Synergistic Interactions between Aβ, Tau, and α-Synuclein: Acceleration of Neuropathology and Cognitive Decline
Open accessAbstract
Alzheimer's disease (AD), the most prevalent age-related neurodegenerative disorder, is characterized pathologically by the accumulation of β-amyloid (Aβ) plaques and tau-laden neurofibrillary tangles. Interestingly, up to 50% of AD cases exhibit a third prevalent neuropathology: the aggregation of α-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, Aβ, tau, and α-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 α-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 Aβ, tau, and α-synuclein pathologies. Our findings also provide additional evidence that the accumulation of α-synuclein alone can significantly disrupt cognition. Together, our data support the notion that Aβ, tau, and α-synuclein interact in vivo to promote the aggregation and accumulation of each other and accelerate cognitive dysfunction.
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3xTg-AD mice readily recapitulated Aβ and tau pathology.
“The 3xTg-AD mice readily recapitulated Aβ and tau pathology, and after breeding with αSynA35T mice the resulting AD-LBV offspring exhibited accelerated cognitive deterioration, and enhanced accumulations of Aβ, αSyn, and tau pathology compared to 3xTg-AD or αSynA53T animals [199].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [199]
AD-LBV mice exhibited increased levels of phosphorylated αSyn (pS129) at younger ages compared with 3xTg-AD or αSyn-A53T animals.
“The AD-LBV mice exhibited increased levels of insoluble αSyn, phosphorylated αSyn (pS129), Aβ1-42, and tau at younger ages compared to the 3xTg-AD or αSyn-A53T animals [199].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [199]
AD-LBV offspring exhibited enhanced accumulations of Aβ pathology compared with 3xTg-AD or αSynA53T animals.
“The 3xTg-AD mice readily recapitulated Aβ and tau pathology, and after breeding with αSynA35T mice the resulting AD-LBV offspring exhibited accelerated cognitive deterioration, and enhanced accumulations of Aβ, αSyn, and tau pathology compared to 3xTg-AD or αSynA53T animals [199].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [199]
AD-LBV offspring exhibited accelerated cognitive deterioration compared with 3xTg-AD or αSynA53T animals.
“The 3xTg-AD mice readily recapitulated Aβ and tau pathology, and after breeding with αSynA35T mice the resulting AD-LBV offspring exhibited accelerated cognitive deterioration, and enhanced accumulations of Aβ, αSyn, and tau pathology compared to 3xTg-AD or αSynA53T animals [199].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [199]
AD-LBV offspring exhibited enhanced accumulations of tau pathology compared with 3xTg-AD or αSynA53T animals.
“The 3xTg-AD mice readily recapitulated Aβ and tau pathology, and after breeding with αSynA35T mice the resulting AD-LBV offspring exhibited accelerated cognitive deterioration, and enhanced accumulations of Aβ, αSyn, and tau pathology compared to 3xTg-AD or αSynA53T animals [199].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [199]
AD-LBV mice exhibited increased levels of insoluble αSyn at younger ages compared with 3xTg-AD or αSyn-A53T animals.
“The AD-LBV mice exhibited increased levels of insoluble αSyn, phosphorylated αSyn (pS129), Aβ1-42, and tau at younger ages compared to the 3xTg-AD or αSyn-A53T animals [199].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [199]
AD-LBV mice exhibited increased levels of Aβ1-42 at younger ages compared with 3xTg-AD or αSyn-A53T animals.
“The AD-LBV mice exhibited increased levels of insoluble αSyn, phosphorylated αSyn (pS129), Aβ1-42, and tau at younger ages compared to the 3xTg-AD or αSyn-A53T animals [199].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [199]
AD-LBV mice exhibited increased levels of tau at younger ages compared with 3xTg-AD or αSyn-A53T animals.
“The AD-LBV mice exhibited increased levels of insoluble αSyn, phosphorylated αSyn (pS129), Aβ1-42, and tau at younger ages compared to the 3xTg-AD or αSyn-A53T animals [199].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [199]
AD-LBV offspring exhibited enhanced accumulations of αSyn pathology compared with 3xTg-AD or αSynA53T animals.
