The DOI matches its Crossref record; 60 of the 60 references it cites were found in a registry or an index; 36 of the 43 sources its claims cite were checked for support.
Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease
Open accessAbstract
OBJECTIVE: To test the hypothesis that plasma total tau (t-tau) and neurofilament light chain (NfL) concentrations may have a differential role in the study of frontotemporal lobar degeneration syndromes (FTLD-S) and clinically diagnosed Alzheimer disease syndromes (AD-S), we determined their diagnostic and prognostic value in FTLD-S and AD-S and their sensitivity to pathologic diagnoses. METHODS: We measured plasma t-tau and NfL with the Simoa platform in 265 participants: 167 FTLD-S, 43 AD-S, and 55 healthy controls (HC), including 82 pathology-proven cases (50 FTLD-tau, 18 FTLD-TDP, 2 FTLD-FUS, and 12 AD) and 98 participants with amyloid PET. We compared cross-sectional and longitudinal biomarker concentrations between groups, their correlation with clinical measures of disease severity, progression, and survival, and cortical thickness. RESULTS: Plasma NfL, but not plasma t-tau, discriminated FTLD-S from HC and AD-S from HC. Both plasma NfL and t-tau were poor discriminators between FLTD-S and AD-S. In pathology-confirmed cases, plasma NfL was higher in FTLD than AD and in FTLD-TDP compared to FTLD-tau, after accounting for age and disease severity. Plasma NfL, but not plasma t-tau, predicted clinical decline and survival and correlated with regional cortical thickness in both FTLD-S and AD-S. The combination of plasma NfL with plasma t-tau did not outperform plasma NfL alone. CONCLUSION: Plasma NfL is superior to plasma t-tau for the diagnosis and prediction of clinical progression of FTLD-S and AD-S. CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that plasma NfL has superior diagnostic and prognostic performance vs plasma t-tau in FTLD and AD.
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Claims the paper makes
48 Own result · 16 Partly supported · 15 Own method · 10 Own interpretation · 9 Supported · 5 No full text of the sources · 2 Not supported · 1 Couldn’t confirm · accuracy not yet measured
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
“Studies of plasma t-tau in AD and FTLD, including the present one, have found no relationship between plasma and CSF t-tau.13”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Disputedcites [13] 13. Mattsson N, Zetterberg H, Janelidze S, et al. Plasma tau in Alzheimer disease. Neu- rology 2016;87:1827-1835. sourceExperimental — accuracy not yet measured
The Results report no significant overall correlation in ADNI, but they also report a significant correlation between plasma tau and CSF total tau in BioFINDER, including an association in the AD dementia subgroup. Thus, this study does not support the blanket claim that no relationship was found. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
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.
- Disputed
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
“We also recently observed that phosphorylated plasma tau at threonine 181 differentiates autopsy-diagnosed AD from FTLD with better accuracy than clinically diagnosed or amyloid PET-defined cases.22”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Disputedcites [22] 22. Advancing Research and Treatment for Frontotemporal Lobar Degeneration (ARTFL) investigators, Thijssen EH, La Joie R, Wolf A, et al. Diagnostic value of plasma phosphorylated tau181 in Alzheimer's disease and frontotemporal lobar de- generation. Nat Med 2020;26:387-397. sourceExperimental — accuracy not yet measured
The Discussion (page not supplied) says the opposite of the claimed comparison: plasma pTau181 differentiated autopsy-diagnosed AD from FTLD with slightly lower accuracy than in clinically diagnosed or PET-defined cases. (LLM, conf=0.95)
Checked by a reasoning model — may be wrong.
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.
- Disputed
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Whereas blood t-tau shows no diagnostic potential for AD, 13 NfL in blood shows a clear increase in AD, 4 and also tracks neurofibrillary tangle load and cognitive decline.14,15”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Abstract
What the sources say
- Partly supportedcites [13] 13. Mattsson N, Zetterberg H, Janelidze S, et al. Plasma tau in Alzheimer disease. Neu- rology 2016;87:1827-1835. sourceExperimental — accuracy not yet measured
The Abstract Conclusions and Discussion say that plasma tau alone is insufficient as an AD biomarker for individual people, supporting the claim about its current diagnostic use. But “no diagnostic potential” is too absolute: the paper reports group-level differences, says plasma tau partly reflects AD pathology, and proposes further study of its biomarker use. No page numbers are available in our copy. (LLM, conf=0.88)
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
Every source the paper cites for this claim was checked and supports it.
In the paper
“Only a single previous study, however, investigated plasma t-tau levels in FTLD-S.38”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Supportedcites [38] 38. Foiani MS, Woollacott IO, Heller C, et al. Plasma tau is increased in frontotemporal dementia. J Neurol Neurosurg Psychiatry 2018;89:804-807. sourceExperimental — accuracy not yet measured
The Introduction (page not provided) says plasma tau had not yet been examined in FTD and identifies this study as investigating it. The Methods, under “Plasma tau measurements” (page not provided), specify a Human Total Tau assay, supporting the citing sentence’s identification of this as an earlier plasma t-tau study. The paper cannot establish how many such studies existed when the later sentence was written. (LLM, conf=0.88)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Specifically, plasma β-amyloid 42/ 40 measured with mass spectrometry is strongly associated with amyloid status determined with amyloid PET scan.43”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Supportedcites [43] 43. Schindler SE, Bollinger JG, Ovod V, et al. High-precision plasma β-amyloid 42/40 predicts current and future brain amyloidosis. Neurology 2019;93:e1647-e1659. source
The Results report that plasma Aβ42/Aβ40 distinguished amyloid PET-positive from PET-negative participants and predicted PET status with an AUC of 0.88. The Discussion identifies the measurement as an immunoprecipitation mass spectrometry assay. Together, these passages support the claimed strong association. (LLM, conf=0.94)
boostedcorrelational- 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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“This further supports that plasma NfL reflects brain pathophysiology, 14”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Supportedcites [14] 14. Ashton NJ, Leuzy A, Lim YM, et al. Increased plasma neurofilament light chain concentration correlates with severity of post-mortem neurofibrillary tangle pathol- ogy and neurodegeneration. Acta Neuropathol Commun 2019;7:5. source
The Conclusion states that plasma NfL reflects CSF biomarker changes, post-mortem neurofibrillary tangle pathology, and neurodegeneration. This supports the citing sentence’s broad claim that plasma NfL reflects brain pathophysiology. (LLM, conf=0.94)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Our results are also consistent with earlier reports showing a high correlation between plasma and CSF NfL. 5”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Supportedcites [5] 5. Rojas JC, Karydas A, Bang J, et al. Plasma neurofilament light chain predicts pro- gression in progressive supranuclear palsy. Ann Clin Transl Neurol 2016;3:216-225. source
The Results report strong positive correlations between plasma and CSF NfL in patients with progressive supranuclear palsy, both at baseline and at one-year follow-up. The Discussion also describes the levels as consistently correlated. (LLM, conf=0.93)
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.
