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Clinical and Biomarker Changes in Dominantly Inherited Alzheimer's Disease
Open accessAbstract
BACKGROUND: The order and magnitude of pathologic processes in Alzheimer's disease are not well understood, partly because the disease develops over many years. Autosomal dominant Alzheimer's disease has a predictable age at onset and provides an opportunity to determine the sequence and magnitude of pathologic changes that culminate in symptomatic disease. METHODS: In this prospective, longitudinal study, we analyzed data from 128 participants who underwent baseline clinical and cognitive assessments, brain imaging, and cerebrospinal fluid (CSF) and blood tests. We used the participant's age at baseline assessment and the parent's age at the onset of symptoms of Alzheimer's disease to calculate the estimated years from expected symptom onset (age of the participant minus parent's age at symptom onset). We conducted cross-sectional analyses of baseline data in relation to estimated years from expected symptom onset in order to determine the relative order and magnitude of pathophysiological changes. RESULTS: Concentrations of amyloid-beta (Aβ)(42) in the CSF appeared to decline 25 years before expected symptom onset. Aβ deposition, as measured by positron-emission tomography with the use of Pittsburgh compound B, was detected 15 years before expected symptom onset. Increased concentrations of tau protein in the CSF and an increase in brain atrophy were detected 15 years before expected symptom onset. Cerebral hypometabolism and impaired episodic memory were observed 10 years before expected symptom onset. Global cognitive impairment, as measured by the Mini-Mental State Examination and the Clinical Dementia Rating scale, was detected 5 years before expected symptom onset, and patients met diagnostic criteria for dementia at an average of 3 years after expected symptom onset. CONCLUSIONS: We found that autosomal dominant Alzheimer's disease was associated with a series of pathophysiological changes over decades in CSF biochemical markers of Alzheimer's disease, brain amyloid deposition, and brain metabolism as well as progressive cognitive impairment. Our results require confirmation with the use of longitudinal data and may not apply to patients with sporadic Alzheimer's disease. (Funded by the National Institute on Aging and others; DIAN ClinicalTrials.gov number, NCT00869817.).
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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.
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“Global cognitive impairment, as measured by the Mini–Mental State Examination and the Clinical Dementia Rating scale, was detected 5 years before expected symptom onset”
- Also stated in: § CLINICAL AND NEUROPSYCHOMETRIC FINDINGS · plain
“Significant differences in CDR-SOB scores were detected between mutation carriers and noncarriers 5 years before expected symptom onset (Fig. 1A and Table 2).”
- Also stated in: § CLINICAL AND NEUROPSYCHOMETRIC FINDINGS · plain
“Significant differences in MMSE scores between mutation carriers and noncarriers were detected at assessments performed 5 years before expected symptom onset”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > Abstract > RESULTS
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.
- Rests on an assumption: The estimated years from expected symptom onset normalizes disease stage based on parental age at onset.
- Rests on an assumption: Mutations in APP, PSEN1, or PSEN2 alter Aβ processing and cause Alzheimer's disease with complete penetrance.
- Also stated in: § CLINICAL AND NEUROPSYCHOMETRIC FINDINGS · 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
“Increased concentrations of tau protein in the CSF and an increase in brain atrophy were detected 15 years before expected symptom onset.”
- Also stated in: § BRAIN ATROPHY · plain
“Increased atrophy of bilateral hippocampi was detected in mutation carriers 15 years before expected symptom onset (Table 2).”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > Abstract > RESULTS
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.
- Rests on an assumption: The estimated years from expected symptom onset normalizes disease stage based on parental age at onset.
- Rests on an assumption: Mutations in APP, PSEN1, or PSEN2 alter Aβ processing and cause Alzheimer's disease with complete penetrance.
- Also stated in: § BRAIN ATROPHY · 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
“Concentrations of amyloid-beta (Aβ)42 in the CSF appeared to decline 25 years before expected symptom onset.”
- Also stated in: § COMBINED MODEL · hedged
“Beginning 25 years before expected symptom onset, Aβ42 concentrations in the CSF in mutation carriers appeared to decline, as compared with those in noncarriers.”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > Abstract > RESULTS
hedgedcorrelational- 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.
- Rests on an assumption: The estimated years from expected symptom onset normalizes disease stage based on parental age at onset.
- Rests on an assumption: Mutations in APP, PSEN1, or PSEN2 alter Aβ processing and cause Alzheimer's disease with complete penetrance.
