C., Turner, R. C., & Editors, A. T. P. M. (2018) · PLoS Medicine · doi:10.1371/journal.pmed.1002518 · Cited by 20
Lombardi, G., Pancani, S., Manca, R., Mitolo, M., Baiardi, S., Massa, F., Coppola, L., Franzese, M., Nicolai, E., Guerini, F. R., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252312916 · Cited by 21
Vasileva-Metodiev, S. Z., Spargo, D. J., Klein, E., Quevenco, F., Cotton, S. E., Sánchez‐Juan, P., Niimi, Y., & Fowler, N. R. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251322978 · Cited by 20
“…due to the subtlety of early cognitive symptoms that may not be detected by clinical assessment, as well as the overlap in clinical presentation with other comorbidities that may cause cognitive and functional decline 16 – 21 ; both under-diagnosis and incorrect diagnoses have been reported.”
Nanomedicine against Alzheimer’s and Parkinson’s Disease
Tandon, A., Singh, S. J., & Chaturvedi, R. K. (2020) · Current Pharmaceutical Design · doi:10.2174/1381612826666201021140904 · Cited by 20
Qu, C., Zou, Y., Ma, Y., Chen, Q., Luo, J., Fan, H., Jia, Z., Gong, Q., & Chen, T. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.841696 · Cited by 19
Zhang, Y., Shen, S., Li, X., Wang, S., Xiao, Z., Cheng, J., & Li, R. (2023) · Neuroscience Letters · doi:10.1016/j.neulet.2023.137609 · Cited by 19
Aye, S., Handels, R. L. H., Winblad, B. G., & Jönsson, L. (2024) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2024.67 · Cited by 19
“Moreover, pathologic confirmation is not mandatory in routine care (11), with diagnosis of AD often relying on clinical criteria, leading to misdiagnosis of pathology rates of up to 25–30% (12).”
The Language of Dementia Science and the Science of Dementia Language
Wray, A. (2016) · Journal of Language and Social Psychology · doi:10.1177/0261927x16663591 · Cited by 20
Ritter, A. R., Cummings, J. L., Nance, C., & Miller, J. B. (2018) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1016/j.trci.2018.06.006 · Cited by 19
“For example, applied to a trial with a 50% response rate, a 20% misdiagnosis rate would effectively reduce the response rate by 10% [13].”
BackgroundMethodFarrar, G., Molinuevo, J. L., & Zanette, M. (2019) · European Journal of Nuclear Medicine and Molecular Imaging · doi:10.1007/s00259-019-04282-y · Cited by 17
Gregson, J., Qizilbash, N., Iwagami, M., Douglas, I., Johnson, M., Pearce, N. E., & Pocock, S. (2019) · European Journal of Neurology · doi:10.1111/ene.14030 · Cited by 18
“Non-specific read codes for dementia were grouped with AD, and the clinical diagnosis of AD is prone to error even when diagnosed by specialists [20].”
BackgroundLack of association between acute stroke, post-stroke dementia, race, and β-amyloid status
Koenig, L. N., McCue, L. M., Grant, E., Massoumzadeh, P., Roe, C. M., Xiong, C., Moulder, K. L., Wang, L. Y., Zazulia, A. R., Kelly, P., et al. (2021) · NeuroImage Clinical · doi:10.1016/j.nicl.2020.102553 · Cited by 18
ICD-11: Neurokognitive Störungen
Jessen, F., & Frölich, L. (2018) · Fortschritte der Neurologie · Psychiatrie · doi:10.1055/s-0044-101607 · Cited by 21
Amyloid PET predicts longitudinal functional and cognitive trajectories in a heterogeneous cohort
Younes, K., Johns, E., Young, C. B., Kennedy, G., Mukherjee, S., Vossler, H. A., Winer, J. R., Cody, K. A., Henderson, V. W., Poston, K. L., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70075 · Cited by 18
“6 In addition, AD pathologies often co-exist alongside other neurodegenerative disorders, and these may influence rates of progression.”