- 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
“Plasma t-tau had no diagnostic utility to differentiate between FTLD-S and AD-S (AUC 0.58, 95% CI 0.49-0.68,p = 0.085), FTLD-S and healthy controls (AUC 0.54, 95% CI 0.45-0.63,p = 0.414), or AD-S and healthy controls (AUC 0.56, 95% CI 0.44-0.68,p = 0.333).”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Diagnostic Value of Plasma t-Tau and NfL
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
“but a poor performance for the discrimination between FTLD-S and AD-S (AUC 0.75, 95% CI 0.68-0.82,p < 0.001)”
- Also stated in: § Abstract · plain
“Both plasma NfL and t-tau were poor discriminators between FLTD-S and AD-S.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Diagnostic Value of Plasma t-Tau and NfL
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § Abstract · 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 AD-S from controls (AUC 0.94, 95% CI 0.89-0.98,p < 0.001)”
- Also stated in: § Abstract · plain
“Plasma NfL, but not plasma t-tau, discriminated FTLD-S from HC and AD-S from HC.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Diagnostic Value of Plasma t-Tau and NfL
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.
- Also stated in: § Abstract · plain
- Probably not a substantial claim. 24
- It may state two separate claims as one. 40
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Total tau (t-tau) is increased in pathology-confirmed AD and is considered a neurodegeneration biomarker in current research AD frameworks.3”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Abstract
What the sources say
- Partly supportedcites [3] 3. Jack CR, Bennett DA, Blennow K, et al. NIA-AA Research Framework: toward a biological definition of Alzheimer's disease. Alzheimers Dement 2018;14:535-562. sourceExperimental — accuracy not yet measured
Section 9.4 places CSF total tau in the framework’s (N) neurodegeneration or neuronal-injury biomarker group. Section 9.3 discusses total tau in AD patients, but does not establish that it is increased specifically in pathology-confirmed AD; its reference to postmortem pathology concerns phosphorylated tau. Page numbers were not available in our copy. (LLM, conf=0.84)
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. 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
“Elevated CSF levels of t-tau and p-tau are considered markers of neurodegeneration and tau pathology in AD and are used in the clinical setting to increase the diagnostic certainty of AD, 1 and together with CSF Aβ42 recommended for diagnostic use in the Alzheimer's Association Appropriate Use Criteria for CSF testing in the diagnosis of AD. 35”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Partly supportedcites [1] 1. Lleo A, Irwin DJ, Illan-Gala I, et al. A 2-step cerebrospinal algorithm for the selection of frontotemporal lobar degeneration subtypes. JAMA Neurol 2018;75:738-745. sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 1 unverifiable. Expand the claim to see per-atom verdicts.
- Partly supportedcites [35] 35. Shaw LM, Arias J, Blennow K, et al. Appropriate use criteria for lumbar puncture and cerebrospinal fluid testing in the diagnosis of Alzheimer's disease. Alzheimers Dement 2018;14:1505-1521. sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable, 1 not checked. Expand the claim to see per-atom verdicts.