- Also stated in: § COMBINED MODEL · hedged
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
“We found that autosomal dominant Alzheimer’s disease was associated with a series of pathophysiological changes over decades in CSF biochemical markers of Alzheimer’s disease, brain amyloid deposition, and brain metabolism as well as progressive cognitive impairment.”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > Abstract > CONCLUSIONS
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.
- Rests on an assumption: The estimated years from expected symptom onset normalizes disease stage based on parental age at onset.
- Rests on an assumption: Mutations in APP, PSEN1, or PSEN2 alter Aβ processing and cause Alzheimer's disease with complete penetrance.
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
“Cerebral hypometabolism and impaired episodic memory were observed 10 years before expected symptom onset.”
- Also stated in: § CLINICAL AND NEUROPSYCHOMETRIC FINDINGS · plain
“We found significant cognitive impairment in mutation carriers, as compared with noncarriers, in the delayed-recall portion of the Logical Memory test21 10 years before expected symptom onset (Table 2).”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > Abstract > RESULTS
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.
- Rests on an assumption: The estimated years from expected symptom onset normalizes disease stage based on parental age at onset.
- Rests on an assumption: Mutations in APP, PSEN1, or PSEN2 alter Aβ processing and cause Alzheimer's disease with complete penetrance.
- Also stated in: § CLINICAL AND NEUROPSYCHOMETRIC FINDINGS · 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
“Plasma Aβ42 levels were elevated in mutation carriers, as compared with noncarriers (Fig. 1I).”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > RESULTS > BIOCHEMICAL MEASURES
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether 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
“Cerebral hypometabolism and impaired episodic memory were observed 10 years before expected symptom onset.”
- Also stated in: § CEREBRAL GLUCOSE METABOLISM · plain
“A significant decrease in cerebral metabolism in the precuneus was detected in mutation carriers 10 years before expected symptom onset (Fig. 1E and Table 2).”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > Abstract > RESULTS
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.
- Rests on an assumption: The estimated years from expected symptom onset normalizes disease stage based on parental age at onset.
- Rests on an assumption: Mutations in APP, PSEN1, or PSEN2 alter Aβ processing and cause Alzheimer's disease with complete penetrance.
- Also stated in: § CEREBRAL GLUCOSE METABOLISM · 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
“patients met diagnostic criteria for dementia at an average of 3 years after expected symptom onset.”
- Also stated in: § CLINICAL AND NEUROPSYCHOMETRIC FINDINGS · plain
“In this cohort, participants had a CDR rating of mild dementia (CDR 1) at a mean of 3.3±5.3 years after the parent’s age of symptom onset.”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > Abstract > RESULTS
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.
- Rests on an assumption: The estimated years from expected symptom onset normalizes disease stage based on parental age at onset.
- Rests on an assumption: Mutations in APP, PSEN1, or PSEN2 alter Aβ processing and cause Alzheimer's disease with complete penetrance.
- Also stated in: § CLINICAL AND NEUROPSYCHOMETRIC FINDINGS · 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
“Aβ deposition, as measured by positron-emission tomography with the use of Pittsburgh compound B, was detected 15 years before expected symptom onset.”
- Also stated in: § Aβ DEPOSITION · plain
“As compared with noncarriers, mutation carriers had significant amyloid deposition in the precuneus 15 years before expected symptom onset (Fig. 1F and Table 2).”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > Abstract > RESULTS
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.
- Rests on an assumption: The estimated years from expected symptom onset normalizes disease stage based on parental age at onset.
- Rests on an assumption: Mutations in APP, PSEN1, or PSEN2 alter Aβ processing and cause Alzheimer's disease with complete penetrance.
- Also stated in: § Aβ DEPOSITION · 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
“Increased concentrations of tau protein in the CSF and an increase in brain atrophy were detected 15 years before expected symptom onset.”
- Also stated in: § BIOCHEMICAL MEASURES · plain
“In mutation carriers, levels of tau in the CSF were increased 15 years before expected symptom onset (Fig. 1G and Table 2).”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > Abstract > RESULTS
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.
- Rests on an assumption: The estimated years from expected symptom onset normalizes disease stage based on parental age at onset.
- Rests on an assumption: Mutations in APP, PSEN1, or PSEN2 alter Aβ processing and cause Alzheimer's disease with complete penetrance.
