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60/100

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Brain scans and imaging

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

Clinicopathological evidence suggests that the pathology of Alzheimer's disease (AD) begins many years before the appearance of cognitive symptoms. Biomarkers are required to identify affected individuals during this asymptomatic ("preclinical") stage to permit intervention with potential disease-modifying therapies designed to preserve normal brain function. Studies of families with autosomal-dominant AD (ADAD) mutations provide a unique and powerful means to investigate AD biomarker changes during the asymptomatic period. In this biomarker study, we collected cerebrospinal fluid (CSF), plasma, and in vivo amyloid imaging cross-sectional data at baseline in individuals from ADAD families enrolled in the Dominantly Inherited Alzheimer Network. Our study revealed reduced concentrations of CSF amyloid-β1-42 (Aβ1-42) associated with the presence of Aβ plaques, and elevated concentrations of CSF tau, ptau181 (phosphorylated tau181), and VILIP-1 (visinin-like protein-1), markers of neurofibrillary tangles and neuronal injury/death, in asymptomatic mutation carriers 10 to 20 years before their estimated age at symptom onset (EAO) and before the detection of cognitive deficits. When compared longitudinally, however, the concentrations of CSF biomarkers of neuronal injury/death within individuals decreased after their EAO, suggesting a slowing of acute neurodegenerative processes with symptomatic disease progression. These results emphasize the importance of longitudinal, within-person assessment when modeling biomarker trajectories across the course of the disease. If corroborated, this pattern may influence the definition of a positive neurodegenerative biomarker outcome in clinical trials.

What this study adds

Evidence grade: Moderate

This is a cross-sectional study. In families carrying inherited Alzheimer's mutations, people with no symptoms already had lower spinal-fluid amyloid-β1-42 and higher tau, ptau181 and VILIP-1 about 10 to 20 years before the age their symptoms were expected to begin. When the same people were followed over time, spinal-fluid markers of nerve-cell injury fell after that expected onset age, which the authors suggest may reflect a slowing of acute damage as the disease progresses and say needs to be corroborated.

Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Fagan, A. M., Xiong, C., Jasielec, M. S., Bateman, R. J., Goate, A. M., Benzinger, T. L., et al. (2014). Longitudinal change in CSF biomarkers in autosomal-dominant Alzheimer's disease. Science translational medicine. https://doi.org/10.1126/scitranslmed.3007901

Vancouver

Fagan AM, Xiong C, Jasielec MS, Bateman RJ, Goate AM, Benzinger TL, et al. Longitudinal change in CSF biomarkers in autosomal-dominant Alzheimer's disease. Science translational medicine. 2014. doi:10.1126/scitranslmed.3007901. PMID: 24598588.

BibTeX

@article{fagan2014-24598588,
  author  = {Fagan, A. M. and Xiong, C. and Jasielec, M. S. and Bateman, R. J. and Goate, A. M. and Benzinger, T. L. and Ghetti, B. and Martins, R. N. and others},
  title   = {{Longitudinal change in CSF biomarkers in autosomal-dominant Alzheimer's disease}},
  journal = {Science translational medicine},
  year    = {2014},
  doi     = {10.1126/scitranslmed.3007901},
  pmid    = {24598588},
  url     = {https://doi.org/10.1126/scitranslmed.3007901}
}

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How to read this study

Design: this is a cross-sectional study. Everyone is measured once, so it cannot show which came first. Read it as a snapshot of how two things go together at one moment.
Size: the record gives no participant count. Look for one in the original before trusting a pattern.
Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded moderate. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Moderate means the abstract mentions a cohort, case-control or longitudinal design. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

Clinicopathological evidence suggests that the pathology of Alzheimer's disease (AD) begins many years before the appearance of cognitive symptoms.
Our study revealed reduced concentrations of CSF amyloid-β1-42 (Aβ1-42) associated with the presence of Aβ plaques, and elevated concentrations of CSF tau, ptau181 (phosphorylated tau181), and VILIP-1 (visinin-like protein-1), markers of neurofibrillary tangles and neuronal injury/death, in asymptomatic mutation carriers 10 to 20 years before their estimated age at symptom onset (EAO) and before the detection of cognitive deficits.
These results emphasize the importance of longitudinal, within-person assessment when modeling biomarker trajectories across the course of the disease.

Why it matters

In families carrying inherited Alzheimer's mutations, people with no symptoms already had lower spinal-fluid amyloid-β1-42 and higher tau, ptau181 and VILIP-1 about 10 to 20 years before the age their symptoms were expected to begin. When the same people were followed over time, spinal-fluid markers of nerve-cell injury fell after that expected onset age, which the authors suggest may reflect a slowing of acute damage as the disease progresses and say needs to be corroborated. The study shows why biomarkers should be tracked within the same person over time; it did not test any treatment and does not show that one works.

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Study details

Study designcross-sectional
Evidence strengthModerate

How this study scored 60/100

Published in a peer-reviewed journal, and it is a snapshot of people at one point in time. Scored zero for sample size, effect reported, studied in people and randomized / blinded because the record does not state it. We have no data on senior author's track record, so that was left out: it earned 58 of the 96 points we could judge it on, which is 60 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Science translational medicine)
Journal's citation record	3 / 4	Science Translational Medicine: journal h-index 365 (OpenAlex, 2026-10-29)
Study design	4 / 12	A snapshot of people at one point in time
Strength of evidence	3 / 5	Rated “moderate” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	1 / 5	2014 — within 20 year(s) of the newest study here
Sample size	0 / 4	Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	0 / 3	Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	6 / 7	Cited 434 times (OpenAlex, 2026-10-10)
Citations per year	4 / 5	31.0 citations a year over 14 year(s) since 2014
Impact for its field and year	5 / 6	Cited 23.6× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	4 / 6	Cited by 54 other studies in this library
Still being cited	3 / 4	Cited 59 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	— / 4	Senior author's record not available — left out of this score
Institution's track record	3 / 3	Harvard University: institution h-index 3,235 (OpenAlex)
Multicenter collaboration	3 / 3	OpenAlex lists 15 institution(s) in 3 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 24598588)
Free to read	0 / 2	Behind a paywall — scores zero
Points	58 / 96	Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 58 of the 96 points we could judge it on is 60 out of 100.
Total	60 / 100	—

What each of these 20 components measures, and what this score is not →

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