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. It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In that study, plasma t-tau was elevated in bvFTD, PPA, and symptomatic MAPT mutation carriers”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Supportedcites [38] 38. Foiani MS, Woollacott IO, Heller C, et al. Plasma tau is increased in frontotemporal dementia. J Neurol Neurosurg Psychiatry 2018;89:804-807. source
The Results report significantly higher plasma tau in bvFTD and PPA than in controls. The Discussion states that, among the genetic groups, increased levels were seen only in the MAPT mutation group; the Methods describe these participants as patients with a measured disease duration. Page numbers are not available in our copy. (LLM, conf=0.94)
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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“For example, the CSF t-tau immunoassay used here relies on a combination of monoclonal antibodies with epitopes in the mid-protein region.In contrast, the plasma t-tau assay detects epitopes going from the N-terminal region to the more distal amino acid 224.39”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Partly supportedcites [39] 39. Cicognola C, Brinkmalm G, Wahlgren J, et al. Novel tau fragments in cerebrospinal fluid: relation to tangle pathology and cognitive decline in Alzheimer's disease. Acta Neuropathol 2019;137:279-296. sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) says standard CSF t-tau immunoassays use monoclonal antibodies with mid-region epitopes. But the Materials and methods section describes the assay detecting fragments ending at amino acid 224 as a CSF assay using neat CSF samples, not a plasma t-tau assay; it also describes those fragments as N-terminally truncated. The plasma-assay portion is therefore unsupported by this paper. (LLM, conf=0.88)
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
“PET scans were read as positive or negative, as previously described and validated against neuropathology.27”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Study Participants
What the sources say
- Partly supportedcites [27] 27. La Joie R, Ayakta N, Seeley WW, et al. Multisite study of the relationships between antemortem [ 11 C]PIB-PET Centiloid values and postmortem measures of Alz- heimer's disease neuropathology. Alzheimers Dement 2019;15:205-216. sourceExperimental — accuracy not yet measured
The Results (Complementary analyses; page unavailable) describe clinicians reading PET scans as positive or negative. The Discussion (Pathology-based thresholds; page unavailable) validates a quantitative Centiloid threshold against neuropathology and compares it with visual reads, but does not establish that the visual-reading method itself was validated against neuropathology. (LLM, conf=0.83)
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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Tau hyperphosphorylation leads to the formation of paired helical filaments that aggregate in neurofibrillary tangles, a defining pathologic hallmark of AD. 3”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Partly supportedcites [3] 3. Jack CR, Bennett DA, Blennow K, et al. NIA-AA Research Framework: toward a biological definition of Alzheimer's disease. Alzheimers Dement 2018;14:535-562. sourceExperimental — accuracy not yet measured
Section 6 (Definition of AD; page unavailable) says paired helical filament (PHF) tau deposits are required, along with Aβ deposits, to meet neuropathologic criteria for AD. Section 9.2 (Tau PET; page unavailable) refers to PHF tangles, while section 9.3 (CSF T-tau and P-tau; page unavailable) associates phosphorylated tau with PHF formation. The paper does not state the claimed causal sequence that tau hyperphosphorylation produces filaments that then aggregate into tangles. (LLM, conf=0.87)
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. 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
“This adds to accumulating evidence supporting that t-tau and NfL reflect different aspects of neurodegeneration and provide different information compared to other neurodegeneration biomarkers, such as FDG-PET, or structural neuroimaging biomarkers, and that their longitudinal trajectories may be differently affected by demographic variables or disease stage.34”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Partly supportedcites [34] 34. Illan-Gala I, Pegueroles J, Montal V, et al. Challenges associated with biomarker-based classification systems for Alzheimer's disease. Alzheimers Dement Amst Neth 2018; 10:346-357. 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.
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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Plasma NfL and plasma t-tau concentrations were determined with commercially available ultrasensitive Single molecule array technology using an HD-1 analyzer (Quanterix, Billerica, MA), by board-certified laboratory technicians blinded to clinical data, as previously described.5”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Study Participants
What the sources say
- Partly supportedcites [5] 5. Rojas JC, Karydas A, Bang J, et al. Plasma neurofilament light chain predicts pro- gression in progressive supranuclear palsy. Ann Clin Transl Neurol 2016;3:216-225. sourceExperimental — accuracy not yet measured
The Subjects and Methods section (Plasma and CSF analyses; page unavailable) says a board-certified laboratory technician measured plasma NfL using an assay transferred onto the Simoa platform. It does not say the technician was blinded to clinical data, and the paper reports total tau measurements in CSF, not plasma. (LLM, conf=0.90)
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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“High CSF t-tau relates to clinical progression in AD 36 and FTLD.37”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Supportedcites [36] 36. Wattmo C, Blennow K, Hansson O. Cerebro-spinal fluid biomarker levels: phos- phorylated tau (T) and total tau (N) as markers for rate of progression in Alzheimer's disease. BMC Neurol 2020;20:10. source
Citation 36 is attached to the AD portion of the sentence; FTLD is attributed to citation 37. In Results > Short-term response to ChEI therapy and longitudinal outcomes (page unavailable), higher CSF total tau was associated with greater annual cognitive deterioration and faster worsening of instrumental daily functioning in patients with AD. The reported correlations were weak. (LLM, conf=0.90)
- Partly supportedcites [37] 37. Ljubenkov PA, Staffaroni AM, Rojas JC, et al. Cerebrospinal fluid biomarkers predict frontotemporal dementia trajectory. Ann Clin Transl Neurol 2018;5:1250-1263. sourceExperimental — accuracy not yet measured
The Results section, “Baseline NfL and total tau predict change in nfvPPA” (page unavailable), reports that higher CSF total tau predicted faster clinical worsening in patients with nfvPPA, an FTD variant. This supports the FTLD-related point cited to this paper, but the finding is specific to nfvPPA rather than FTLD generally. The citing sentence assigns the Alzheimer disease point to a different citation, so it is not judged here. (LLM, conf=0.86)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In agreement with our results, no associations were found between plasma t-tau and baseline measures of disease severity or brain volume and AD pathophysiology (as measured by the CSF tau/Aβ 1-42 ratio).38”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Supportedcites [38] 38. Foiani MS, Woollacott IO, Heller C, et al. Plasma tau is increased in frontotemporal dementia. J Neurol Neurosurg Psychiatry 2018;89:804-807. source
The Results report no significant correlations between plasma tau and disease duration or cross-sectional brain volumes. They also report no difference in plasma tau between groups classified by the CSF t-tau/Aβ1-42 ratio, supporting the stated lack of association with that index of AD pathology. (LLM, conf=0.90)
