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The arsenic exposure hypothesis for Alzheimer disease
Gong G, OʼBryant SE.. Alzheimer disease and associated disorders, 2010-10-01
Topic: Amyloid, tau and blood-test diagnosis
Prior research has shown that arsenic exposure induces changes that coincide with most of the developmental, biochemical, pathologic, and clinical features of Alzheimer disease (AD) and associated disorders. On the basis of this literature, we propose the Arsenic Exposure Hypothesis for AD that is inclusive of and cooperative with the existing hypotheses. Arsenic toxicity induces hyperphosphorylation of protein tau and overtranscription of the amyloid precursor protein, which are involved in the formation of neurofibrillary tangles and brain amyloid plaques, consistent with the amyloid hypothesis of AD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Gong, G., & OʼBryant, S. E. (2010). The arsenic exposure hypothesis for Alzheimer disease. Alzheimer disease and associated disorders. https://doi.org/10.1097/wad.0b013e3181d71bc7
Vancouver
Gong G, OʼBryant SE. The arsenic exposure hypothesis for Alzheimer disease. Alzheimer disease and associated disorders. 2010. doi:10.1097/wad.0b013e3181d71bc7. PMID: 20473132.
BibTeX
@article{gong2010-20473132,
author = {Gong, G. and OʼBryant, S. E.},
title = {{The arsenic exposure hypothesis for Alzheimer disease}},
journal = {Alzheimer disease and associated disorders},
year = {2010},
doi = {10.1097/wad.0b013e3181d71bc7},
pmid = {20473132},
url = {https://doi.org/10.1097/wad.0b013e3181d71bc7}
}
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Key findings
- On the basis of this literature, we propose the Arsenic Exposure Hypothesis for AD that is inclusive of and cooperative with the existing hypotheses.
- Arsenic toxicity induces hyperphosphorylation of protein tau and overtranscription of the amyloid precursor protein, which are involved in the formation of neurofibrillary tangles and brain amyloid plaques, consistent with the amyloid hypothesis of AD.
- Arsenic exposure has been associated with cardiovascular diseases and associated risk factors, which is in agreement with the vascular hypothesis of AD.
- Arsenic exposure invokes brain inflammatory responses, which resonates with the inflammatory hypotheses of AD.
Why it matters
This paper proposes the Arsenic Exposure Hypothesis for Alzheimer's disease, suggesting arsenic toxicity induces tau hyperphosphorylation and overtranscription of amyloid precursor protein. It is a hypothesis based on prior literature, not a clinical trial, so it does not show that reducing arsenic exposure treats, cures or prevents Alzheimer's disease.
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Study details
- Evidence strengthLow
How this study scored 38/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Alzheimer disease and associated disorders) |
| Journal's citation record | 1 / 4 | Alzheimer Disease & Associated Disorders: journal h-index 131 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2010 — 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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 117 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 6.5 citations a year over 18 year(s) since 2010 |
| Impact for its field and year | 3 / 6 | Cited 3.2× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 2 / 4 | Cited 17 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Sid E. O’Bryant: h-index 63 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Texas Tech University Health Sciences Center: institution h-index 356 (OpenAlex) |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 20473132) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 38 / 100 | — |
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