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38/100

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Disease mechanisms

Topic: Disease mechanisms in lab and animal studies

Plain-language summary

Dose-dependent decrease of Aβ40 levels in vivo confirmed suppression of BACE1 activity by both inhibitors. Prolonged treatment caused a reduction in spine formation of layer V pyramidal neurons, which recovered after withdrawal of inhibitors. Congruently, the rate of spontaneous and miniature excitatory postsynaptic currents in pyramidal neurons and hippocampal long-term potentiation were reduced in animals treated with BACE1 inhibitors. These effects were not detected in Bace1(-/-) mice treated with SCH1682496, confirming BACE1 as the pharmacological target. Described structural and functional changes were associated with cognitive deficits as revealed in behavioral tests. Our findings indicate important functions to BACE1 in structural and functional synaptic plasticity in the mature brain, with implications for cognition.

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

APA 7th

Filser, S., Ovsepian, S. V., Masana, M., Blazquez-Llorca, L., Elvang, A. B., Volbracht, C., et al. (2015). Pharmacological inhibition of BACE1 impairs synaptic plasticity and cognitive functions. Biological psychiatry. https://doi.org/10.1016/j.biopsych.2014.10.013

Vancouver

Filser S, Ovsepian SV, Masana M, Blazquez-Llorca L, Elvang AB, Volbracht C, et al. Pharmacological inhibition of BACE1 impairs synaptic plasticity and cognitive functions. Biological psychiatry. 2015. doi:10.1016/j.biopsych.2014.10.013. PMID: 25599931.

BibTeX

@article{filser2015-25599931,
  author  = {Filser, Severin and Ovsepian, Saak V and Masana, Mercè and Blazquez-Llorca, Lidia and Elvang, Anders Brandt and Volbracht, Christiane and Müller, Marianne B and Jung, Christian K E and others},
  title   = {{Pharmacological inhibition of BACE1 impairs synaptic plasticity and cognitive functions}},
  journal = {Biological psychiatry},
  year    = {2015},
  doi     = {10.1016/j.biopsych.2014.10.013},
  pmid    = {25599931},
  url     = {https://doi.org/10.1016/j.biopsych.2014.10.013}
}

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How to read this study

Design: our record does not state a study design, so check the methods section of the original before weighing the result.
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Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

Dose-dependent decrease of Aβ40 levels in vivo confirmed suppression of BACE1 activity by both inhibitors.
Prolonged treatment caused a reduction in spine formation of layer V pyramidal neurons, which recovered after withdrawal of inhibitors.
Congruently, the rate of spontaneous and miniature excitatory postsynaptic currents in pyramidal neurons and hippocampal long-term potentiation were reduced in animals treated with BACE1 inhibitors.
These effects were not detected in Bace1(-/-) mice treated with SCH1682496, confirming BACE1 as the pharmacological target.
Described structural and functional changes were associated with cognitive deficits as revealed in behavioral tests.

Study details

Evidence strengthLow

How this study scored 38/100

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 21 of the 56 points we could judge it on, which is 38 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Biological psychiatry)
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	2015 — 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)
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 25599931)
Free to read	— / 2	Access not recorded — left out of this score
Points	21 / 56	Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 21 of the 56 points we could judge it on is 38 out of 100.
Total	38 / 100	—

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