“The 3xTg-AD mice readily recapitulated Aβ and tau pathology, and after breeding with αSynA35T mice the resulting AD-LBV offspring exhibited accelerated cognitive deterioration, and enhanced accumulations of Aβ, αSyn, and tau pathology compared to 3xTg-AD or αSynA53T animals [199].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [199]
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Cites
1 retracted
Tsigelny, I. F., Crews, L., Desplats, P., Shaked, G. M., Sharikov, Y., Mizuno, H., Spencer, B., Rockenstein, E., Trejo, M., Platoshyn, O., et al. (2008) · PLoS ONE · doi:10.1371/journal.pone.0003135 · Cited by 281 · see citing works
RetractedTriple-Transgenic Model of Alzheimer’s Disease with Plaques and Tangles
Oddo, S., Caccamo, A., Shepherd, J. D., Murphy, M. P., Golde, T. E., Kayed, R., Metherate, R., Mattson, M. P., Akbari, Y., & LaFerla, F. M. (2003) · Neuron · doi:10.1016/s0896-6273(03)00434-3 · Cited by 4,126 · see citing works
Self-citationMemory deficits associated with senescence: A neurophysiological and behavioral study in the rat.
Barnes, C. A. (1979) · Journal of Comparative and Physiological Psychology · doi:10.1037/h0077579 · Cited by 2,088 · see citing works
Jarrett, J. T., Berger, E. P., & Lansbury, P. T. (1993) · Biochemistry · doi:10.1021/bi00069a001 · Cited by 2,022 · see citing works
α-Synuclein is phosphorylated in synucleinopathy lesions
Fujiwara, H., Hasegawa, M., Dohmae, N., Kawashima, A., Masliah, E., Goldberg, M., Shen, J., Takio, K., & Iwatsubo, T. (2002) · Nature Cell Biology · doi:10.1038/ncb748 · Cited by 1,906 · see citing works
Suzuki, N., Cheung, T. T., Cai, X.-D., Odaka, A., Otvos, L., Eckman, C., Golde, T. E., & Younkin, S. G. (1994) · Science · doi:10.1126/science.8191290 · Cited by 1,471 · see citing works
Billings, L. M., Oddo, S., Green, K. N., McGaugh, J. L., & LaFerla, F. M. (2005) · Neuron · doi:10.1016/j.neuron.2005.01.040 · Cited by 1,294 · see citing works
Self-citationNeuronal α-Synucleinopathy with Severe Movement Disorder in Mice Expressing A53T Human α-Synuclein
Giasson, B. I., Duda, J. E., Quinn, S. M., Zhang, B., Trojanowski, J. Q., & Lee, V. M.-Y. (2002) · Neuron · doi:10.1016/s0896-6273(02)00682-7 · Cited by 1,266 · see citing works
Self-citationThe Lewy body variant of Alzheimer's disease: A clinical and pathologic entity
Hansen, L., Salmon, D., Galasko, D., Masliah, E., Katzman, R., DeTeresa, R., Thal, L., Pay, M. M., Hofstetter, R., Klauber, M., et al. (1990) · Neurology · doi:10.1212/wnl.40.1.1 · Cited by 1,068 · see citing works
Initiation and Synergistic Fibrillization of Tau and Alpha-Synuclein
Giasson, B. I., Forman, M. S., Higuchi, M., Golbe, L. I., Graves, C. L., Kotzbauer, P. T., Trojanowski, J. Q., & Lee, V. M.-Y. (2003) · Science · doi:10.1126/science.1082324 · Cited by 879 · cited 13× · see citing works
“Importantly, plaques, tangles, and LBs do not develop in high enough individual frequency to explain their co-occurrence simply by statistical overlap; thus, it has been hypothesized that A , tau, and -syn promote the accumulation of one another (Giasson et al., 2003; Lee et al., 2004).”