- Also stated in: § BIOCHEMICAL MEASURES · plain
- It may state two separate claims as one. 11
- Probably not a substantial claim. 5
In the paper
“The decrease by half in Aβ42 in the CSF and the increase in tau in the CSF were similar in magnitude to those typically observed in late-onset sporadic Alzheimer’s disease.26”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > RESULTS > BIOCHEMICAL MEASURES
What the sources say
- Not checked yetcites [26] Fagan AM Roe CM Xiong C Mintun MA Morris JC Holtzman DM Cerebrospinal fluid tau/beta-amyloid(42) ratio as a prediction of cognitive decline in non-demented older adults Arch Neurol 2007 64 343 349 17210801 source
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
A 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
“Noncarriers had stable CDR-SOB scores of 0 throughout the relative age range, whereas carriers had increasing CDR-SOB scores at higher values of estimated years from expected symptom onset.”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > RESULTS > CLINICAL AND NEUROPSYCHOMETRIC FINDINGS
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.
- Rests on an assumption: The estimated years from expected symptom onset normalizes disease stage based on parental age at onset.
- Rests on an assumption: Mutations in APP, PSEN1, or PSEN2 alter Aβ processing and cause Alzheimer's disease with complete penetrance.
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
“There was no detectable amyloid deposition in noncarriers. All noncarriers had PIB-PET SUVR values of less than 0.88.”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > RESULTS > Aβ DEPOSITION
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Our findings suggest that once initiated, Alzheimer’s disease processes are likely independent of absolute age but rather depend on the start of processes such as Aβ misfolding and other modulating factors.”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > 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.
It may state two separate claims as one.
- Rests on an assumption: The estimated years from expected symptom onset normalizes disease stage based on parental age at onset.
- Rests on an assumption: Mutations in APP, PSEN1, or PSEN2 alter Aβ processing and cause Alzheimer's disease with complete penetrance.
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
“Our results support the hypothesis of a pathophysiological cascade and suggest the possibility of a common pathophysiology between autosomal dominant Alzheimer’s disease and the much more common “sporadic” form.”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > DISCUSSION
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“If autosomal dominant Alzheimer’s disease is similar to late-onset Alzheimer’s disease, this finding suggests that Alzheimer’s dementia will eventually develop in persons with positive scans for amyloid deposition.”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > 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.
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
“With the use of estimates of years from expected symptom onset, the order and magnitude of changes indicate that genetic mutations cause increased Aβ42, which is followed by brain amyloidosis, tauopathy, brain atrophy, and decreased glucose metabolism. After these biologic changes, cognitive impairment can be detected, which culminates in clinical impairment and eventually dementia.”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > 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.
- Rests on an assumption: The estimated years from expected symptom onset normalizes disease stage based on parental age at onset.
- Rests on an assumption: Mutations in APP, PSEN1, or PSEN2 alter Aβ processing and cause Alzheimer's disease with complete penetrance.
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
“a linear mixed model was used to model each marker as a function of estimated years from expected symptom onset, mutation status (carrier or noncarrier), and apolipoprotein E (APOE) status (positive or negative).”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > METHODS > STATISTICAL ANALYSIS
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
In the paper
“initial and ongoing quality control and matching between site scanners were performed according to the Alzheimer’s Disease Neuroimaging Initiative (ADNI) protocol.19”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > METHODS > BRAIN IMAGING
What the sources say
- Not checked yetcites [19] Mueller SG Weiner MW Thal LJ The Alzheimer’s disease neuroimaging initiative Neuroimaging Clin N Am 2005 15 869 877 16443497 PMC2376747 source
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
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
“All values had to meet quality-control standards, including a coefficient of variation of 25% or less, kit “controls” within the expected range as defined by the manufacturer, and measurement consistency between plates of a common sample that was included in each run.”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > METHODS > BIOCHEMICAL ANALYSIS
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.
None of the sources cited for this claim have been checked yet.
In the paper
“The age at clinical onset of autosomal dominant Alzheimer’s disease is similar between generations14 and is affected mostly by the mutation type and background family genetics.15”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > Abstract > CONCLUSIONS
What the sources say
- Not checked yetcites [14] Lopera F Ardilla A Martínez A Clinical features of early-onset Alzheimer disease in a large kindred with an E280A presenilin-1 mutation JAMA 1997 277 793 799 9052708 source
- Not checked yetcites [15] Wijsman EM Daw EW Yu X APOE and other loci affect age-at-onset in Alzheimer’s disease families with PS2 mutation Am J Med Genet B Neuropsychiatr Genet 2005 132B 14 20 15389756 source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
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
“after adjustment for the correlation among family members.”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > METHODS > STATISTICAL ANALYSIS
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.
