Evidence map›Paper›PMID 41021123›Full record

ReviewMetabolic brain disease2025

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

Abstract readReview
PubMed Publisher
In one paragraph

Review in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. The interactions of copper, glutamate, and cuproptosis: insights into brain health and Alzheimer's disease pathology.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Review
  7. Article
  8. [Fiber photometry-based analysis of transcranial magneto-acoustic electrical stimulation effects on synaptic plasticity in the hippocampal CA1 region of APP/PS1 mice].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2026
    Article
  9. Article
  10. Review
  11. Article
  12. Frontiers in pharmacology · 2026
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Rasoul EbrahimiSchool of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0009-0004-0991-7752
Zahra GolzariSchool of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0009-0004-1776-1401
Mahsa Heidari-ForoozanStudent Research Committee, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0000-0003-3969-8015
Abolfazl KhosraviSchool of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0009-0006-7608-2155
Samin Ghaheri SharghiSchool of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0009-0005-3669-8978
Mobina SalehStudents Research Committee, Shahrekord University of Medical Sciences, Shahrekord, Iran.ORCID 0009-0005-5865-2970
Shakiba SalarvandianNeuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0000-0002-8323-2717
Khadijeh EsmaeilpourDepartment of Psychology, University of Toronto Mississagua, Mississauga, ON, Canada. Kh.esmaeilpour@utoronto.ca.ORCID 0000-0002-5349-9285

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

Alzheimer DiseaseNeuronal PlasticityAmyloid beta-PeptidesAnimalsHippocampusHumansLong-Term PotentiationOxidative StressSynapsesAmyloid beta-PeptidesAlzheimer’s diseaseHippocampusLong-term potentiationSynaptic plasticity

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.