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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 41 out of 100. Risk genes beyond APOE

Topic: Disease mechanisms in lab and animal studies

Alzheimer's disease (AD) is the most frequent cause of dementia in the elderly. Few cases are familial (FAD), due to autosomal dominant mutations in presenilin-1 (PS1), presenilin-2 (PS2) or amyloid precursor protein (APP). The three proteins are involved in the generation of amyloid-beta (Aβ) peptides, providing genetic support to the hypothesis of Aβ pathogenicity. However, clinical trials focused on the Aβ pathway failed in their attempt to modify disease progression, suggesting the existence of additional pathogenic mechanisms. Ca2+ dysregulation is a feature of cerebral aging, with an increased frequency and anticipated age of onset in several forms of neurodegeneration, including AD. Interestingly, FAD-linked PS1 and PS2 mutants alter multiple key cellular pathways, including Ca2+ signaling. By generating novel tools for measuring Ca2+ in living cells, and combining different approaches, we showed that FAD-linked PS2 mutants significantly alter cell Ca2+ signaling and brain network activity, as summarized below.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Pendin, D., Fasolato, C., Basso, E., Filadi, R., Greotti, E., Galla, L., et al. (2021). Familial Alzheimer's disease presenilin-2 mutants affect Ca2+ homeostasis and brain network excitability. Aging clinical and experimental research. https://doi.org/10.1007/s40520-019-01341-0

Vancouver

Pendin D, Fasolato C, Basso E, Filadi R, Greotti E, Galla L, et al. Familial Alzheimer's disease presenilin-2 mutants affect Ca2+ homeostasis and brain network excitability. Aging clinical and experimental research. 2021. doi:10.1007/s40520-019-01341-0. PMID: 31606858.

BibTeX

@article{pendin2021-31606858,
  author  = {Pendin, Diana and Fasolato, Cristina and Basso, Emy and Filadi, Riccardo and Greotti, Elisa and Galla, Luisa and Gomiero, Chiara and Leparulo, Alessandro and others},
  title   = {{Familial Alzheimer's disease presenilin-2 mutants affect Ca2+ homeostasis and brain network excitability}},
  journal = {Aging clinical and experimental research},
  year    = {2021},
  doi     = {10.1007/s40520-019-01341-0},
  pmid    = {31606858},
  url     = {https://doi.org/10.1007/s40520-019-01341-0}
}

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's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.

Key findings

Study details

How this study scored 41/100
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 3 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomized / 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; Multicenter collaboration left out, no data; Indexed in PubMed 2 of 2; Free to read left out, no data. 23 of the 56 points it could be judged on, which is 41 of 100. Total 41 of 100.23 of the 56 points we could judge = 41 of 100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / 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, multicenter 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.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Aging clinical and experimental research)
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)
Randomized / blinded 0 / 2 No randomization 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
Multicenter collaboration — / 3 Institutions not listed — left out of this score
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 31606858)
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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