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
“There were no significant differences in the presence of an APOE ε4 allele or sex between asymptomatic mutation carriers and noncarriers.”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > RESULTS > STUDY PARTICIPANTS
plainn = 128- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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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
“Clinicians who performed the assessments were not aware of the mutation status of participants.”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > METHODS > CLINICAL ASSESSMENTS
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
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
“Owing to the younger age of the cohort, the prevalence of confounders such as vascular risk factors was low (<15%) in this cohort and not significantly different between carriers and noncarriers.”
§ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease > DISCUSSION
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
The estimated years from expected symptom onset normalizes disease stage based on parental age at onset.
“The estimated year from expected symptom onset normalizes the stage of disease on the basis of the parental age of onset.”
The paper relies on this without support.
Mutations in APP, PSEN1, or PSEN2 alter Aβ processing and cause Alzheimer's disease with complete penetrance.
“Mutations in one of three genes (APP, PSEN1, and PSEN2) have been identified that cause alterations in Aβ processing and lead to Alzheimer’s disease with complete penetrance.”
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
“Efforts continue to be placed on the early detection of AD as changes in brain chemistry begin to occur 20 years or more prior to the onset of noticeable cognitive symptoms [137,138,139,140].”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [138]
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
“and that progression of biomarker measures is also a continuous process that begins before symptoms [9–14]”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [9]
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
“Consequently, a widely held view is that amyloid biomarkers represent the earliest evidence of AD neuropathologic change currently detectable in living persons [9,11,72,103,104].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [9]
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
“Abundant human and animal data implicate A and T in the primary pathogenesis of AD [9,100], including the observation that the age-related exponential increase in prevalence of A (by biomarkers and neuropathology) anticipates the age-related exponential increase in prevalence of clinically defined possible/probable “AD” by around 15 years [53,212].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [9]
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
“Nevertheless, neuroimaging and biomarker studies show consistencies in the sequential onset of amyloid deposition, tau, FDG-PET hypometabolism, grey matter atrophy, and clinical presentation between late-onset and autosomal-dominant Alzheimer’s disease (Bateman et al., 2012; Benzinger et al., 2013; Young et al., 2014; Gordon et al., 2018; Oxtoby et al., 2018), suggesting substantial commonalities”
From White matter diffusion alterations precede symptom onset in autosomal dominant Alzheimer’s disease (2018) · cites this paper as Bateman et al., 2012
Experimental — accuracy not yet measured
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
“So far, biomarker studies demonstrated the successive development of primary pathologies including amyloid-β and tau (as measured by biofluid and molecular PET markers) followed by alterations of medial temporal and parietal grey matter (as measured by volumetric MRI and FDG-PET) in both sporadic late-onset Alzheimer’s disease (Jack et al., 2012) and genetically-caused Alzheimer’s disease (Bateman”
From White matter diffusion alterations precede symptom onset in autosomal dominant Alzheimer’s disease (2018) · cites this paper as Bateman et al., 2012
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
“In defense of this strategy, the expression of Aβ42 plaques in humans with highly penetrant APP and PSEN mutations occurs as much as 10–20 years before serious cognitive loss75,76, so in this regard the temporal dynamics of the 5×FAD mouse is actually a reasonable match to prodromal autosomal dominant forms of AD in humans.”
From Magnetic resonance microscopy maps widespread effects of Alzheimer’s disease on brain structures and behavior in mice (2026) · cites this paper as [75]
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
“Thus, it is suggested that CSF p-tau biomarkers likely indicate an active process of tau secretion, and one that is correlated with cerebral Aβ deposition in early disease.20, 21, 22”
From Cerebrospinal fluid p-tau231 as an early indicator of emerging pathology in Alzheimer's disease (2022) · cites this paper as [20]
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
“Increases in CSF p-tau occur before both tau PET20,63,64 and established measures of neuronal death (e.g., neurofilament light, magnetic resonance imaging or [18F]FDG PET), thus CSF p-tau cannot merely reflect NFT leakage from dying neurons.”
From Cerebrospinal fluid p-tau231 as an early indicator of emerging pathology in Alzheimer's disease (2022) · cites this paper as [20]
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
“a timeline which mimics that of humans with both dominantly inherited AD and late-onset sporadic AD (Bateman et al., 2012).”
From Inhibiting USP16 rescues stem cell aging and memory in an Alzheimer’s model (2022) · cites this paper as Bateman et al., 2012
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The first biomarkers to become abnormal in carriers of deterministic AD mutations are those of Aβ [9–11,14].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [9]
The cited source says what the claim attributes to it.