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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Plasma NfL increases upon neuronal injury and correlates with clinical progression and survival in FTLD syndromes (FTLD-S) and AD syndromes (AD-S).[4][5][6][7][8]”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Abstract
What the sources say
- Partly supportedcites [4] 4. Mattsson N, Andreasson U, Zetterberg H, Blennow K; for the Alzheimer's Disease Neuroimaging Initiative. Association of plasma neurofilament light with neuro- degeneration in patients with Alzheimer disease. JAMA Neurol 2017;74:557. sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) describes plasma NfL as a marker of neuronal injury and reports associations with cognitive and imaging decline in AD. It notes elevated levels in frontotemporal dementia, but does not establish a correlation with clinical progression in FTLD syndromes; neither the Discussion nor the Results addresses survival in either syndrome. (LLM, conf=0.88)
- Partly supportedcites [5] 5. Rojas JC, Karydas A, Bang J, et al. Plasma neurofilament light chain predicts pro- gression in progressive supranuclear palsy. Ann Clin Transl Neurol 2016;3:216-225. sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) describes blood NfL as a marker of neuronal injury, and the Results and Discussion link higher baseline plasma NfL to faster clinical decline in PSP. This copy does not establish a plasma NfL association with progression and survival across FTLD-S and AD-S; its survival-related finding concerns ALS patients. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [6] 6. Bridel C, van Wieringen WN, Zetterberg H, et al. Diagnostic value of cerebrospinal fluid neurofilament light protein in neurology: a systematic review and meta-analysis. JAMA Neurol 2019;76:1035. source
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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Also in agreement with the present results are those from 2 large AD cohorts, in which plasma t-tau was associated with faster clinical decline.13”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Partly supportedcites [13] 13. Mattsson N, Zetterberg H, Janelidze S, et al. Plasma tau in Alzheimer disease. Neu- rology 2016;87:1827-1835. sourceExperimental — accuracy not yet measured
The Results section reports that higher plasma tau was associated with accelerated cognitive decline in ADNI. The Methods section describes ADNI as prospectively followed but BioFINDER as cross-sectional, so the paper does not establish faster clinical decline in both cohorts. Page numbers were not available in our copy. (LLM, conf=0.90)
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 cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Whereas blood t-tau shows no diagnostic potential for AD, 13 NfL in blood shows a clear increase in AD, 4 and also tracks neurofibrillary tangle load and cognitive decline.14,15”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Abstract
What the sources say
- Partly supportedcites [4] 4. Mattsson N, Andreasson U, Zetterberg H, Blennow K; for the Alzheimer's Disease Neuroimaging Initiative. Association of plasma neurofilament light with neuro- degeneration in patients with Alzheimer disease. JAMA Neurol 2017;74:557. sourceExperimental — accuracy not yet measured
The Results section on diagnostic groups reports higher plasma NfL in AD dementia than in controls, and the Results section on cognition reports an association with faster cognitive decline. The paper does not measure neurofibrillary tangle load. Its biochemical-marker results show a weak correlation with CSF phosphorylated tau in the full cohort, which does not establish that NfL tracks tangle load. (LLM, conf=0.88)
- Supportedcites [14] 14. Ashton NJ, Leuzy A, Lim YM, et al. Increased plasma neurofilament light chain concentration correlates with severity of post-mortem neurofibrillary tangle pathol- ogy and neurodegeneration. Acta Neuropathol Commun 2019;7:5. source
The Discussion reports that plasma NfL is increased in AD, despite overlap with other diagnostic groups, and rises with the severity of post-mortem neurofibrillary tangle pathology. The Results section reports an association between plasma NfL and subsequent MMSE scores, supporting the cognitive-decline component. (LLM, conf=0.92)
- Partly supportedcites [15] 15. Mattsson N, Cullen NC, Andreasson U, Zetterberg H, Blennow K. Association be- tween longitudinal plasma neurofilament light and neurodegeneration in patients with Alzheimer disease. JAMA Neurol 2019;76:791. sourceExperimental — accuracy not yet measured
The Abstract and Discussion report that changes in plasma NfL correlate with worsening cognition, and the Abstract reports associations with CSF tau biomarkers. The paper does not report measuring neurofibrillary tangle load, so the claim that NfL tracks tangle load is not established by this source. (LLM, conf=0.87)
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“This contrasts with a strong correlation of plasma and CSF t-tau concentration in Creutzfeldt-Jakob disease, in which the range of t-tau concentrations and species in plasma and CSF is higher than in AD or FTLD.40”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Partly supportedcites [40] 40. Staffaroni AM, Kramer AO, Casey M, et al. Association of blood and cerebrospinal fluid tau level and other biomarkers with survival time in sporadic Creutzfeldt-Jakob disease. JAMA Neurol 2019;76:969-977. sourceExperimental — accuracy not yet measured
The Baseline Characteristics section reports a strong correlation between plasma and CSF total tau in sporadic CJD (r = 0.74). The Discussion mentions greater serum tau elevations in CJD than in other neurodegenerative conditions, but it does not establish that concentration ranges in both fluids exceed those in AD or FTLD. Our copy does not compare tau species diversity across these diseases. Page numbers were not available in the indexed passages. (LLM, conf=0.88)
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Plasma biomarkers are powerful diagnostic and prognostic clinical tools. 1”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Abstract
What the sources say
- Partly supportedcites [1] 1. Lleo A, Irwin DJ, Illan-Gala I, et al. A 2-step cerebrospinal algorithm for the selection of frontotemporal lobar degeneration subtypes. JAMA Neurol 2018;75:738-745. sourceExperimental — accuracy not yet measured
The Biofluid Collection and Analysis and Discussion sections describe cerebrospinal fluid (CSF) biomarkers and their diagnostic use in distinguishing neurodegenerative pathologies. The Discussion also notes that CSF neurofilament light correlates with disease progression, but the paper does not establish that plasma biomarkers are diagnostic or prognostic clinical tools. Page numbers are unavailable in our copy. (LLM, conf=0.83)
boosted- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may be too vague to check against evidence. It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Plasma t-tau was weakly elevated and correlated with more severe longitudinal hypometabolism in patients with AD compared to controls.13”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Supportedcites [13] 13. Mattsson N, Zetterberg H, Janelidze S, et al. Plasma tau in Alzheimer disease. Neu- rology 2016;87:1827-1835. source
The Results section (“Plasma tau in different diagnostic groups”; page unavailable) reports higher plasma tau in patients with AD dementia than in cognitively normal controls. The Results section on brain metabolism reports that higher plasma tau was associated with greater longitudinal decline in FDG-PET, a measure of brain metabolism; the Discussion characterizes the associations as mild. (LLM, conf=0.88)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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Every source the paper cites for this claim was checked and supports it.