Self-citationCerami, C., Boccardi, M., Meli, C., Panzavolta, A., Funghi, G., Festari, C., Cappa, S. F., Chatzikostopoulos, T., Chicherio, C., Clarens, M. F., et al. (2025) · Journal of Neuropsychology · doi:10.1111/jnp.12431 · Cited by 18
“Clinical neuropsychological examination alone has shown little accuracy to identify the underlying pathology responsible for NCDs (Beach et al., 2012; Bertoux et al., 2020), while biomarkers can exclude or confirm an aetiology (Dubois et al., 2021; Frisoni et al., 2024).”
Fluid biomarkers for neurodegenerative diseases: a comprehensive update
Valletta, M., Briel, N., Yuksekel, I., Barboure, M. C., Coward, A. R., Houwer, J. F. H. D., Fawad, A., González-Mayoral, A., Iaccarino, G., Martínez‐Dubarbie, F., et al. (2025) · Alzheimer s Research & Therapy · doi:10.1186/s13195-025-01919-z · Cited by 25
“Indeed, a substantial portion of clinically diagnosed cases of AD and other neurodegenerative diseases are not confirmed at autopsy [137].”
Giau, V. V., Senanarong, V., Bagyinszky, E., Limwongse, C., An, S. S. A., & Kim, S. (2018) · Neuropsychiatric Disease and Treatment · doi:10.2147/ndt.s180174 · Cited by 18
“No additional causative gene(s) were reported for AD except the above three genes, but additional possible risk factor genes were also discovered, such as ABCA7, SORL1, or CLU.(7,8) In addition, the overlapping clinical and neuropathologic features correspondence: sangYun Kim Department of Neurology, Seoul National Un…”
BackgroundAmyloid‐β, cortical thickness, and subsequent cognitive decline in cognitively normal oldest‐old
Pelkmans, W., Legdeur, N., ten Kate, M., Barkhof, F., Yaqub, M. M., Holstege, H. H., van Berckel, B. N. M., Scheltens, P., van der Flier, W. M., Visser, P. J., et al. (2021) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.51273 · Cited by 17
“Possibly, other pathological factors, such as hippocampal sclerosis, TDP-43 pathology, ARTAG, argyrophilic grain disease (AGD), primary age-related tauopathy (PART), and cerebrovascular disease, may contribute to atrophy in these regions, which at old ages become increasingly more common.(15,16,50) Such pathologies ma…”
BackgroundRatcliff, R., Scharre, D. W., & McKoon, G. (2021) · Journal of Experimental Psychology General · doi:10.1037/xge0001133 · Cited by 17
Predictive Utility of Plasma Amyloid and Tau for Cognitive Decline in Cognitively Normal Adults
Lee, Y.-J., Lin, S., Peng, S., Lin, Y., Chen, T.-B., Wang, P.-N., & Cheng, I. H. (2023) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2023.15 · Cited by 18
“A discrepancy exists between pathological and clinical diagnoses of AD; autopsy reveals no brain neuropathological change characteristic of AD in about 10–30% of patients clinically diagnosed with the disease in dementia centers (5).”