In the citing paper
“In dominantly inherited AD, hypometabolism on FDG-PET can be detected as early as 10 years before symptom onset [112].”
From The use of neuroimaging techniques in the early and differential diagnosis of dementia (2023) · cites this paper as [112]
The cited source says what the claim attributes to it.
In the citing paper
“While this clearly indicates a major role for Aβ in AD pathology (Jack et al., 2013; Selkoe and Hardy, 2016), even in these genetic forms, a decades-long asymptomatic phase is present (Bateman et al., 2012).”
From The Major Risk Factors for Alzheimer’s Disease: Age, Sex, and Genes Modulate the Microglia Response to Aβ Plaques (2019) · cites this paper as Bateman et al., 2012
The cited source says what the claim attributes to it.
In the citing paper
“In humans, CSF Aβ concentrations begin changing before tau levels; amyloid deposition occurs in the brain decades before the onset of clinical symptoms (3–5).”
From An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice (2014) · cites this paper as [5]
In the citing paper
“PET scanning and CSF analysis revealed that the pathological changes are initiated two decades before the appearance of symptoms [38].”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [38]
In the citing paper
“However, atrophy of individual cortical regions occurs earlier1,2,22,25.”
From Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease (2019) · cites this paper as [1]
In the citing paper
“Cross-sectional and longitudinal data analyses of DIAN and other large Alzheimer’s disease cohorts have demonstrated that the pathological processes in Alzheimer’s disease begin more than two decades before the onset of clinical symptoms.”
From Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease (2019) · cites this paper as [1]
In the citing paper
“The accumulation of amyloid-β in the brain (estimated 15–20 years before clinical onset) is followed by declines in cortical metabolism (estimated 10–15 years before clinical onset) and brain atrophy (5–10 years before clinical onset)1,2,22,25.”
From Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease (2019) · cites this paper as [1]
In the citing paper
“These pathological changes can be assessed by magnetic resonance imaging (MRI), positron-emission tomography (PET), and measurement of amyloid-β and tau protein levels in the cerebrospinal fluid (CSF)1–4.”
From Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease (2019) · cites this paper as [1]
In the citing paper
“ADAD work has revealed a temporal ordering of biomarkers consistent with theoretical models,6–8 and indications that pathology progressively appears in new regions of the brain as the disease worsens7.”
From Spatial patterns of neuroimaging biomarker change in individuals from families with autosomal dominant Alzheimer's disease: a longitudinal study (2018) · cites this paper as [6]
In the citing paper
“Our findings are consistent with prior studies suggesting that physiologic changes may be detectable before behavioral changes become manifest in a variety of neurological and neurodevelopmental disorders [36–43].”
From EEG power at 3 months in infants at high familial risk for autism (2017) · cites this paper as [36]
In the citing paper
“Between the appearance of amyloid plaques and neuronal tangles in the human brain, to the ultimate dementia in patients, up to twenty years may elapse (Bateman et al. , 2012; Villemagne et al. , 2013; Jansen et al. , 2015).”
From Spatial Transcriptomics and In Situ Sequencing to Study Alzheimer’s Disease (2020) · cites this paper as Bateman et al., 2012
In the citing paper
“Previous cross-sectional studies indicate that Aβ42 levels decrease in the CSF as Aβ starts to accumulate, before fibrillar plaques can be detected with PET7–11.”
From Earliest accumulation of β-amyloid occurs within the default-mode network and concurrently affects brain connectivity (2017) · cites this paper as [7]
In the citing paper
“Amyloid accumulation probably starts many years before the onset of symptoms,2,26,27 and initiation of anti-amyloid treatment only after dementia develops may be too late to affect the clinical course of the disease.28”
From Two Phase 3 Trials of Bapineuzumab in Mild-to-Moderate Alzheimer's Disease (2014) · cites this paper as [2]
In the citing paper
“Multiple lines of evidence indicate that aberrant Aβ production or clearance is an early component in the pathogenesis of Alzheimer’s disease.1–3”
From Two Phase 3 Trials of Bapineuzumab in Mild-to-Moderate Alzheimer's Disease (2014) · cites this paper as [2]
In the citing paper
“characterized by early deposition of Aβ in the precuneus and other cortical regions comprising the default mode network, followed sequentially by regional cortical hypometabolism, accumulation of tau pathology, hippocampal volume loss, and onset of symptomatic cognitive impairment”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Bateman et al., 2012
In the citing paper
“Extensive biomarker and imaging studies indicate that amyloid-β aggregation is the earliest pathological event in Alzheimer’s disease, followed at a later stage by pathological changes of tau aggregation extending beyond the limbic system to the neocortex, which correlates with brain atrophy and cognitive decline2,3.”