BackgroundInfluentialSelf-citationIntravesicular Localization and Exocytosis of α-Synuclein and its Aggregates
Lee, H.-J., Patel, S. S., & Lee, S. (2005) · Journal of Neuroscience · doi:10.1523/jneurosci.0692-05.2005 · Cited by 798 · see citing works
Oddo, S., Billings, L., Kesslak, J. P., Cribbs, D. H., & LaFerla, F. M. (2004) · Neuron · doi:10.1016/j.neuron.2004.07.003 · Cited by 780 · see citing works
Self-citationHamilton, R. L. (2000) · Brain Pathology · doi:10.1111/j.1750-3639.2000.tb00269.x · Cited by 754 · see citing works
Masliah, E., Rockenstein, E., Veinbergs, I., Sagara, Y., Mallory, M., Hashimoto, M., & Mucke, L. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.211412398 · Cited by 607 · see citing works
Constitutive Phosphorylation of the Parkinson's Disease Associated α-Synuclein
Okochi, M., Walter, J., Koyama, A., Nakajo, S., Baba, M., Iwatsubo, T., Meijer, L., Kahle, P. J., & Haass, C. (2000) · Journal of Biological Chemistry · doi:10.1074/jbc.275.1.390 · Cited by 521 · see citing works
Temporal Profile of Amyloid-β (Aβ) Oligomerization in an in Vivo Model of Alzheimer Disease
Oddo, S., Caccamo, A., Tran, L., Lambert, M. P., Glabe, C. G., Klein, W. L., & LaFerla, F. M. (2006) · Journal of Biological Chemistry · doi:10.1074/jbc.m507892200 · Cited by 379 · see citing works
Self-citationCognitive decline is faster in Lewy body variant than in Alzheimer's disease
Olichney, J., Galasko, D. R., Salmon, D. P., Hofstetter, C. R., Hansen, L. A., Katzman, R., & Thal, L. J. (1998) · Neurology · doi:10.1212/wnl.51.2.351 · Cited by 305 · see citing works
Age-dependent sexual dimorphism in cognition and stress response in the 3xTg-AD mice
Clinton, L. K., Billings, L. M., Green, K. N., Caccamo, A., Ngo, J., Oddo, S., McGaugh, J. L., & LaFerla, F. M. (2007) · Neurobiology of Disease · doi:10.1016/j.nbd.2007.06.013 · Cited by 299 · see citing works
Self-citationCognitive differences in dementia patients with autopsy-verified AD, Lewy body pathology, or both
Kraybill, M., Larson, E. B., Tsuang, D. W., Teri, L. L., McCormick, W. C., Bowen, J. D., Kukull, W. A., Leverenz, J. B., & Cherrier, M. M. (2005) · Neurology · doi:10.1212/01.wnl.0000165987.89198.65 · Cited by 286 · see citing works
-Synuclein Phosphorylation Enhances Eosinophilic Cytoplasmic Inclusion Formation in SH-SY5Y Cells
Smith, W. W. (2005) · Journal of Neuroscience · doi:10.1523/jneurosci.0482-05.2005 · Cited by 264 · see citing works
The Lewy-Body Variant of Alzheimer's Disease
Förstl, H., Burns, A. S., Luthert, P. J., Cairns, N. J., & Levy, R. (1993) · The British Journal of Psychiatry · doi:10.1192/bjp.162.3.385 · Cited by 221 · see citing works
Mandal, P. K., Pettegrew, J. W., Masliah, E., Hamilton, R. L., & Mandal, R. (2006) · Neurochemical Research · doi:10.1007/s11064-006-9140-9 · Cited by 219 · see citing works
Lee, V. M. ‐., Giasson, B. I., & Trojanowski, J. Q. (2004) · Trends in Neurosciences · doi:10.1016/j.tins.2004.01.007 · Cited by 185 · see citing works
Self-citationKotzbauer, P. T. (2004) · Experimental Neurology · doi:10.1016/j.expneurol.2004.01.007 · Cited by 176 · see citing works
Age-dependent cognitive decline and amygdala pathology in α-synuclein transgenic mice
Freichel, C., Neumann, M., Ballard, T. M., Müller, V., Woolley, M. L., Ozmen, L., Borroni, E., Kretzschmar, H. A., Haass, C., Spooren, W. P. J. M., et al. (2006) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2006.06.013 · Cited by 173 · see citing works