In the paper
“but the effect sizes were small, pathologic data were not available, and analyses for prediction of disease progression with clinical scales, neuropsychological testing, and survival were not conducted.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Supportedcites [38] 38. Foiani MS, Woollacott IO, Heller C, et al. Plasma tau is increased in frontotemporal dementia. J Neurol Neurosurg Psychiatry 2018;89:804-807. source
The Results report generally poor discrimination between patients and controls, and the Discussion notes extensive overlap in plasma tau levels, consistent with small effects. The Discussion calls for future studies with pathological confirmation; the Methods describe progression analyses using neurofilament light chain and brain atrophy, not clinical scales, neuropsychological tests, or survival. No page numbers are available in our copy. (LLM, conf=0.88)
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In acute conditions, like traumatic brain injury and hypoxic brain injury, plasma t-tau concentrations measured using the same technology as the one employed here increase rapidly and show an apparent half-life of around 10 hours, 41 which contrasts with the half-life of CSF t-tau, which is about 20 days.42”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Partly supportedcites [41] 41. Zetterberg H. Review: tau in biofluids: relation to pathology, imaging and clinical features. Neuropathol Appl Neurobiol 2017;43:194-199. sourceExperimental — accuracy not yet measured
The Plasma tau section reports rapid increases after hypoxic brain injury and concussion, and says tau’s half-life appears to be measured in hours in plasma versus weeks in CSF. It does not give the specific estimates of approximately 10 hours and 20 days. The section identifies Simoa as a blood-tau measurement platform, but does not establish that it is the same assay used by the citing authors. (LLM, conf=0.87)
- Not checked — no full text of the sourcecites [42] 42. Sato C, Barthélemy NR, Mawuenyega KG, et al. Tau kinetics in neurons and the human central nervous system. Neuron 2018;98:861-864. source
hedgeddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The combination of CSF t-tau and NfL discriminated between early onset AD and FTLD, 9 and both analytes may be useful for the diagnosis and prognosis of FTLD.1,[10][11][12]”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Abstract
What the sources say
- Partly supportedcites [1] 1. Lleo A, Irwin DJ, Illan-Gala I, et al. A 2-step cerebrospinal algorithm for the selection of frontotemporal lobar degeneration subtypes. JAMA Neurol 2018;75:738-745. sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) says NfL is elevated in FTD and correlates with disease progression, supporting its potential prognostic use, but cautions that it lacks disease specificity. The paper uses t-tau among biomarkers that help exclude AD in FTLD-related syndromes; it does not establish t-tau as a prognostic marker for FTLD. (LLM, conf=0.86)
- Partly supportedcites [10] 10. Irwin DJ, Lleo A, Xie SX, et al. Ante mortem cerebrospinal fluid tau levels correlate with postmortem tau pathology in frontotemporal lobar degeneration. Ann Neurol 2017;82:247-258. sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) reports possible diagnostic utility for a CSF p-tau-to-t-tau ratio in distinguishing FTLD subtypes, which offers limited support for a role for t-tau. The Results and Discussion assess diagnostic accuracy for p-tau, not t-tau alone. Our copy does not establish diagnostic or prognostic utility for NfL, or prognostic utility for t-tau. (LLM, conf=0.82)
- Partly supportedcites [11] 11. Grossman M, Elman L, McCluskey L, et al. Phosphorylated tau as a candidate bio- marker for amyotrophic lateral sclerosis. JAMA Neurol 2014;71:442-448. sourceExperimental — accuracy not yet measured
The Results (page unavailable) report that CSF t-tau distinguished ALS from a four-repeat-tau comparison group, which offers limited support for diagnostic usefulness within the FTLD spectrum. The paper does not evaluate NfL, and its Results state that CSF levels were not related to progression rate; it therefore does not support the claim that both analytes may aid FTLD diagnosis and prognosis. (LLM, conf=0.86)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“These results may be related to limitations of the methodology to measure plasma t-tau, and the measurement of phosphorylated species of tau may have better clinical performance, as suggested by recent studies.44”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Could not verifycites [44] 44. Blennow K, Chen C, Cicognola C, et al. Cerebrospinal fluid tau fragment correlates with tau PET: a candidate biomarker for tangle pathology. Brain 2020;143:650-660. sourceExperimental — accuracy not yet measured
The Introduction and CSF collection and biomarker analyses sections discuss assays for cerebrospinal-fluid tau, not plasma tau. The Discussion compares CSF tau measures with tau PET, but does not say that limitations in measuring plasma total tau explain its performance or that plasma phosphorylated tau has better clinical performance. Searches for plasma assay limitations and plasma p-tau found no passage addressing those claims; page numbers were unavailable in our copy. (LLM, conf=0.76)
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Could not verify
Every source the paper cites for this claim was checked and supports it.
In the paper
“This study also replicated the findings of previous investigations supporting that, in AD, high plasma NfL correlates with faster worsening in global cognition and faster atrophy rates.4,15”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Supportedcites [4] 4. Mattsson N, Andreasson U, Zetterberg H, Blennow K; for the Alzheimer's Disease Neuroimaging Initiative. Association of plasma neurofilament light with neuro- degeneration in patients with Alzheimer disease. JAMA Neurol 2017;74:557. source
The Results section (‘Plasma NFL and Cognition and Neuroimaging’; page not provided) reports that higher plasma NFL was associated over time with accelerated decline in cognitive measures, including MMSE and ADAS-COG 11, and in imaging measures of atrophy. The Discussion says these correlations were strongest in the MCI and AD dementia groups. (LLM, conf=0.93)
- Supportedcites [15] 15. Mattsson N, Cullen NC, Andreasson U, Zetterberg H, Blennow K. Association be- tween longitudinal plasma neurofilament light and neurodegeneration in patients with Alzheimer disease. JAMA Neurol 2019;76:791. source
The paper’s introduction states that plasma NfL levels in AD correlate with future atrophy and cognitive decline. The Discussion further reports that worsening cognition and atrophy correlated with increasing NfL in all diagnostic groups, with the strongest correlations in patients with mild cognitive impairment. (LLM, conf=0.90)
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.
