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53/100

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Lewy body dementia

Topic: Brain proteins, microglia and lab models

Alzheimer's disease (AD), the most prevalent age-related neurodegenerative disorder, is characterized pathologically by the accumulation of beta-amyloid (Abeta) plaques and tau-laden neurofibrillary tangles. Interestingly, up to 50% of AD cases exhibit a third prevalent neuropathology: the aggregation of alpha-synuclein into Lewy bodies. Importantly, the presence of Lewy body pathology in AD is associated with a more aggressive disease course and accelerated cognitive dysfunction. Thus, Abeta, tau, and alpha-synuclein may interact synergistically to promote the accumulation of each other. In this study, we used a genetic approach to generate a model that exhibits the combined pathologies of AD and dementia with Lewy bodies (DLB). To achieve this goal, we introduced a mutant human alpha-synuclein transgene into 3xTg-AD mice. As occurs in human disease, transgenic mice that develop both DLB and AD pathologies (DLB-AD mice) exhibit accelerated cognitive decline associated with a dramatic enhancement of Abeta, tau, and alpha-synuclein pathologies. Our findings also provide additional evidence that the accumulation of alpha-synuclein alone can significantly disrupt cognition. Together, our data support the notion that Abeta, tau, and alpha-synuclein interact in vivo to promote the aggregation and accumulation of each other and accelerate cognitive dysfunction.

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

APA 7th

Clinton, L. K., Blurton-Jones, M., Myczek, K., Trojanowski, J. Q., & LaFerla, F. M. (2010). Synergistic Interactions between Abeta, tau, and alpha-synuclein: acceleration of neuropathology and cognitive decline. The Journal of neuroscience : the official journal of the Society for Neuroscience. https://doi.org/10.1523/jneurosci.0490-10.2010

Vancouver

Clinton LK, Blurton-Jones M, Myczek K, Trojanowski JQ, LaFerla FM. Synergistic Interactions between Abeta, tau, and alpha-synuclein: acceleration of neuropathology and cognitive decline. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2010. doi:10.1523/jneurosci.0490-10.2010. PMID: 20505094.

BibTeX

@article{clinton2010-20505094,
  author  = {Clinton, L. K. and Blurton-Jones, M. and Myczek, K. and Trojanowski, J. Q. and LaFerla, F. M.},
  title   = {{Synergistic Interactions between Abeta, tau, and alpha-synuclein: acceleration of neuropathology and cognitive decline}},
  journal = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
  year    = {2010},
  doi     = {10.1523/jneurosci.0490-10.2010},
  pmid    = {20505094},
  url     = {https://doi.org/10.1523/jneurosci.0490-10.2010}
}

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Key findings

Importantly, the presence of Lewy body pathology in AD is associated with a more aggressive disease course and accelerated cognitive dysfunction.
As occurs in human disease, transgenic mice that develop both DLB and AD pathologies (DLB-AD mice) exhibit accelerated cognitive decline associated with a dramatic enhancement of Abeta, tau, and alpha-synuclein pathologies.
Our findings also provide additional evidence that the accumulation of alpha-synuclein alone can significantly disrupt cognition.

Why it matters

Mice with amyloid, tau and alpha-synuclein pathology together showed faster cognitive decline and more accumulation of all three proteins than mice with alpha-synuclein alone. This is animal work suggesting these proteins interact to worsen disease, but it does not test a treatment in people.

Study details

Evidence strengthLow

How this study scored 53/100

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 (The Journal of neuroscience : the official journal of the Society for Neuroscience)
Journal's citation record	4 / 4	Journal of Neuroscience: journal h-index 651 (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	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	6 / 7	Cited 579 times (OpenAlex, 2026-10-10)
Citations per year	4 / 5	32.2 citations a year over 18 year(s) since 2010
Impact for its field and year	4 / 6	Cited 19.5× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	4 / 6	Cited by 32 other studies in this library
Still being cited	3 / 4	Cited 105 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	4 / 4	Last-listed author Frank M. LaFerla: h-index 114 (OpenAlex, whole career)
Institution's track record	2 / 3	University of Pennsylvania: institution h-index 1,859 (OpenAlex)
Multi-centre collaboration	1 / 3	OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 20505094)
Free to read	0 / 2	Behind a paywall — scores zero
Total	53 / 100	—

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

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