From Interplay between innate immunity and Alzheimer disease: APOE and TREM2 in the spotlight (2018) · cites this paper as [3]
In the citing paper
“An alternative design will test Aβ-based interventions in asymptomatic FAD subjects with presenilin 1 mutations, as their age of symptomatic onset is reasonably predictable [259, 260].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [259]
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Metadata
- Authors
- Bateman, R. J., Xiong, C., Benzinger, T. L. S., Fagan, A. M., Goate, A., Fox, N. C., Marcus, D. S., Cairns, N. J., Xie, X., Blazey, T. M., Holtzman, D. M., Santacruz, A., Buckles, V., Oliver, A., Moulder, K., Aisen, P. S., Ghetti, B., Klunk, W. E., McDade, E., Martins, R. N., Masters, C. L., Mayeux, R., Ringman, J. M., Rossor, M. N., Schofield, P. R., Sperling, R. A., Salloway, S., & Morris, J. C.
- Affiliations
- Washington University in St. Louis (US)
- University of Pittsburgh (US)
- Edith Cowan University (AU)
- Mental Health Research Institute (AU)
- Columbia University Irving Medical Center (US)
- University of California, Los Angeles (US)
- UNSW Sydney (AU)
- Brigham and Women's Hospital (US)
- Brown University (US)
- ORCID
- Bateman, Randall J.
- Xiong, Chengjie
- Benzinger, Tammie L.S.
- Fagan, Anne M.
- Goate, Alison
- Fox, Nick C.
- Marcus, Daniel S.
- Blazey, Tyler M.
- Holtzman, David M.
- Santacruz, Anna
- Oliver, Angela
- Ghetti, Bernardino
- Klunk, William E.
- McDade, Eric
- Martins, Ralph N.
- Masters, Colin L.
- Mayeux, Richard
- Ringman, John M.
- Rossor, Martin N.
- Schofield, Peter R.
- Sperling, Reisa A.
- Salloway, Stephen
- Morris, John C.
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2012-08-30
- Volume
- 367
- Issue
- 9
- Pages
- 795-804
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- PMC
- PMC3474597
- OpenAlex
- W2171250577
- Semantic Scholar
- f9e95e5b9f5f5f7439a49c2f9832d72c680590a1
- Cited by
- 3,814
- References
- 33
- Citations by year
- 2026: 227 · 2025: 276 · 2024: 297 · 2023: 300 · 2022: 290 · 2021: 340 · 2020: 345 · 2019: 267 · 2018: 266 · 2017: 225 · 2016: 232 · 2015: 240 · 2014: 238 · 2013: 223 · 2012: 40
- FWCI
- 168.71
- Type
- journal article
- Language
- en
- Open access
- green
- research.vumc.nl
- Licence
- other-oa
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion, other-oa)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
- UWA Profiles and Research Repository (UWA) (submittedVersion)
- Australasian Journal of Paramedicine (submittedVersion)
- Digital Academic REpository of VU University Amsterdam (Vrije Universiteit Amsterdam) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Minerva Access (University of Melbourne) (submittedVersion)
- Pure Amsterdam UMC (submittedVersion, other-oa)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Funders
- National Institute for Health and Care Research (NF-SI-0508-10123)
- National Institutes of Health (UL1TR000124, UL1TR000448)
- National Institute on Aging (UF1AG032438, U19AG032438, U19AG010483)
- National Institute of Neurological Disorders and Stroke (P30NS048056)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Clinical Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- autosomal dominant Alzheimer's disease, preclinical Alzheimer's disease, amyloid-beta, tau protein, cerebrospinal fluid biomarkers, amyloid deposition, Pittsburgh compound B PET, brain atrophy, brain hypometabolism, episodic memory impairment, cognitive impairment, age of symptom onset, disease progression, DIAN
- MeSH terms
- Alzheimer Disease, Brain, Cerebrospinal Fluid, Cross-Sectional Studies, Female, Genes, Dominant, Glucose, Humans, Longitudinal Studies, Magnetic Resonance Imaging, Male, Middle Aged, Mutation, Neuropsychological Tests, Biomarkers, Amyloid beta-Peptides, Age of Onset
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-05, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-05 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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