BackgroundAssessing preparedness for Alzheimer disease‐modifying therapies in Australasian health care systems
Brodtmann, A. G., Darby, D., Oboudiyat, C., Mahoney, C., Heron, C. J. L., Panegyres, P. K., & Brew, B. J. (2023) · The Medical Journal of Australia · doi:10.5694/mja2.51880 · Cited by 18
Talyansky, S. D., Guen, Y. L., Kasireddy, N. M., Belloy, M. E., & Greicius, M. D. (2023) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01626-6 · Cited by 21
“extensive inclusions [20, 14]. In humans, LB pathology was found to be more severe among AD–LB+ subjects who have an APOE-ε4 allele [16, 20, 51]. However, when Kaivola et al. (2022) categorized pathologically confirmed cases from the cohort in [11] by not only LB but also AD pathology status, APOE-ε4 was not associate…”
BackgroundResultInfluentialShevtsova, K. V., Rozhkov, D. O., Grishina, D., Grinyuk, V. V., Zakharov, V. V., Kashakanova, N., Koberskaya, N., Kosivtsova, O., Lokshina, A. V., Starchina, Y., et al. (2024) · Neurology, neuropsychiatry, Psychosomatics · doi:10.14412/2074-2711-2024-3-96-102 · Cited by 16
Coart, E., Barrado, L. G., Duits, F. H., Scheltens, P., van der Flier, W. M., Teunissen, C. E., van der Vies, S. M., Burzykowski, T., & Initiative, A. D. N. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-142886 · Cited by 17
“The first, ‘optimistic’ prior in accordance with [4, 28, 29], suggested a sensitivity and specificity of about 90%, with 5% probability that sensitivity and specificity were below 80%.”
Meyer, P., McSweeney, M., Gonneaud, J., & Villeneuve, S. (2019) · Progress in molecular biology and translational science · doi:10.1016/bs.pmbts.2019.05.001 · Cited by 20
“there is a mismatch between clinical and neuropathological diagnoses for up to 30% of individuals diagnosed with dementia.(92) These misdiagnoses include individuals diagnosed as having AD dementia when they have no AD pathology (false positive) and individuals incorrectly diagnosed with another dementia when they hav…”
BackgroundDay, G. S., Cruchaga, C., Wingo, T. S., Schindler, S. E., Coble, D. W., & Morris, J. C. (2019) · JAMA Network Open · doi:10.1001/jamanetworkopen.2019.13491 · Cited by 17
Peters, R. K., Breitner, J. C. S., James, S., Jicha, G. A., Meyer, P., Richards, M., Smith, A. D., Yassine, H. N., Abner, E. L., Hainsworth, A. H., et al. (2021) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1002/trc2.12202 · Cited by 19
“23 When T2DM has been examined as a risk factor for Alzheimer’s pathology, no association is observed; T2DM is associated with cerebrovascular pathology, however.”
BackgroundIacono, D., Zandi, P. P., Gross, M. D., Markesbery, W. R., Pletniková, O., Rudow, G. L., & Troncoso, J. C. (2015) · Oncotarget · doi:10.18632/oncotarget.4118 · Cited by 18
“A previous large autopsy-cohort study [77] showed that 30% of subjects diagnosed with probable AD have insufficient AD neuropathological changes at autopsy to satisfy a diagnosis of definite AD.”
Happich, M., Kirson, N. Y., Desai, U. S., et al. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-150685 · Cited by 17
“Indeed, the rate of misdiagnosis for multiple types of dementia is substantial in both clinical and research settings, even when strict diagnostic criteria are used, as shown by neuropathological and neuroimaging evaluations [3–5].”
MethodJasiecki, J., Limon-Sztencel, A., Żuk, M., Chmara, M., Cysewski, D., Limon, J., & Wasąg, B. (2019) · Scientific Reports · doi:10.1038/s41598-019-41578-3 · Cited by 17
Dementia is not synonymous with Alzheimer’s disease
Jack, C. R., Holtzman, D. M., & Sperling, R. A. (2019) · Science Translational Medicine · doi:10.1126/scitranslmed.aav0511 · Cited by 17
“In addition, in older individuals, Alzheimer’s Clinical Syndrome is most often seen in the presence of combinations of neuropathological abnormalities rather than a single disease (2).”
