Clinton, Lani K., et al. "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, vol. 30, no. 21, 2010, pp. 7281-9.
Clinton LK, Blurton-Jones M, Myczek K, et al. Synergistic Interactions between Abeta, tau, and alpha-synuclein: acceleration of neuropathology and cognitive decline. J Neurosci. 2010;30(21):7281-9.
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, 30(21), 7281-9. https://doi.org/10.1523/JNEUROSCI.0490-10.2010
Clinton LK, et al. Synergistic Interactions Between Abeta, Tau, and Alpha-synuclein: Acceleration of Neuropathology and Cognitive Decline. J Neurosci. 2010 May 26;30(21):7281-9. PubMed PMID: 20505094.
TY - JOUR
T1 - Synergistic Interactions between Abeta, tau, and alpha-synuclein: acceleration of neuropathology and cognitive decline.
AU - Clinton,Lani K,
AU - Blurton-Jones,Mathew,
AU - Myczek,Kristoffer,
AU - Trojanowski,John Q,
AU - LaFerla,Frank M,
PY - 2010/5/28/entrez
PY - 2010/5/28/pubmed
PY - 2010/6/16/medline
SP - 7281
EP - 9
JF - The Journal of neuroscience : the official journal of the Society for Neuroscience
JO - J Neurosci
VL - 30
IS - 21
N2 - 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.
SN - 1529-2401
UR - https://www.unboundmedicine.com/medline/citation/20505094/Synergistic_Interactions_between_Abeta_tau_and_alpha_synuclein:_acceleration_of_neuropathology_and_cognitive_decline_
L2 - http://www.jneurosci.org/cgi/pmidlookup?view=long&pmid=20505094
DB - PRIME
DP - Unbound Medicine