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It may state two separate claims as one.
- 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
“Most pathology-confirmed FTLD cases had at least some degree of AD co-pathology, but this did not influence the performance of plasma t-tau or NfL.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
plain- Asserted: passes — The authors put it forward as true.
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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
“participants in the FTLD-S group without a mutation had similar plasma NfL concentrations (46.1 ± 23 pg/mL) compared to GRN (88.1 ± 60 pg/mL, p = 0.43) and MAPT (30.1 ± 17 pg/mL, p = 0.89) mutation carriers, but lower than those with a C9orf72 repeat expansion (88.1 ± 57, p = 0.049).”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Differences in Plasma t-Tau and NfL Concentrations by Clinical Group
plain- 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.
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
“In the whole sample, plasma NfL correlated with MMSE (r = -0.26,p < 0.001), the language and executive cognitive composites (r = -0.22 and r = -0.22,respectively, all p < 0.001), and CDR+NACC/FTLD-SB (r = 0.41, p < 0.001) scores.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Relationship Between Plasma Biomarkers, Age, and Clinical Measures
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.
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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
“The relationship between baseline NfL and worse disease severity was significant in all FTLD-S subgroups (except for nfvPPA and CBS) and both typical amnestic and nonamnestic AD presentations (supplementary table e-4, 10.5061/dryad.12jm63xvv).”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Relationship Between Baseline Plasma Biomarkers and Clinical Progression
plaincorrelational- Asserted: passes — The authors put it forward as true.
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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
“In FTLD-S, baseline plasma t-tau concentrations were associated with worse decline (3.7 points change in CDR+NACC/FTLD-SB score per log t-tau pg/mL increase per year, 95% CI 1.4 to 6.0, p = 0.006).”
- Also stated in: § Relationship Between Baseline Plasma Biomarkers and Clinical Progression · plain
“However, this effect was evident only in the bvFTD and PSP FTLD-S subgroups (3.6 points change in CDR+NACC/FTLD-SB, 95% CI 0. 1-7.1, p = 0.015 and 11.8 points change in CDR+NACC/FTLD-SB, 95% CI 0.3-23.3,p = 0.023) and was not observed in the AD-S group.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Relationship Between Baseline Plasma Biomarkers and Clinical Progression
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Also stated in: § Relationship Between Baseline Plasma Biomarkers and Clinical Progression · 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
“In contrast, plasma NfL showed strong correlations with cortical thickness in frontal regions in FTLD-S and the right lateral temporal lobe, right inferior parietal, and left superior frontal in the AD-S group (figure 4, E and F).”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Relationship Between Plasma Biomarkers and Cortical Thickness
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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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
“Neither plasma t-tau nor plasma NfL predicted survival in the AD-S group (table 2).”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Survival Analyses
plain- Asserted: passes — The authors put it forward as true.
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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
“Plasma NfL, but not plasma t-tau, predicted clinical decline and survival and correlated with regional cortical thickness in both FTLD-S and AD-S.”
- Also stated in: § Relationship Between Baseline Plasma Biomarkers and Clinical Progression · plain
“baseline plasma NfL concentrations related to faster annual worsening in both FTLD-S (2.4 point change per log NfL ng/mL increase per year, 95% CI 0.78-2.4,p < 0.001) and AD-S (4.6 points change per log NfL ng/mL increase per year, 95% CI 1.2-5.5, p = 0.002).”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Abstract
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Also stated in: § Relationship Between Baseline Plasma Biomarkers and Clinical Progression · 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
“In contrast, age and plasma NfL were moderately correlated in AD-S and HC (r = 0.51 and r = 0.63, respectively, all p < 0.001), but not in FTLD-S (r = 0.02, p = 0.79).”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Relationship Between Plasma Biomarkers, Age, and Clinical Measures
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.
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 final sample included 265 participants: 167 FTLD-S (43 bvFTD, 28 nfvPPA, 18 svPPA, 36 PSP, 32 CBS, and 10 ALS-FTD), 43 AD-S, and 55 HC.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Sample Composition and Demographics
plainn = 265- 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.
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Probably not a substantial 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
“As shown in table 2, in FTLD-S, only the clinical phenotype was independently associated with shorter survival, whereas in AD-S, only the CDR+NACC/FTLD-SB score was independently associated with shorter survival.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Survival Analyses
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.
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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
“Plasma t-tau | 0.80 (0.40-1.60) | 0.514 | 0.98 (0.12-7.71) | 0.984”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
plain- Asserted: passes — The authors put it forward as true.
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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
“but it is nonspecific and has weak discriminatory power between FTLD and AD or between FTLD clinical subtypes.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer 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.
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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
“We applied Cox regression analyses to estimate survival, controlling for age at diagnosis, sex, disease severity at symptom onset, and primary clinical phenotype (only in the FTLD-S group).”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Statistical 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.
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
“This may also explain the weak correlation of plasma and CSF t-tau and the poor diagnostic performance of plasma t-tau in chronic neurodegeneration.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer 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.
In the paper
“The combination of CSF t-tau and NfL discriminated between early onset AD and FTLD, 9 and both analytes may be useful for the diagnosis and prognosis of FTLD.1,[10][11][12]”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Abstract
What the sources say
- Not checked — no full text of the sourcecites [9] 9. Sjogren M, Rosengren L, Minthon L, Davidsson P, Blennow K, Wallin A. Cyto- skeleton proteins in CSF distinguish frontotemporal dementia from AD. Neurology 2000;54:1960-1964. source
plaincorrelational- 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
“Age at plasma sampling, education, MMSE, and CDR+NACC/FTLD-SB was similar in FTLD-S and AD-S.The HC group, however, was younger than both disease groups (table 1).”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Sample Composition and Demographics
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.