BackgroundInfluentialQuispialaya, K. M., Therriault, J., Aliaga, A., Benedet, A. L., Ashton, N. J., Karikari, T. K., Macedo, A. C., Rahmouni, N., Tissot, C., Arias, J. F., et al. (2024) · Neurology · doi:10.1212/wnl.0000000000210211 · Cited by 17
An AI‐first framework for multimodal data in Alzheimer's disease and related dementias
Jasodanand, V. H., Bellitti, M., & Kolachalama, V. B. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70719 · Cited by 19
“34 Withaccesstolarge, deeply phenotyped cohorts like NACC, which includes hundreds of variables ranging from neuropsychological testing to autopsy findings, MLoffersawaytointegratemultifaceteddataintoactionableoutputs.”
Vöglein, J., Kostova, I., Arzberger, T., Roeber, S., Schmitz, P., Simons, M., Ruf, V., Windl, O., Herms, J. W., Dieterich, M., et al. (2021) · European Journal of Neurology · doi:10.1111/ene.14800 · Cited by 17
Pitfalls of predicting age‐related traits by polygenic risk scores
Escott‐Price, V., & Schmidt, K. M. (2023) · Annals of Human Genetics · doi:10.1111/ahg.12520 · Cited by 15
“The determination of variant effect sizes in GWAS faces the problem that the diagnostic accuracy for Alzheimer’s disease and other dementias is generally poor (Beach et al., 2012; Escott-Price et al., 2019), introducing uncertainty into the observed odds ratios.”
BackgroundAnkeny, S. E., Bacci, J. R., Decourt, B., Sabbagh, M. N., & Mielke, M. M. (2024) · Neurology and Therapy · doi:10.1007/s40120-024-00658-x · Cited by 22
Chandra, S. R. (2017) · The Indian Journal of Medical Research · doi:10.4103/ijmr.ijmr_74_17 · Cited by 16
Lithgow, B., Dastgheib, Z. A., Anssari, N., Mansouri, B., Blakley, B. W., Ashiri, M., & Moussavi, Z. (2021) · Medical & Biological Engineering & Computing · doi:10.1007/s11517-021-02409-8 · Cited by 16
Evaluation of Cognitive Impairment in Older Adults
Scharre, D. W., & Trzepacz, P. T. (2013) · FOCUS The Journal of Lifelong Learning in Psychiatry · doi:10.1176/appi.focus.11.4.482 · Cited by 17
Towards pharmacological prevention of Alzheimer disease
Llibre‐Guerra, J. J., McDade, E., Schindler, S. E., Clifford, D. B., Supnet, C. B., Atri, A., & Bateman, R. J. (2025) · Nature Reviews Neurology · doi:10.1038/s41582-025-01154-y · Cited by 18
The Role of Amyloid- and Tau PET in the New Era of Alzheimer Disease Therapies
Chiotis, K., Wang, Y., Joie, R. L., & Rabinovici, G. D. (2025) · Journal of Nuclear Medicine · doi:10.2967/jnumed.124.268339 · Cited by 18
Su, S., Esparza, T. J., & Brody, D. L. (2022) · PLoS ONE · doi:10.1371/journal.pone.0276107 · Cited by 16
“The accuracy of 51 clinical diagnosis of AD at the National Institute of Aging and National Institute of Aging sponsored AD 52 centers varies depending on the clinical and neuropathologic criteria used [7].”
MethodDiagnosing and Treating Alzheimer Disease During the Early Stage
Burke, A. D., & Goldfarb, D. (2023) · The Journal of Clinical Psychiatry · doi:10.4088/jcp.li21019ah3c · Cited by 16
Lower mortality risk in APOE4 carriers with normal cognitive ageing
Pirraglia, E., Glodzik, L., & Shao, Y. (2023) · Scientific Reports · doi:10.1038/s41598-023-41078-5 · Cited by 16
Relationship of Hippocampal Volume to Amyloid Burden across Diagnostic Stages of Alzheimer's Disease
Trzepacz, P. T., Hochstetler, H. M., Yu, P., Castelluccio, P., Witte, M. M., Dell’Agnello, G., Degenhardt, E. K., & Initiative, A. D. N. (2015) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000441351 · Cited by 15
Piccoli, E., Rossi, G., Rossi, T., Pelliccioni, G., D’Amato, I., Tagliavini, F., & Fede, G. D. (2016) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2016.01.134 · Cited by 15
“An overlapping among clinical features of AD and other neurodegenerative diseases, such as the frontotemporal lobar degeneration spectrum and prion diseases, is well acknowledged and thought to cause misdiagnosis in a moderate number of patients (Beach et al., 2012; Cruchaga et al., 2012).”