Neural Stem Cells Improve Memory in an Inducible Mouse Model of Neuronal Loss
Yamasaki, T. R., Blurton-Jones, M. M., Morrissette, D. A., Kitazawa, M., Oddo, S., & LaFerla, F. M. (2007) · Journal of Neuroscience · doi:10.1523/jneurosci.1627-07.2007 · Cited by 158 · see citing works
Self-citationNeurotransmitters in basal ganglia and cortex of Alzheimer's disease with and without Lewy bodies
Langlais, P. J., Thai, L., Hansen, L. A., Galasko, D., Alford, M. F., & Masliah, E. (1993) · Neurology · doi:10.1212/wnl.43.10.1927 · Cited by 144 · see citing works
Casein kinase 1 delta mRNA is upregulated in Alzheimer disease brain
Yasojima, K., Kuret, J., DeMaggio, A. J., McGeer, E. G., & McGeer, P. L. (2000) · Brain Research · doi:10.1016/s0006-8993(00)02200-9 · Cited by 116 · see citing works
Postina, R. (2008) · Current Alzheimer Research · doi:10.2174/156720508783954668 · Cited by 110 · see citing works
Tau phosphorylation increases in symptomatic mice overexpressing A30P α-synuclein
Frasier, M. A., Walzer, M., McCarthy, L., Magnuson, D. J., Lee, J. M., Haas, C. A., Kahle, P. J., & Wolozin, B. L. (2004) · Experimental Neurology · doi:10.1016/j.expneurol.2004.07.016 · Cited by 103 · see citing works
Lehman, E. J. H. (2003) · Human Molecular Genetics · doi:10.1093/hmg/ddg322 · Cited by 85 · see citing works
Blurton-Jones, M. M., & Tuszynski, M. H. (2006) · The Journal of Comparative Neurology · doi:10.1002/cne.21122 · Cited by 56 · see citing works
Self-citationDetection of Lewy Bodies in Trisomy 21 (Down's Syndrome)
Raghavan, R., Khin-Nu, C., Brown, A., Irving, D., Ince, P. G., Day, K. A., Tyrer, S. P., & Perry, R. H. (1993) · Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques · doi:10.1017/s0317167100047405 · Cited by 54 · see citing works
“Emerging Alzheimer’s disease therapies: focusing on the future”
Trojanowski, J. Q. (2002) · Neurobiology of Aging · doi:10.1016/s0197-4580(02)00123-9 · Cited by 38 · see citing works
Self-citation
Flagged first, then by citations
Cited by
Sorted by citations
Protein misfolding, aggregation, and conformational strains in neurodegenerative diseases
Soto, C., & Pritzkow, S. (2018) · Nature Neuroscience · doi:10.1038/s41593-018-0235-9 · Cited by 1,180 · see citing works
Saman, S., Kim, W., Raya, M., Visnick, Y., Miro, S., Saman, S., Jackson, B., McKee, A. C., Alvarez, V. E., Lee, N. C. Y., et al. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.m111.277061 · Cited by 985 · see citing works
Tau and Aβ imaging, CSF measures, and cognition in Alzheimer’s disease
Brier, M. R., Gordon, B., Friedrichsen, K., McCarthy, J., Stern, A., Christensen, J., Owen, C., Aldea, P., Su, Y., Hassenstab, J., et al. (2016) · Science Translational Medicine · doi:10.1126/scitranslmed.aaf2362 · Cited by 734 · see citing works
Robinson, J. L., Lee, E. B., Xie, S. X., Rennert, L., Suh, E., Bredenberg, C., Caswell, C., Van Deerlin, V. M., Yan, N., Yousef, A., et al. (2018) · Brain · doi:10.1093/brain/awy146 · Cited by 729 · see citing works
Self-citationProtein transmission in neurodegenerative disease
Peng, C., Trojanowski, J. Q., & Lee, V. M.-Y. (2020) · Nature Reviews Neurology · doi:10.1038/s41582-020-0333-7 · Cited by 625 · see citing works
