Home › Research › Inflammation and the immune system
Neuroinflammation induced by amyloid-forming pancreatic amylin: Rationale for a mechanistic hypothesis
Noah S Leibold, Florin Despa. Biophysical chemistry, 2024-04-22
Topic: Gut, metabolism and diet
Amylin is a systemic neuroendocrine hormone co-expressed and co-secreted with insulin by pancreatic β-cells. In persons with thype-2 diabetes, amylin forms pancreatic amyloid triggering inflammasome and interleukin-1β signaling and inducing β-cell apoptosis. Here, we summarize recent progress in understanding the potential link between amyloid-forming pancreatic amylin and Alzheimer's disease (AD). Clinical data describing amylin pathology in AD alongside mechanistic studies in animals are reviewed. Data from multiple research teams indicate higher amylin concentrations are associated with increased frequency of cognitive impairment and amylin co-aggregates with β-amyloid in AD-type dementia. Evidence from rodent models further suggests cerebrovascular amylin accumulation as a causative factor underlying neurological deficits. Analysis of relevant literature suggests that modulating the amylin-interleukin-1β pathway may provide an approach for counteracting neuroinflammation in AD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Leibold, N. S., & Despa, F. (2024). Neuroinflammation induced by amyloid-forming pancreatic amylin: Rationale for a mechanistic hypothesis. Biophysical chemistry. https://doi.org/10.1016/j.bpc.2024.107252
Vancouver
Leibold NS, Despa F. Neuroinflammation induced by amyloid-forming pancreatic amylin: Rationale for a mechanistic hypothesis. Biophysical chemistry. 2024. doi:10.1016/j.bpc.2024.107252. PMID: 38663120.
BibTeX
@article{leibold2024-38663120,
author = {Leibold, Noah S and Despa, Florin},
title = {{Neuroinflammation induced by amyloid-forming pancreatic amylin: Rationale for a mechanistic hypothesis}},
journal = {Biophysical chemistry},
year = {2024},
doi = {10.1016/j.bpc.2024.107252},
pmid = {38663120},
url = {https://doi.org/10.1016/j.bpc.2024.107252}
}
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
- Data from multiple research teams indicate higher amylin concentrations are associated with increased frequency of cognitive impairment and amylin co-aggregates with β-amyloid in AD-type dementia.
- Analysis of relevant literature suggests that modulating the amylin-interleukin-1β pathway may provide an approach for counteracting neuroinflammation in AD.
Study details
- Evidence strengthLow
How this study scored 43/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / 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, multicenter collaboration and free to read, so those were left out: it earned 24 of the 56 points we could judge it on, which is 43 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Biophysical chemistry) |
| 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 | 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 | 4 / 5 | 2024 — within 3 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 | — / 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 |
| Multicenter collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 38663120) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 24 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 24 of the 56 points we could judge it on is 43 out of 100. |
| Total | 43 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
Free copy unknown: no free-copy check has an answer for this record yet. That does not mean it is paywalled.
Related
Studies in the library that share something with this one. The line above each title says what.
Related studies in Inflammation and the immune system
Also tagged “peptide-1”
285 studies in the library carry the topic tag “peptide-1”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 285 tagged studies.