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Impaired Synaptic Plasticity Mechanisms in Alzheimer's Disease
Rasoul Ebrahimi, Zahra Golzari, Mahsa Heidari-Foroozan, Abolfazl Khosravi, Samin Ghaheri Sharghi, Mobina Saleh, Shakiba Salarvandian, Khadijeh Esmaeilpour. Metabolic brain disease, 2025-09-29
Topic: Disease mechanisms in lab and animal studies
Alzheimer's disease (AD) is the most common form of dementia, characterized by progressive cognitive decline driven by a complex interplay of genetic, environmental, and lifestyle factors. Increasing evidence highlights impaired synaptic plasticity as a major contributor to early cognitive deficits, often preceding neuronal loss. In particular, disruption of long-term potentiation (LTP) within the hippocampus, a region essential for learning and memory, plays a central role. Accumulation of amyloid β (Aβ) plaques and hyperphosphorylated tau proteins compromises synaptic integrity, leading to reduced synaptic density and altered protein expression critical for excitatory signaling. Additional mechanisms, including microglial activation and mitochondrial dysfunction, further aggravate synaptic impairment through inflammation and oxidative stress. Understanding these interconnected molecular and cellular disruptions offers crucial insight into the pathways underlying synaptic dysfunction in AD. By elucidating these mechanisms, future research can inform novel therapeutic strategies aimed at preserving synaptic function and slowing disease progression.
Key findings
- In particular, disruption of long-term potentiation (LTP) within the hippocampus, a region essential for learning and memory, plays a central role.
- Accumulation of amyloid β (Aβ) plaques and hyperphosphorylated tau proteins compromises synaptic integrity, leading to reduced synaptic density and altered protein expression critical for excitatory signaling.
- Additional mechanisms, including microglial activation and mitochondrial dysfunction, further aggravate synaptic impairment through inflammation and oxidative stress.
- Understanding these interconnected molecular and cellular disruptions offers crucial insight into the pathways underlying synaptic dysfunction in AD.
- By elucidating these mechanisms, future research can inform novel therapeutic strategies aimed at preserving synaptic function and slowing disease progression.
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 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 (Metabolic brain disease) |
| 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 | 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 | — / 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 41021123) |
| 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
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 8 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
APA 7th
Ebrahimi, R., Golzari, Z., Heidari-Foroozan, M., Khosravi, A., Sharghi, S. G., Saleh, M., et al. (2025). Impaired Synaptic Plasticity Mechanisms in Alzheimer's Disease. Metabolic brain disease. https://doi.org/10.1007/s11011-025-01712-9
Vancouver
Ebrahimi R, Golzari Z, Heidari-Foroozan M, Khosravi A, Sharghi SG, Saleh M, et al. Impaired Synaptic Plasticity Mechanisms in Alzheimer's Disease. Metabolic brain disease. 2025. doi:10.1007/s11011-025-01712-9. PMID: 41021123.
BibTeX
@article{ebrahimi2025-41021123,
author = {Ebrahimi, Rasoul and Golzari, Zahra and Heidari-Foroozan, Mahsa and Khosravi, Abolfazl and Sharghi, Samin Ghaheri and Saleh, Mobina and Salarvandian, Shakiba and Esmaeilpour, Khadijeh},
title = {{Impaired Synaptic Plasticity Mechanisms in Alzheimer's Disease}},
journal = {Metabolic brain disease},
year = {2025},
doi = {10.1007/s11011-025-01712-9},
pmid = {41021123},
url = {https://doi.org/10.1007/s11011-025-01712-9}
}
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