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Adiponectin Receptor Agonist Ameliorates Synaptic Dysfunction in 3xTg Alzheimer's Disease Mouse Model by Activation of AMPK
Jenna Bloemer, Priyanka D Pinky, Vishnu Suppiramaniam, Miranda N Reed. CNS neuroscience & therapeutics, 2025-09
Topic: Gut, metabolism and diet
Incubation of hippocampal slices with AdipoRon ameliorated long-term potentiation (LTP) and basal synaptic transmission deficits in 3xTg-AD mice. AdipoRon was unable to restore these parameters in the presence of the AMPK inhibitor, Compound C. AdipoRon altered presynaptic parameters by a mechanism that did not appear to be solely dependent on AMPK. AdipoRon slice incubation was associated with activation of AMPK, inhibition of GSK3β, and altered glutamatergic receptor subunit phosphorylation based on Western blot analysis. Activation of adiponectin receptors restores synaptic function in an AD model in part through AMPK signaling. These results warrant further investigation into adiponectin receptor agonists as a novel approach for AD prevention or treatment.
Key findings
- Incubation of hippocampal slices with AdipoRon ameliorated long-term potentiation (LTP) and basal synaptic transmission deficits in 3xTg-AD mice.
- AdipoRon was unable to restore these parameters in the presence of the AMPK inhibitor, Compound C.
- AdipoRon altered presynaptic parameters by a mechanism that did not appear to be solely dependent on AMPK.
- AdipoRon slice incubation was associated with activation of AMPK, inhibition of GSK3β, and altered glutamatergic receptor subunit phosphorylation based on Western blot analysis.
- Activation of adiponectin receptors restores synaptic function in an AD model in part through AMPK signaling.
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 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 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 (CNS neuroscience & therapeutics) |
| 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 | 2025 — 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 | Laboratory or animal study (title names “3xtg”) — scores zero |
| 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 40984655) |
| 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 →
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APA 7th
Bloemer, J., Pinky, P. D., Suppiramaniam, V., & Reed, M. N. (2025). Adiponectin Receptor Agonist Ameliorates Synaptic Dysfunction in 3xTg Alzheimer's Disease Mouse Model by Activation of AMPK. CNS neuroscience & therapeutics. https://doi.org/10.1111/cns.70616
Vancouver
Bloemer J, Pinky PD, Suppiramaniam V, Reed MN. Adiponectin Receptor Agonist Ameliorates Synaptic Dysfunction in 3xTg Alzheimer's Disease Mouse Model by Activation of AMPK. CNS neuroscience & therapeutics. 2025. doi:10.1111/cns.70616. PMID: 40984655.
BibTeX
@article{bloemer2025-40984655,
author = {Bloemer, Jenna and Pinky, Priyanka D and Suppiramaniam, Vishnu and Reed, Miranda N},
title = {{Adiponectin Receptor Agonist Ameliorates Synaptic Dysfunction in 3xTg Alzheimer's Disease Mouse Model by Activation of AMPK}},
journal = {CNS neuroscience \& therapeutics},
year = {2025},
doi = {10.1111/cns.70616},
pmid = {40984655},
url = {https://doi.org/10.1111/cns.70616}
}