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Role of Aβ in Alzheimer's-related synaptic dysfunction
Huiqin Zhang, Xuefan Jiang, Lina Ma, Wei Wei, Zehui Li, Surui Chang, Jiayu Wen, Jiahui Sun et al.. Frontiers in cell and developmental biology, 2022-08-26
Topic: Disease mechanisms in lab and animal studies
Synaptic dysfunction is closely related to Alzheimer's disease (AD) which is also recognized as synaptic disorder. β-amyloid (Aβ) is one of the main pathogenic factors in AD, which disrupts synaptic plasticity and mediates the synaptic toxicity through different mechanisms. Aβ disrupts glutamate receptors, such as NMDA and AMPA receptors, which mediates calcium dyshomeostasis and damages synapse plasticity characterized by long-term potentiation (LTP) suppression and long-term depression (LTD) enhancement. As Aβ stimulates and Ca2+ influx, microglial cells and astrocyte can be activated and release cytokines, which reduces glutamate uptake and further impair synapse function. Besides, extracellular glutamate accumulation induced by Aβ mediates synapse toxicity resulting from reduced glutamate receptors and glutamate spillovers. Aβ also mediates synaptic dysfunction by acting on various signaling pathways and molecular targets, disrupting mitochondria and energy metabolism. In addition, Aβ overdeposition aggravates the toxic damage of hyperphosphorylated tau to synapses. Synaptic dysfunction plays a critical role in cognitive impairment of AD. The review addresses the possible mechanisms by which Aβ mediates AD-related synaptic impairment from distant perspectives.
Key findings
- Besides, extracellular glutamate accumulation induced by Aβ mediates synapse toxicity resulting from reduced glutamate receptors and glutamate spillovers.
- Aβ also mediates synaptic dysfunction by acting on various signaling pathways and molecular targets, disrupting mitochondria and energy metabolism.
- In addition, Aβ overdeposition aggravates the toxic damage of hyperphosphorylated tau to synapses.
- Synaptic dysfunction plays a critical role in cognitive impairment of AD.
- The review addresses the possible mechanisms by which Aβ mediates AD-related synaptic impairment from distant perspectives.
Study details
- Evidence strengthLow
How this study scored 41/100
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 23 of the 56 points we could judge it on, which is 41 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Frontiers in cell and developmental biology) |
| 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 | 3 / 5 | 2022 — within 6 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 36092715) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 23 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 23 of the 56 points we could judge it on is 41 out of 100. |
| Total | 41 / 100 | — |
What each of these 20 components measures, and what this score is not →
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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APA 7th
Zhang, H., Jiang, X., Ma, L., Wei, W., Li, Z., Chang, S., et al. (2022). Role of Aβ in Alzheimer's-related synaptic dysfunction. Frontiers in cell and developmental biology. https://doi.org/10.3389/fcell.2022.964075
Vancouver
Zhang H, Jiang X, Ma L, Wei W, Li Z, Chang S, et al. Role of Aβ in Alzheimer's-related synaptic dysfunction. Frontiers in cell and developmental biology. 2022. doi:10.3389/fcell.2022.964075. PMID: 36092715.
BibTeX
@article{zhang2022-36092715,
author = {Zhang, Huiqin and Jiang, Xuefan and Ma, Lina and Wei, Wei and Li, Zehui and Chang, Surui and Wen, Jiayu and Sun, Jiahui and others},
title = {{Role of Aβ in Alzheimer's-related synaptic dysfunction}},
journal = {Frontiers in cell and developmental biology},
year = {2022},
doi = {10.3389/fcell.2022.964075},
pmid = {36092715},
url = {https://doi.org/10.3389/fcell.2022.964075}
}
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