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Modified Glutamatergic Postsynapse in Neurodegenerative Disorders
Bruno José Moraes, Patrícia Coelho, Lígia Fão, Ildete Luísa Ferreira, A Cristina Rego. Neuroscience, 2019-12-27
Topic: Disease mechanisms in lab and animal studies
The postsynaptic density (PSD) is a complex subcellular domain important for postsynaptic signaling, function, and plasticity. The PSD is present at excitatory synapses and specialized to allow for precise neuron-to-neuron transmission of information. The PSD is localized immediately underneath the postsynaptic membrane forming a major protein network that regulates postsynaptic signaling and synaptic plasticity. Glutamatergic synaptic dysfunction affecting PSD morphology and signaling events have been described in many neurodegenerative disorders, either sporadic or familial forms. Thus, in this review we describe the main protein players forming the PSD and their activity, as well as relevant modifications in key components of the postsynaptic architecture occurring in Huntington's, Parkinson's and Alzheimer's diseases.
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APA 7th
Moraes, B. J., Coelho, P., Fão, L., Ferreira, I. L., & Rego, A. C. (2021). Modified Glutamatergic Postsynapse in Neurodegenerative Disorders. Neuroscience. https://doi.org/10.1016/j.neuroscience.2019.12.002
Vancouver
Moraes BJ, Coelho P, Fão L, Ferreira IL, Rego AC. Modified Glutamatergic Postsynapse in Neurodegenerative Disorders. Neuroscience. 2021. doi:10.1016/j.neuroscience.2019.12.002. PMID: 31887357.
BibTeX
@article{moraes2021-31887357,
author = {Moraes, Bruno José and Coelho, Patrícia and Fão, Lígia and Ferreira, Ildete Luísa and Rego, A Cristina},
title = {{Modified Glutamatergic Postsynapse in Neurodegenerative Disorders}},
journal = {Neuroscience},
year = {2021},
doi = {10.1016/j.neuroscience.2019.12.002},
pmid = {31887357},
url = {https://doi.org/10.1016/j.neuroscience.2019.12.002}
}
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Key findings
- The postsynaptic density (PSD) is a complex subcellular domain important for postsynaptic signaling, function, and plasticity.
- The PSD is present at excitatory synapses and specialized to allow for precise neuron-to-neuron transmission of information.
- The PSD is localized immediately underneath the postsynaptic membrane forming a major protein network that regulates postsynaptic signaling and synaptic plasticity.
- Glutamatergic synaptic dysfunction affecting PSD morphology and signaling events have been described in many neurodegenerative disorders, either sporadic or familial forms.
- Thus, in this review we describe the main protein players forming the PSD and their activity, as well as relevant modifications in key components of the postsynaptic architecture occurring in Huntington's, Parkinson's and Alzheimer's diseases.
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 (Neuroscience) |
| 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 | 2021 — 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 31887357) |
| 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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