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.

54/100

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Lewy body dementia

Topic: Brain proteins, microglia and lab models

Disorders characterized by α-synuclein (α-syn) accumulation, Lewy body formation and parkinsonism (and in some cases dementia) are collectively known as Lewy body diseases. The molecular mechanism (or mechanisms) through which α-syn abnormally accumulates and contributes to neurodegeneration in these disorders remains unknown. Here, we provide an overview of current knowledge and prevailing hypotheses regarding the conformational, oligomerization and aggregation states of α-syn and their role in regulating α-syn function in health and disease. Understanding the nature of the various α-syn structures, how they are formed and their relative contributions to α-syn-mediated toxicity may inform future studies aiming to develop therapeutic prevention and intervention.

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

APA 7th

Lashuel, H. A., Overk, C. R., Oueslati, A., & Masliah, E. (2013). The many faces of α-synuclein: from structure and toxicity to therapeutic target. Nature reviews. Neuroscience. https://doi.org/10.1038/nrn3406

Vancouver

Lashuel HA, Overk CR, Oueslati A, Masliah E. The many faces of α-synuclein: from structure and toxicity to therapeutic target. Nature reviews. Neuroscience. 2013. doi:10.1038/nrn3406. PMID: 23254192.

BibTeX

@article{lashuel2013-23254192,
  author  = {Lashuel, H. A. and Overk, C. R. and Oueslati, A. and Masliah, E.},
  title   = {{The many faces of α-synuclein: from structure and toxicity to therapeutic target}},
  journal = {Nature reviews. Neuroscience},
  year    = {2013},
  doi     = {10.1038/nrn3406},
  pmid    = {23254192},
  url     = {https://doi.org/10.1038/nrn3406}
}

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.

Key findings

Disorders characterized by α-synuclein (α-syn) accumulation, Lewy body formation and parkinsonism (and in some cases dementia) are collectively known as Lewy body diseases.
The molecular mechanism (or mechanisms) through which α-syn abnormally accumulates and contributes to neurodegeneration in these disorders remains unknown.
Here, we provide an overview of current knowledge and prevailing hypotheses regarding the conformational, oligomerization and aggregation states of α-syn and their role in regulating α-syn function in health and disease.
Understanding the nature of the various α-syn structures, how they are formed and their relative contributions to α-syn-mediated toxicity may inform future studies aiming to develop therapeutic prevention and intervention.

Why it matters

This review summarizes current knowledge and hypotheses about the different structural and aggregation states of alpha-synuclein and their possible role in Lewy body diseases, noting that the mechanism of toxicity remains unknown. It is a discussion of alpha-synuclein biology, not a treatment, cure or prevention for Alzheimer's disease.

Study details

Evidence strengthLow

How this study scored 54/100

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.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Nature reviews. Neuroscience)
Journal's citation record	4 / 4	Nature reviews. Neuroscience: journal h-index 572 (OpenAlex, 2026-10-29)
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	2013 — 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 / 7	Cited 1,631 times (OpenAlex, 2026-10-10)
Citations per year	5 / 5	108.7 citations a year over 15 year(s) since 2013
Impact for its field and year	4 / 6	Cited 11.7× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	2 / 6	Cited by 7 other studies in this library
Still being cited	4 / 4	Cited 330 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	4 / 4	Last-listed author Eliezer Masliah: h-index 195 (OpenAlex, whole career)
Institution's track record	2 / 3	University of California San Diego: institution h-index 1,852 (OpenAlex)
Multi-centre collaboration	1 / 3	OpenAlex lists 2 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 23254192)
Free to read	0 / 2	Behind a paywall — scores zero
Total	54 / 100	—

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

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

Studies this one cites

Referenced by this study and also in the alzhub library, so you can read them here.

Later studies that cite this one

7 studies in the alzhub library list this one in their references.

Related studies in Lewy body dementia

Also in Lewy body dementia

39 studies in the library are filed under Lewy body dementia with no topic tag they share with another; these are this study's neighbours in a fixed tour of them. The Lewy body dementia hub.

Similar studies

More on Lewy body dementia

See all studies in Lewy body dementia →