In the paper
“The microtubule-associated protein tau has been implicated in the pathophysiology of Alzheimer disease (AD) and frontotemporal lobar degeneration (FTLD) and can be measured in plasma with ultrasensitive immunoassays.2”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Abstract
What the sources say
- Not checked — no full text of the sourcecites [2] 2. Randall J, Mörtberg E, Provuncher GK, et al. Tau proteins in serum predict neuro- logical outcome after hypoxic brain injury from cardiac arrest: results of a pilot study. Resuscitation 2013;84:351-356. source
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.
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
“Fluid biomarker concentrations were log-transformed using the natural log to fulfill the normal distribution assumption.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Statistical 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.
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 participants gave their written informed consent to participate in the study.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Standard Protocol Approvals, Registrations, and Patient Consents
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.
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
“Plasma NfL is superior to plasma t-tau for the diagnosis and prediction of clinical progression of FTLD-S and AD-S.”
- Also stated in: § Discussion · plain
“The main findings of this study are that (1) only plasma NfL provided between-group clinical discrimination, predicted disease progression and survival, and correlated with neuroimage measures of neurodegeneration; and”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Abstract
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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It may state two separate claims as one.
- Also stated in: § Discussion · plain
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 study was approved by the UCSF Institutional Review Board and was conducted following the Declaration of Helsinki.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Standard Protocol Approvals, Registrations, and Patient Consents
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.
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
“Fifteen MRIs were excluded from final neuroimaging analyses: 8 because of low image quality (i.e., significant movement artifact) or preprocessing errors and 7 because they were performed in a different MRI scanner.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > MRI Acquisition and Preprocessing
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.
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
“Then, we studied the correlation between neuropsychology testing variables and plasma biomarkers with partial correlations adjusting for age and education, to account for the well-known effect of these variables on cognitive performance.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Statistical Analysis
boostedcorrelational- 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
“This may be related to differential expression of tau species in each compartment or different sensitivities of the techniques used for detection.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > 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. 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
“Clinical diagnosis was made by clinicians blinded to fluid biomarker results.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Study Participants
plain- Asserted: passes — The authors put it forward as true.
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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
“To study longitudinal changes in plasma biomarkers, we used linear mixed-effects models controlling for age, sex, CDR+NACC/FTLD-SB, and time between samples in the subset of participants with 2 plasma samples (n = 123, mean time between samples = 1.2 ± 0.4 years).”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Statistical Analysis
plainn = 123- Asserted: passes — The authors put it forward as true.
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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
“Of note, we checked that the assumption of proportionality of hazards was fulfilled.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > 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.
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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
“We studied a sizeable FTLD-S cohort with available pathologic data (i.e., 70 cases or 42% of the FTLD-S sample).”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
plainn = 70- 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.
It may state two separate claims as one.
- Rests on an assumption: The analyses of frontotemporal lobar degeneration pathologic subtypes assume that the 70 cases with available pathologic data are representative of the entire frontotemporal lobar degeneration syndrome cohort.
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
“and that plasma and CSF NfL may provide equivalent prognostic information, with the added value of plasma being more convenient for clinical use.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer 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
“Plasma t-tau may not be equivalent to other blood-based neurodegeneration biomarkers, which should be considered for the refinement of biomarker-based classification schemes.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
hedged- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“NfL has emerged as a nonspecific CSF and plasma biomarker of neuronal injury in degenerative and nondegenerative disorders.6”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Not checked — no full text of the sourcecites [6] 6. Bridel C, van Wieringen WN, Zetterberg H, et al. Diagnostic value of cerebrospinal fluid neurofilament light protein in neurology: a systematic review and meta-analysis. JAMA Neurol 2019;76:1035. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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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
“However, our results in the AD-S group should be interpreted cautiously due to its relatively small size and the lack of AD participants at the preclinical stage.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > 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. It may state two separate claims as one.
In the paper
“Our results, however, are in line with a recent European multicenter study of plasma NfL in genetic FTLD.50”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
What the sources say
- Not checked — no full text of the sourcecites [50] 50. van der Ende EL, Meeter LH, Poos JM, et al. Serum neurofilament light chain in genetic frontotemporal dementia: a longitudinal, multicentre cohort study. Lancet Neurol 2019;18:1103-1111. 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.
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 study is not representative of genetic FTLD forms, because it included only a small number of participants with genetic FTLD and did not include prodromal forms of disease.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > 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.
The paper relies on this without support.
Studies of plasma NfL and t-tau in pathology-confirmed FTLD and AD are scarce, and it is unknown whether their concentrations are affected by comorbid AD presenting in the context of primary FTLD pathology.
“Studies of plasma NfL and t-tau in pathology-confirmed FTLD and AD are scarce, and it is unknown if their concentrations are affected by comorbid AD presenting in the context of primary FTLD pathology.”
The paper relies on this without support.
The analyses of frontotemporal lobar degeneration pathologic subtypes assume that the 70 cases with available pathologic data are representative of the entire frontotemporal lobar degeneration syndrome cohort.
“We studied a sizeable FTLD-S cohort with available pathologic data (i.e., 70 cases or 42% of the FTLD-S sample).”
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
“NfL in CSF is elevated in frontotemporal lobar degeneration, but concentrations do not differentiate frontotemporal lobar degeneration from non-frontotemporal lobar degeneration pathology, nor do they distinguish the different protein opathies in frontotemporal lobar degeneration.47,49,50”
From Advances and controversies in frontotemporal dementia: diagnosis, biomarkers, and therapeutic considerations (2022) · cites this paper as [50]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“NfL concentrations in plasma correlate well with those in CSF.47,50”
From Advances and controversies in frontotemporal dementia: diagnosis, biomarkers, and therapeutic considerations (2022) · cites this paper as [50]
In the citing paper
“However, high levels of NfL are not specific to bvFTD as this biomarker can be strongly elevated in several other neurodegenerative conditions as well [2,40,41].”