BackgroundChallenges in the Neuropathological Diagnosis of Dementias
Jellinger, K. A. (2012) · International Journal of Neuropathology · doi:10.7726/ijn.2013.1002 · Cited by 15
“The misdiagnosis rate should be considered when estimating numbers for AD studies (Beach et al., 2012).”
BackgroundSmith, T. O., Cross, J., Poland, F. M., Clay, F., Brookes, A., Maidment, I. D., Penhale, B., Laidlaw, K., & Fox, C. (2017) · Current Alzheimer Research · doi:10.2174/1567205014666170908094931 · Cited by 16
Alzheimer’s disease is associated with prostate cancer: a population-based study
Lin, H., Kao, L., Chung, S., Huang, C., Shia, B., & Huang, C. (2018) · Oncotarget · doi:10.18632/oncotarget.24139 · Cited by 15
“First, studies that rely on diagnostic codes for an AD diagnosis are susceptible to misclassification [36, 37].”
BackgroundReduced Retinal Thickness Predicts Age-Related Changes in Cognitive Function
Mammadova, N., Neppl, T. K., Denburg, N. L., & Greenlee, M. H. W. (2020) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2020.00081 · Cited by 15
Integrated bioinformatics-based identification of diagnostic markers in Alzheimer disease
Chen, D., Zhang, Y., Qiao, R., Kong, X., Zhong, H., Wang, X., Zhu, J., & Li, B. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.988143 · Cited by 17
“Although it is possible to detect Aβ plaques and tau-related neurodegeneration by imaging and from analytes in the cerebrospinal fluid (Jack and Holtzman, 2013), about 40% of nondemented normal elderly people show AD neuropathology including senile plaques and neurofibrillary tangles (Jack and Holtzman, 2013); convers…”
BackgroundMapping CSF biomarker profiles onto NIA–AA guidelines for Alzheimer’s disease
Alexopoulos, P., Roesler, J., Thierjung, N., Werle, L., Buck, D., Yakushev, I. Y., Gleixner, L. S., Kagerbauer, S. M., Ortner, M., Grimmer, T., et al. (2015) · European Archives of Psychiatry and Clinical Neuroscience · doi:10.1007/s00406-015-0628-7 · Cited by 17
“The detected atypical for AD biomarker profiles in patients suffering from AD dementia can be attributed to the relatively low, in the absence of biomarker data, accuracy of current clinical AD diagnostic methods in predicting histopathologic diagnoses (sensitivity 71–88 %, specificity 44–71 %) validated by the standa…”
Coexistence of Cerebral Microbleeds and Amyloid Pathology in Patients with Cognitive Complaints
Lim, E. Y., Ryu, S. Y., Shim, Y. S., Yang, D. W., & Cho, A.-H. (2020) · Journal of Clinical Neurology · doi:10.3988/jcn.2020.16.1.83 · Cited by 15
Pressman, P., & Rabinovici, G. D. (2014) · Elsevier eBooks · doi:10.1016/b978-0-12-385157-4.00475-9 · Cited by 17
Therapeutic news in Alzheimer’s disease: Soon a disease-modifying therapy?
Villain, N. (2022) · Revue Neurologique · doi:10.1016/j.neurol.2022.02.456 · Cited by 14
“However, it is now known that approximately one-third of patients with Alzheimer's type dementia do not have Alzheimer's pathology [13].”
