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Alzheimer's Disease is Type 3 Diabetes-Evidence Reviewed
de la Monte SM, Wands JR. Journal of Diabetes Science and Technology, 2008-11
Topic: Amyloid, tau and blood-test diagnosis
This influential review article proposed that Alzheimer's disease could be considered a brain-specific form of diabetes, arguing that impaired insulin and insulin-like growth factor signaling in the brain drives amyloid buildup, tau tangles, oxidative stress, and energy failure - the hallmark features of Alzheimer's - and coined the term 'type 3 diabetes' for this concept.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
de la Monte, S. M., & Wands, JR. (2008). Alzheimer's Disease is Type 3 Diabetes-Evidence Reviewed. Journal of Diabetes Science and Technology. https://doi.org/10.1177/193229680800200619
Vancouver
de la Monte SM, Wands JR. Alzheimer's Disease is Type 3 Diabetes-Evidence Reviewed. Journal of Diabetes Science and Technology. 2008. doi:10.1177/193229680800200619. PMID: 19885299.
BibTeX
@article{delamonte2008-6d507843,
author = {de la Monte, S. M. and Wands, JR.},
title = {{Alzheimer's Disease is Type 3 Diabetes-Evidence Reviewed}},
journal = {Journal of Diabetes Science and Technology},
year = {2008},
doi = {10.1177/193229680800200619},
pmid = {19885299},
url = {https://doi.org/10.1177/193229680800200619}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- Reviews evidence that brain insulin/IGF-1 signaling is impaired early in Alzheimer's disease, before major clinical symptoms
- Argues that this brain insulin resistance can drive amyloid-beta accumulation, tau hyperphosphorylation, oxidative stress, and mitochondrial dysfunction
- Notes that experimentally inducing brain insulin resistance in animals (e.g., via streptozotocin) produces Alzheimer's-like brain changes
- Proposes the term 'type 3 diabetes' to describe Alzheimer's disease as a brain-selective, insulin-resistant condition distinct from but related to type 1 and type 2 diabetes
Why it matters
This review proposed that impaired brain insulin and IGF-1 signaling drives the hallmark features of Alzheimer's and coined the term 'type 3 diabetes' for the concept. It is a hypothesis-generating review, not a clinical trial, so it does not show that treating insulin resistance prevents or cures Alzheimer's.
Study details
- Evidence strengthPreliminary
Limitations
This is a narrative review/hypothesis paper synthesizing prior data, not a new empirical study with its own population or effect size; the 'type 3 diabetes' framing remains debated and is not an accepted clinical diagnostic category.
How this study scored 32/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people, randomised / blinded and indexed in PubMed 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, 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 20 of the 62 points we could judge it on, which is 32 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of Diabetes Science and Technology) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 2 / 5 | Rated “preliminary” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2008 — 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 | — / 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 | 0 / 6 | No other study in this library cites it |
| 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 | 0 / 2 | No PubMed ID and no DOI — scores zero (not stated in the record — scored 0) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 20 / 62 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 20 of the 62 points we could judge it on is 32 out of 100. |
| Total | 32 / 100 | — |
What each of these 20 components measures, and what this score is not →
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