In the citing paper
“Similar to what was observed in CSF, serum and plasma NfL are elevated in FTD compared to AD, but with limited utility in discriminating FTD from AD.”
From New developments of biofluid‐based biomarkers for routine diagnosis and disease trajectories in frontotemporal dementia (2022) · cites this paper as [87]
In the citing paper
“For example, higher levels of both CSF and plasma NfL have been observed in FTD‐TDP than in FTD‐tau cases, but with high within‐group variability.”
From New developments of biofluid‐based biomarkers for routine diagnosis and disease trajectories in frontotemporal dementia (2022) · cites this paper as [87]
In the citing paper
“Several studies have already indicated that baseline NfL concentrations in both CSF and blood could reflect the aggressiveness of the disease as it can predict rate of disease progression in the different clinicopathological phenotypes in both sporadic and familial FTD.”
From New developments of biofluid‐based biomarkers for routine diagnosis and disease trajectories in frontotemporal dementia (2022) · cites this paper as [87]
In the citing paper
“It appears to be more specific for AD pathology, at least compared to frontotemporal dementia and chronic traumatic encephalopathy (85, 91, 92), but it is increased in prion disease (83).”
From All the Tau We Cannot See (2023) · cites this paper as [92]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated major: it would touch a result — a value a result rests on, reported and recomputed p-values on opposite sides of the significance level, two passages that conflict with no sign which is right, or a cited work retracted before this paper was published.
In the paper
“Fifteen MRIs were excluded from final neuroimaging analyses: 8 because of low image quality (i.e., significant movement artifact) or preprocessing errors and 7 because they were performed in a different MRI scanner.The remaining 225 MRIs (160 FTLD-S, 29 AD-S, and 51 HC) were processed”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > MRI Acquisition and Preprocessing
Reported 225 · recomputed 240
Rated major: it would touch a result — a value a result rests on, reported and recomputed p-values on opposite sides of the significance level, two passages that conflict with no sign which is right, or a cited work retracted before this paper was published.
In the paper
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
“plasma levels of t-tau only predicted clinical decline in some clinical subgroups of FTLD-S (bvFTD and PSP) but not in the whole FTLD-S and AD-S groups.”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Relationship Between Baseline Plasma Biomarkers and Clinical Progression
“In FTLD-S, baseline plasma t-tau concentrations were associated with worse decline (3.7 points change in CDR+NACC/FTLD-SB score per log t-tau pg/mL increase per year, 95% CI 1.4 to 6.0, p = 0.006).”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Additional information
“High t-tau and high NfL represent levels superior to 2.2 ng/mL and 42 ng/mL, respectively (median split).”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
“t-Tau, pg/mL e , median (Q1, Q3) | 2.2 (1.8, 2.9) ns | 2.5 (1.9, 3.2) ns | 2.2 (1.8, 2.7) ns | p = 0.427”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Additional information
“High t-tau and high NfL represent levels superior to 2.2 ng/mL and 42 ng/mL, respectively (median split).”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Survival Analyses
“FTLD-S participants with high NfL concentrations (≥42 pg/mL) showed increased mortality compared to those with low concentrations (<42 pg/mL, log-rank 14.4, p < 0.001).”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Additional information
“High t-tau and high NfL represent levels superior to 2.2 ng/mL and 42 ng/mL, respectively (median split).”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > Discussion
“| t-Tau, pg/mL e , median (Q1, Q3) | 2.2 (1.8, 2.9) ns | 2.5 (1.9, 3.2) ns | 2.2 (1.8, 2.7) ns | p = 0.427 |”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
“The remaining 225 MRIs (160 FTLD-S, 29 AD-S, and 51 HC) were processed with the CAT12 toolbox”
§ Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease > MRI Acquisition and Preprocessing
Reported 225 · recomputed 240
Citations
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Metadata
- Authors
- Illán-Gala, I., Lleo, A., Karydas, A., Staffaroni, A. M., Zetterberg, H., Sivasankaran, R., Grinberg, L. T., Spina, S., Kramer, J. H., Ramos, E. M., Coppola, G., La Joie, R., Rabinovici, G. D., Perry, D. C., Gorno-Tempini, M. L., Seeley, W. W., Miller, B. L., Rosen, H. J., Blennow, K., Boxer, A. L., & Rojas, J. C.
- Affiliations
- From the Sant Pau Memory Unit, Department of Neurology (I.I.-G., A.L.), Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, Spain; Memory and Aging Center (A.K., A.M.S., L.T.G., S.S., J.H.K., R.L.J., G.D.R., D.C.P., M.L.G.-T., W.W.S., B.L.M., H.J.R., A.L.B., J.C.R.), Department of Neurology (I.I.-G.), University of California San Francisco; Department of Psychiatry and Neurochemistry (H.Z., K.B.), Institute of Neuroscience and Physiology,...
- Universitat Autònoma de Barcelona (ES)
- Venue
- Neurology
- Published
- 2021-02-02
- Volume
- 96
- Issue
- 5
- Pages
- e671-e683
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- PMC
- PMC7884995
- OpenAlex
- W3106237074
- Cited by
- 150
- References
- 56
- Citations by year
- 2026: 10 · 2025: 27 · 2024: 32 · 2023: 29 · 2022: 34 · 2021: 12
- FWCI
- 10.94
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- 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
- neurofilament light chain, frontotemporal lobar degeneration, Alzheimer's disease, FTLD-TDP, FTLD-tau, plasma biomarkers, Simoa, survival prediction
- MeSH terms
- Adult, Aged, Alzheimer Disease, Brain
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