Self-citationA gut bacterial amyloid promotes α-synuclein aggregation and motor impairment in mice
Sampson, T. R., Challis, C., Jain, N., Moiseyenko, A., Ladinsky, M. S., Shastri, G. G., Thron, T., Needham, B. D., Horvath, I., Debelius, J. W., et al. (2020) · eLife · doi:10.7554/elife.53111 · Cited by 439 · see citing works
α-synuclein in the pathophysiology of Alzheimer’s disease
Twohig, D., & Nielsen, H. M. (2019) · Molecular Neurodegeneration · doi:10.1186/s13024-019-0320-x · Cited by 374 · see citing works
Yamada, K., Cirrito, J. R., Stewart, F. R., Jiang, H., Finn, M. B., Holmes, B. B., Binder, L. I., Mandelkow, E.-M., Diamond, M. I., Lee, V. M.-Y., et al. (2011) · The Journal of Neuroscience · doi:10.1523/jneurosci.2569-11.2011 · Cited by 351 · see citing works
Cerebrospinal fluid biomarkers in Parkinson disease
Parnetti, L., Castrioto, A., Chiasserini, D., Persichetti, E., Tambasco, N., El-Agnaf, O., & Calabresi, P. (2013) · Nature Reviews Neurology · doi:10.1038/nrneurol.2013.10 · Cited by 209 · see citing works
Long, J. M., Ray, B., & Lahiri, D. K. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.m112.366336 · Cited by 198 · see citing works
Mixed neuropathologies and estimated rates of clinical progression in a large autopsy sample
Brenowitz, W. D., Hubbard, R. A., Keene, C. D., Hawes, S. E., Longstreth, W. T., Woltjer, R. L., & Kukull, W. A. (2017) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2016.09.015 · Cited by 188 · see citing works
Neuropathology of multiple system atrophy: New thoughts about pathogenesis
Jellinger, K. A. (2014) · Movement Disorders · doi:10.1002/mds.26052 · Cited by 181 · see citing works
Exosomes and stem cells in degenerative disease diagnosis and therapy
Chang, Y.-H., Wu, K.-C., Harn, H.-J., Lin, S.-Z., & Ding, D.-C. (2018) · Cell Transplantation · doi:10.1177/0963689717723636 · Cited by 159 · see citing works
Kim, D. S., Choi, H.-I., Wang, Y., Luo, Y., Hoffer, B. J., & Greig, N. H. (2017) · Cell Transplantation · doi:10.1177/0963689717721234 · Cited by 136 · see citing works
Alzheimer’s disease: Ablating single master site abolishes tau hyperphosphorylation
Stefanoska, K., Gajwani, M., Tan, A. R. P., Ahel, H. I., Asih, P. R., Volkerling, A., Poljak, A., & Ittner, A. (2022) · Science Advances · doi:10.1126/sciadv.abl8809 · Cited by 128 · see citing works
RETRACTED: Soluble α-Synuclein Is a Novel Modulator of Alzheimer's Disease Pathophysiology
Larson, M. E., Sherman, M. A., Greimel, S., Kuskowski, M., Schneider, J. A., Bennett, D. A., & Lesné, S. E. (2012) · The Journal of Neuroscience · doi:10.1523/jneurosci.0581-12.2012 · Cited by 128 · see citing works
Retractedα-Synuclein in Cerebrospinal Fluid of Alzheimer's Disease and Mild Cognitive Impairment
Korff, A., Liu, C., Ginghina, C., Shi, M., Zhang, J., & Initiative, F. T. A. D. N. (2013) · Journal of Alzheimer’s Disease · doi:10.3233/jad-130458 · Cited by 95 · see citing works
Dehghan, E., Zhang, Y., Saremi, B., Yadavali, S., Hakimi, A., Dehghani, M., Goodarzi, M., Tu, X., Robertson, S., Lin, R., et al. (2017) · Nature Communications · doi:10.1038/s41467-017-02394-3 · Cited by 92 · see citing works
Kawahata, I., & Fukunaga, K. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21113779 · Cited by 71 · see citing works
Ciccone, L., Shi, C., di Lorenzo, D., Van Baelen, A.-C., & Tonali, N. (2020) · Molecules · doi:10.3390/molecules25102439 · Cited by 69 · see citing works