BackgroundThe Biochemical Biomarkers Determination in Alzheimer Dementia
Bîrluțiu, V., Ștef, L., Mitariu, S. I. C., Roman-Filip, C., DUICA, L. C., Antonescu, E., Pîrlog, M. C., Purnichi, T., Silişteanu, S. C., & Manea, M. M. (2018) · Revista de Chimie · doi:10.37358/rc.18.11.6702 · Cited by 14
Deatsch, A. E., Perovnik, M., Namías, M., Trošt, M., Jeraj, R., & Initiative, A. D. N. (2022) · Physics in Medicine and Biology · doi:10.1088/1361-6560/ac8f10 · Cited by 15
Observational studies in Alzheimer disease: bridging preclinical studies and clinical trials
Brenowitz, W. D., & Yaffe, K. S. (2022) · Nature Reviews Neurology · doi:10.1038/s41582-022-00733-7 · Cited by 16
Characteristics of amnestic patients with hypometabolism patterns suggestive of Lewy body pathology
Silva‐Rodríguez, J., Labrador‐Espinosa, M. Á., Moscoso, A., Schöll, M., Mir, P., Grothe, M. J., & Initiative, A. D. N. (2023) · Brain · doi:10.1093/brain/awad194 · Cited by 14
“5,6 Lewy body pathology is typically associated with a distinct clinical syndrome, dementia with Lewy bodies, that is characterized by hallmark diagnostic features such as REM sleep behaviour disorder, visual hallucinations, parkinsonism and cognition fluctuations, in addition to a typically more…”
Atypical clinical variants of Alzheimer’s disease: are they really atypical?
Whitwell, J. L. (2024) · Frontiers in Neuroscience · doi:10.3389/fnins.2024.1352822 · Cited by 15
Hiya, S., Maldonado‐Díaz, C., Rohde, S. K., Gonzales, M. M., Canbeldek, L., Mahadevan, L. S. K., Yokoda, R. T., Sullivan, A. C., Parker, A. S., White, C. L., et al. (2024) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlae134 · Cited by 14
Florbetapir positron emission tomography and cerebrospinal fluid biomarkers
Hake, A. M., Trzepacz, P. T., Wang, S., Yu, P., Case, M. G., Hochstetler, H. M., Witte, M. M., Degenhardt, E. K., Dean, R. A., & Initiative, A. D. N. (2015) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2015.03.002 · Cited by 14
“…from the National Institute on Aging (NIA) Alzheimer’s Disease Centers collected from 2005 to 2010 found ranges for sensitivity of 70.9% to 87.3% and specificity of 44.3% to 70.8% when clinical diagnoses of possible and probable AD dementia are compared with post-mortem histopathology diagnosis [2].”
InfluentialRECENT ADVANCES IN ALZHEIMER'S DISEASE: CAUSES AND TREATMENT
Kaur, K., Kaur, R., & Kaur, M. (2016) · International Journal of Pharmacy and Pharmaceutical Sciences · Cited by 14
Detecting semantic changes in Alzheimer’s disease with vector space models
Fraser, K., & Hirst, G. (2016) · Language Resources and Evaluation · Cited by 14
Dumba, M., Khan, S. R., Patel, N., Perry, L., Malhotra, P., Perry, R. J., Nijran, K. S., Barwick, T. D., Wallitt, K. L., & Win, Z. (2019) · British Journal of Radiology · doi:10.1259/bjr.20181027 · Cited by 14
Association of Hippocampal Subfield Volumes with Amyloid-Beta Deposition in Alzheimer’s Disease
Baek, M. S., Lee, N., Kim, J. W., & Hong, J. Y. (2022) · Journal of Clinical Medicine · doi:10.3390/jcm11061526 · Cited by 14
“Since the diagnosis of AD or prodromal AD based on the clinical history and structural imaging is not always related to the pathologic findings [13], other types of dementia that also demonstrate hippocampal atrophy, such as limbic-predominant age-related TDP-43 encephalopathy [14] and Lewy body dementia [15,16], may…”
BackgroundBeier, K., Nussbeck, S. Y., & Wemheuer, W. M. (2015) · Journal of Biorepository Science for Applied Medicine · doi:10.2147/bsam.s75245 · Cited by 14
“66,67 Brain autopsies would allow researchers to exclude such patients from the evaluation of clinical studies with the benefit of hindsight and therefore make studies more precise in smaller case numbers.”
