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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Digital health tools

Topic: Disease mechanisms in lab and animal studies

Neurodegenerative diseases, including Alzheimer's disease (AD), target specific and functionally connected neuronal networks, raising the possibility that neurodegeneration may spread through abnormal patterns of neural network activity. AD is associated with high levels of amyloid-beta (A beta) peptides in the brain, synaptic depression, aberrant excitatory neuronal activity, and cognitive decline. However, the relationships among these alterations and their underlying mechanisms are poorly understood. In experimental models of AD, high concentrations of pathogenic A beta assemblies reduce glutamatergic transmission and enhance long-term depression at the synaptic level. At the network level, they cause dysrhythmias, including neuronal synchronization, epileptiform activity, seizures, and postictal suppression. Both synaptic depression and aberrant network synchronization likely interfere with activity-dependent synaptic regulation, which is critical for learning and memory. Abnormal patterns of neuronal activity across functionally connected brain regions may also trigger and perpetuate trans-synaptic mechanisms of neurodegeneration. It remains to be determined if synaptic depression and network dysrhythmias are mechanistically related, which of them is primary or secondary, and whether normalization of one will prevent the other as well as cognitive dysfunction in AD.

Key findings

Study details

How this study scored 36/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record left out, no data; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 1 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited left out, no data; Citations per year left out, no data; Impact for its field and year left out, no data; Cited by studies here left out, no data; Still being cited left out, no data; Senior author's track record left out, no data; Institution's track record left out, no data; Multi-centre collaboration left out, no data; Indexed in PubMed 2 of 2; Free to read 0 of 2. 21 of the 58 points it could be judged on, which is 36 of 100. Total 36 of 100.21 of the 58 points we could judge = 36 of 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 and multi-centre collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Neuromolecular medicine)
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 1 / 5 2010 — within 20 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 19838821)
Free to read 0 / 2 Behind a paywall — scores zero
Points 21 / 58 Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100.
Total 36 / 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

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.

APA 7th

Palop, J. J., & Mucke, L. (2010). Synaptic depression and aberrant excitatory network activity in Alzheimer's disease: two faces of the same coin? Neuromolecular medicine. https://doi.org/10.1007/s12017-009-8097-7

Vancouver

Palop JJ, Mucke L. Synaptic depression and aberrant excitatory network activity in Alzheimer's disease: two faces of the same coin? Neuromolecular medicine. 2010. doi:10.1007/s12017-009-8097-7. PMID: 19838821.

BibTeX

@article{palop2010-19838821,
  author  = {Palop, J. J. and Mucke, L.},
  title   = {{Synaptic depression and aberrant excitatory network activity in Alzheimer's disease: two faces of the same coin?}},
  journal = {Neuromolecular medicine},
  year    = {2010},
  doi     = {10.1007/s12017-009-8097-7},
  pmid    = {19838821},
  url     = {https://doi.org/10.1007/s12017-009-8097-7}
}

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