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Evidence that iron accelerates Alzheimer's pathology: a CSF biomarker study
Scott Ayton, Ibrahima Diouf, Ashley Ian Bush, Alzheimer’s disease Neuroimaging Initiative. Journal of neurology, neurosurgery, and psychiatry, 2017-09-22
Topic: Plasma and spinal-fluid biomarkers
In subjects with biomarker-confirmed Alzheimer's pathology, high CSF ferritin (>6.2 ng/mL) was associated with accelerated depreciation of CSF Aβ1-42 (reporting increased plaque formation; p=0.0001). CSF ferritin was neither associated with changes in CSF tau in the same subjects, nor longitudinal changes in CSF tau or Aβ1-42 in subjects with low baseline pathology. In simulation modelling of the natural history of Aβ deposition, which we estimated to occur over 31.4 years, we predicted that it would take 12.6 years to reach the pathology threshold value of CSF Aβ from healthy normal levels, and this interval is not affected by CSF ferritin. CSF ferritin influences the fall in CSF Aβ over the next phase, where high CSF ferritin accelerated the transition from threshold preclinical Aβ levels to the average level of Alzheimer's subjects from 18.8 to 10.8 years. Iron might facilitate Aβ deposition in Alzheimer's and accelerate the disease process.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Ayton, S., Diouf, I., Bush, A. I., & Alzheimer’s disease Neuroimaging Initiative. (2018). Evidence that iron accelerates Alzheimer's pathology: a CSF biomarker study. Journal of neurology, neurosurgery, and psychiatry. https://doi.org/10.1136/jnnp-2017-316551
Vancouver
Ayton S, Diouf I, Bush AI, Alzheimer’s disease Neuroimaging Initiative. Evidence that iron accelerates Alzheimer's pathology: a CSF biomarker study. Journal of neurology, neurosurgery, and psychiatry. 2018. doi:10.1136/jnnp-2017-316551. PMID: 28939683.
BibTeX
@article{ayton2018-28939683,
author = {Ayton, Scott and Diouf, Ibrahima and Bush, Ashley Ian and {Alzheimer’s disease Neuroimaging Initiative}},
title = {{Evidence that iron accelerates Alzheimer's pathology: a CSF biomarker study}},
journal = {Journal of neurology, neurosurgery, and psychiatry},
year = {2018},
doi = {10.1136/jnnp-2017-316551},
pmid = {28939683},
url = {https://doi.org/10.1136/jnnp-2017-316551}
}
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Key findings
- In subjects with biomarker-confirmed Alzheimer's pathology, high CSF ferritin (>6.2 ng/mL) was associated with accelerated depreciation of CSF Aβ1-42 (reporting increased plaque formation; p=0.0001).
- CSF ferritin was neither associated with changes in CSF tau in the same subjects, nor longitudinal changes in CSF tau or Aβ1-42 in subjects with low baseline pathology.
- In simulation modelling of the natural history of Aβ deposition, which we estimated to occur over 31.4 years, we predicted that it would take 12.6 years to reach the pathology threshold value of CSF Aβ from healthy normal levels, and this interval is not affected by CSF ferritin.
- CSF ferritin influences the fall in CSF Aβ over the next phase, where high CSF ferritin accelerated the transition from threshold preclinical Aβ levels to the average level of Alzheimer's subjects from 18.8 to 10.8 years.
- Iron might facilitate Aβ deposition in Alzheimer's and accelerate the disease process.
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Study details
- Study designlongitudinal study
- Participants296
- Evidence strengthModerate
How this study scored 64/100
Published in a peer-reviewed journal, and it is a longitudinal study following the same people over time. Scored zero for effect reported and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record, multi-centre collaboration and free to read, so those were left out: it earned 36 of the 56 points we could judge it on, which is 64 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of neurology, neurosurgery, and psychiatry) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 7 / 12 | A longitudinal study following the same people over 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 | 2 / 5 | 2018 — within 10 year(s) of the newest study here |
| Sample size | 2 / 4 | 296 participants |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 28939683) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 36 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 36 of the 56 points we could judge it on is 64 out of 100. |
| Total | 64 / 100 | — |
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