Pradeep, T., Bray, M. J. C., Arun, S., Richey, L. N., Jahed, S., Bryant, B. R., LoBue, C., Lyketsos, C. G., Kim, P. S., & Peters, M. E. (2019) · International Review of Psychiatry · doi:10.1080/09540261.2019.1682529 · Cited by 16
“Regarding actual misdiagnosis, even subtle rates of misdiagnoses have a significant impact on clinical trial enrollment as even a 20% misdiagnosis rate, when coupled with a 50% study response rate, would double the subjects necessary to maintain the same statistical power (Beach et al., 2012).”
BackgroundMedical Informatics Platform (MIP): A Pilot Study Across Clinical Italian Cohorts
Redolfi, A., Francesco, S. D., Palesi, F., Galluzzi, S., Muscio, C., Castellazzi, G., Tiraboschi, P., Savini, G., Nigri, A., Bottini, G., et al. (2020) · Frontiers in Neurology · doi:10.3389/fneur.2020.01021 · Cited by 14
“The International Working Group (IWG) criteria (1, 2) define Alzheimer’s Dementia (AD) as a construct based on the combination of brain amyloidosis and tauopathy (3– 6).”
BackgroundGenetic Influences on Hippocampal Subfields
Vilor‐Tejedor, N., Evans, T. E., Adams, H. H. H., Gónzalez‐de‐Echávarri, J. M., Molinuevo, J. L., Guigó, R., Gispert, J. D., & Operto, G. (2021) · Neurology Genetics · doi:10.1212/nxg.0000000000000591 · Cited by 12
The Social Construction of Dementia
Wray, A. (2020) · Oxford University Press eBooks · doi:10.1093/oso/9780190917807.003.0004 · Cited by 14
Pathophysiological subtypes of Alzheimer’s disease based on cerebrospinal fluid proteomicsPreprint
Tijms, B. M., Gobom, J., Reus, L. M., Jansen, I. E., Hong, S., Dobričić, V., Kilpert, F., ten Kate, M., Barkhof, F., Tsolaki, M., et al. (2020) · medRxiv · doi:10.1101/2020.03.25.20043158 · Cited by 14
Alzheimer’s disease cortical morphological phenotypes are associated with TOMM40′523-APOE haplotypes
Honea, R. A., Hunt, S. L., Lepping, R. J., Vidoni, E. D., Morris, J. K., Watts, A. S., Michaelis, E. K., Burns, J. M., & Swerdlow, R. H. (2023) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2023.09.001 · Cited by 12
“Clinical evaluation results were used to determine dementia status, which were reviewed along with psychometric battery results and finalized at a consensus diagnostic conference attended by clinicians and psychometricians using the NINCDSADRDA criteria as well as the McKann NIA-AA workgroup diagnostic guidelines (Bea…”
Alzheimer's disease detection using data fusion with a deep supervised encoder
Trinh, M., Shahbaba, R., Stark, C. E. L., & Ren, Y. (2024) · Frontiers in Dementia · doi:10.3389/frdem.2024.1332928 · Cited by 13
“We compare the performance of these ensemble models with the individual models across all pipelines to determine the optimal DR and fusion strategy.”