The relevance of cerebrospinal fluid α-synuclein levels to sporadic and familial Alzheimer’s disease
for the Dominantly Inherited Alzheimer Network (DIAN), Twohig, D., Rodriguez-Vieitez, E., Sando, S. B., Berge, G., Lauridsen, C., Møller, I., Grøntvedt, G. R., Bråthen, G., Patra, K., et al. (2018) · Acta Neuropathologica Communications · doi:10.1186/s40478-018-0624-z · Cited by 68 · see citing works
Han, S.-H., Park, J.-C., & Mook-Jung, I. (2016) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2015.12.004 · Cited by 67 · see citing works
Selective lowering of synapsins induced by oligomeric α-synuclein exacerbates memory deficits
Larson, M. E., Greimel, S. J., Amar, F., LaCroix, M., Boyle, G., Sherman, M. A., Schley, H., Miel, C., Schneider, J. A., Kayed, R., et al. (2017) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1704698114 · Cited by 61 · see citing works
Criteria for the neuropathological diagnosis of dementing disorders: routes out of the swamp?
Jellinger, K. A. (2009) · Acta Neuropathologica · doi:10.1007/s00401-008-0466-z · Cited by 60 · see citing works
Bidirectional modulation of Alzheimer phenotype by alpha-synuclein in mice and primary neurons
Khan, S. S., LaCroix, M., Boyle, G., Sherman, M. A., Brown, J. L., Amar, F., Aldaco, J., Lee, M. K., Bloom, G. S., & Lesné, S. E. (2018) · Acta Neuropathologica · doi:10.1007/s00401-018-1886-z · Cited by 41 · see citing works
Moszczynski, A. J., Harvey, M., Fulcher, N., de Oliveira, C., McCunn, P., Donison, N., Bartha, R., Schmid, S., Strong, M. J., & Volkening, K. (2019) · Acta Neuropathologica Communications · doi:10.1186/s40478-019-0816-1 · Cited by 15 · see citing works
- Authors
- Clinton, L. K., Blurton-Jones, M., Myczek, K., Trojanowski, J. Q., & LaFerla, F. M.
- Affiliations
- University of California, Irvine (US)
- University of Pennsylvania (US)
- Corresponding author
- LaFerla, Frank M.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2010-05-26
- Volume
- 30
- Issue
- 21
- Pages
- 7281-7289
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3308018
- OpenAlex
- W1973166472
- Cited by
- 576
- References
- 34
- Citations by year
- 2026: 25 · 2025: 51 · 2024: 28 · 2023: 37 · 2022: 44 · 2021: 34 · 2020: 61 · 2019: 35 · 2018: 24 · 2017: 26 · 2016: 43 · 2015: 25 · 2014: 39 · 2013: 35 · 2012: 22
- FWCI
- 22.10
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (T32 AG00096, AG00096, AG16573)
- National Institute on Aging (AG00096, P50 AG 16573, T32 AG00096, AG027544, R29AG015409, AG 16573, K01AG029378, P50AG016573, R01AG027544, T32AG000096)
- National Institute of Neurological Disorders and Stroke (NS053488, P50NS053488)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, dementia with Lewy bodies, alpha-synuclein, amyloid-beta, tau protein, Lewy bodies, cognitive decline, 3xTg-AD mice, transgenic mouse model, neurodegeneration
- MeSH terms
- Age Factors, Alzheimer Disease, Animals, Avoidance Learning, Brain, Cognition Disorders, Disease Models, Animal, Humans, Inhibition, Psychological, Mice, Inbred C57BL, Mice, Transgenic, Motor Activity, Mutation, Phosphorylation, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Lewy Bodies, tau Proteins, Gene Expression Regulation, Developmental, Maze Learning, Mice, alpha-Synuclein, Presenilin-1
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