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.

39/100

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Disease mechanisms

Topic: Disease mechanisms in lab and animal studies

Dendrites and dendritic spines are dynamic structures with pivotal roles in brain connectivity and have been recognized as the locus of long-term synaptic plasticity related to cognitive processes such as learning and memory. In neurodegenerative diseases, the spine dynamic morphology alteration, such as shape and spine density, affects functional characteristics leading to synaptic dysfunction and cognitive impairment. Recent evidence implicates dendritic spine dysfunction as a critical feature in the pathogenesis of dementia, particularly Alzheimer's disease. The alteration of spine morphology and their loss is correlated with the cognitive decline in Alzheimer's disease patients even in the absence of neuronal loss, however, the underlying mechanisms are poorly understood. Currently, the microRNAs have emerged as essential regulators of synaptic plasticity. The changes in neuronal microRNA expression that contribute to the modification of synaptic function through the modulation of dendritic spine morphology or by regulating the local protein translation to synaptic transmission are determinant for synapse formation and synaptic plasticity. Focusing on microRNA and its targets may provide insight into new therapeutic opportunities. In this review we summarize the experimental evidence of the role that the microRNA plays in dendritic spine remodeling and synaptic plasticity and its potential therapeutic approach in Alzheimer's disease. Targeting synaptic deficits through the structural alteration of dendritic spines could form part of therapeutic strategies to improve synaptic plasticity and to ameliorate cognitive impairments in Alzheimer's disease and other neurological diseases.

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

APA 7th

Reza-Zaldivar, E. E., Hernández-Sápiens, M. A., Minjarez, B., Gómez-Pinedo, U., Sánchez-González, V. J., Márquez-Aguirre, A. L., et al. (2020). Dendritic Spine and Synaptic Plasticity in Alzheimer's Disease: A Focus on MicroRNA. Frontiers in cell and developmental biology. https://doi.org/10.3389/fcell.2020.00255

Vancouver

Reza-Zaldivar EE, Hernández-Sápiens MA, Minjarez B, Gómez-Pinedo U, Sánchez-González VJ, Márquez-Aguirre AL, et al. Dendritic Spine and Synaptic Plasticity in Alzheimer's Disease: A Focus on MicroRNA. Frontiers in cell and developmental biology. 2020. doi:10.3389/fcell.2020.00255. PMID: 32432108.

BibTeX

@article{rezazaldivar2020-32432108,
  author  = {Reza-Zaldivar, Edwin Estefan and Hernández-Sápiens, Mercedes Azucena and Minjarez, Benito and Gómez-Pinedo, Ulises and Sánchez-González, Victor Javier and Márquez-Aguirre, Ana Laura and Canales-Aguirre, Alejandro Arturo},
  title   = {{Dendritic Spine and Synaptic Plasticity in Alzheimer's Disease: A Focus on MicroRNA}},
  journal = {Frontiers in cell and developmental biology},
  year    = {2020},
  doi     = {10.3389/fcell.2020.00255},
  pmid    = {32432108},
  url     = {https://doi.org/10.3389/fcell.2020.00255}
}

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 names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.

Key findings

Currently, the microRNAs have emerged as essential regulators of synaptic plasticity.
The changes in neuronal microRNA expression that contribute to the modification of synaptic function through the modulation of dendritic spine morphology or by regulating the local protein translation to synaptic transmission are determinant for synapse formation and synaptic plasticity.
Focusing on microRNA and its targets may provide insight into new therapeutic opportunities.
In this review we summarize the experimental evidence of the role that the microRNA plays in dendritic spine remodeling and synaptic plasticity and its potential therapeutic approach in Alzheimer's disease.
Targeting synaptic deficits through the structural alteration of dendritic spines could form part of therapeutic strategies to improve synaptic plasticity and to ameliorate cognitive impairments in Alzheimer's disease and other neurological diseases.

Study details

Evidence strengthLow

How this study scored 39/100

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 22 of the 56 points we could judge it on, which is 39 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	2 / 5	2020 — within 10 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 32432108)
Free to read	— / 2	Access not recorded — left out of this score
Points	22 / 56	Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 22 of the 56 points we could judge it on is 39 out of 100.
Total	39 / 100	—

What each of these 20 components measures, and what this score is not →

Read the original

Free copy unknown: no free-copy check has an answer for this record yet. That does not mean it is paywalled.

Related studies in Disease mechanisms

Also tagged “dendritic”

287 studies in the library carry the topic tag “dendritic”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 287 tagged studies.

Similar studies

More on Disease mechanisms

See all studies in Disease mechanisms →