Soleimani‐Meigooni, D. N., Smith, R. A., Provost, K., Lesman‐Segev, O. H., Allen, I. E., Chen, M. K., Cho, H., Edwards, L., Janelidze, S., Joie, R. L., et al. (2024) · Annals of Neurology · doi:10.1002/ana.27008 · Cited by 13
Insights into cognitive aging and Alzheimer’s disease using amyloid PET and structural MRI scans
Duara, R., Barker, W., Loewenstein, D., Greig, M. T., Rodriguez, R. A., Goryawala, M., Zhou, Q., & Adjouadi, M. (2015) · Clinical and Translational Imaging · doi:10.1007/s40336-015-0110-6 · Cited by 15
“accuracy of 70–80 % [2], can be enhanced by the use of biomarkers, including those that detect brain amyloid concentrations (PET amyloid imaging) and neurodegeneration (structural MRI and regional glucose metabolism using fluorodeoxyglucose PET scans) [3, 4].”
BackgroundSun, H. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-170059 · Cited by 13
Beheshti, I., Initiative, A. D. N., Geddert, N., Perron, J., Gupta, V., Albensi, B. C., & Ko, J. H. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220585 · Cited by 13
“8%) when compared to postmortem diagnosis [4].”
Pascoal, T. A., Leuzy, A., Therriault, J., Chamoun, M., Lussier, F. Z., Tissot, C., Strandberg, O. T., Palmqvist, S., Stomrud, E., Ferreira, P. C. L., et al. (2023) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.12390 · Cited by 15
Wrapper Methods to Correct Mislabelled Training Data
Young, J., Ashburner, J., & Sebastien Ourselin, A. (2013) · International Workshop on Pattern Recognition in NeuroImaging · doi:10.1109/prni.2013.51 · Cited by 13
Correlation of florbetaben PET imaging and the amyloid peptide Aß42 in cerebrospinal fluid
Schipke, C. G., Koglin, N., Bullich, S., Joachim, L. K., Haas, B., Seibyl, J. P., Barthel, H., Sabri, O., & Peters, O. (2016) · Psychiatry Research Neuroimaging · doi:10.1016/j.pscychresns.2016.10.011 · Cited by 13
Metadata
- Authors
- Beach, T. G., Monsell, S. E., Phillips, L. E., & Kukull, W.
- Affiliations
- Banner Sun Health Research Institute (US)
- University of Washington (US)
- Corresponding author
- Beach, Thomas G.
- Venue
- Journal of Neuropathology & Experimental Neurology
- Publisher
- Oxford University Press (OUP)
- Published
- 2012-04
- Volume
- 71
- Issue
- 4
- Pages
- 266-273
- ISSN
- 0022-3069 (ISSN-L)
- 1554-6578
- PMC
- PMC3331862
- OpenAlex
- W1974300727
- Semantic Scholar
- 59ed18597d0cb2e750fc7f3c928871aedf079d0a
- Cited by
- 1,103
- References
- 56
- Citations by year
- 2026: 71 · 2025: 94 · 2024: 94 · 2023: 92 · 2022: 91 · 2021: 84 · 2020: 117 · 2019: 90 · 2018: 74 · 2017: 69 · 2016: 66 · 2015: 71 · 2014: 34 · 2013: 46 · 2012: 9
- FWCI
- 36.35
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuropathology & Experimental Neurology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Michael J. Fox Foundation for Parkinson's Research (P30 AG19610)
- Arizona Department of Health Services (P30 AG19610, U01 AG016976)
- National Alzheimer's Coordinating Center (U01AG016976)
- Arizona Biomedical Research Commission (P30 AG19610)
- National Institute on Aging (U01AG016976, P30AG019610, U19AG010483)
- 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
- Social Sciences › Psychology › Applied Psychology › Psychological Testing and Assessment
- Keywords
- Alzheimer's disease, diagnostic accuracy, neuropathologic diagnosis, sensitivity and specificity, neuritic plaques, misdiagnosis, dementia, Lewy body disease, frontotemporal lobar degeneration, argyrophilic grain disease, hippocampal sclerosis, cerebrovascular disease
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Female, Humans, Male, Middle Aged, United States, Databases, Factual, National Institute on Aging (U.S.)
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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