The DOI matches its Crossref record; 56 of the 56 references it cites were found in a registry or an index.
β-Amyloid peptides enhance α-synuclein accumulation and neuronal deficits in a transgenic mouse model linking Alzheimer's disease and Parkinson's disease
Open accessAbstract
Alzheimer's disease and Parkinson's disease are associated with the cerebral accumulation of β-amyloid and α-synuclein, respectively. Some patients have clinical and pathological features of both diseases, raising the possibility of overlapping pathogenetic pathways. We generated transgenic (tg) mice with neuronal expression of human β-amyloid peptides, α-synuclein, or both. The functional and morphological alterations in doubly tg mice resembled the Lewy-body variant of Alzheimer's disease. These mice had severe deficits in learning and memory, developed motor deficits before α-synuclein singly tg mice, and showed prominent age-dependent degeneration of cholinergic neurons and presynaptic terminals. They also had more α-synuclein-immunoreactive neuronal inclusions than α-synuclein singly tg mice. Ultrastructurally, some of these inclusions were fibrillar in doubly tg mice, whereas all inclusions were amorphous in α-synuclein singly tg mice. β-Amyloid peptides promoted aggregation of α-synuclein in a cell-free system and intraneuronal accumulation of α-synuclein in cell culture. β-Amyloid peptides may contribute to the development of Lewy-body diseases by promoting the aggregation of α-synuclein and exacerbating α-synuclein-dependent neuronal pathologies. Therefore, treatments that block the production or accumulation of β-amyloid peptides could benefit a broader spectrum of disorders than previously anticipated.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Compared to animals expressing only hαSyn or hAPP, the hαSyn/hAPP animals had marked cholinergic neuron loss, intraneuronal LRP, florid Aβ plaques, exhibited marked motor dysfunction and had significant learning and memory deficits [198].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [198]
In the citing paper
“Compared to animals expressing only hαSyn or hAPP, the hαSyn/hAPP animals had marked cholinergic neuron loss, intraneuronal LRP, florid Aβ plaques, exhibited marked motor dysfunction and had significant learning and memory deficits [198].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [198]
In the citing paper
“Compared to animals expressing only hαSyn or hAPP, the hαSyn/hAPP animals had marked cholinergic neuron loss, intraneuronal LRP, florid Aβ plaques, exhibited marked motor dysfunction and had significant learning and memory deficits [198].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [198]
In the citing paper
“The hαSyn/hAPP model recapitulated many of the clinical symptoms and pathology of AD-LBV.”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [198]
In the citing paper
“Compared to animals expressing only hαSyn or hAPP, the hαSyn/hAPP animals had marked cholinergic neuron loss, intraneuronal LRP, florid Aβ plaques, exhibited marked motor dysfunction and had significant learning and memory deficits [198].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [198]
In the citing paper
“Further evidence of a link between αSyn and Aβ pathology was offered from studies using mice expressing wt human αSyn (hαSyn) and human APP (hAPP) (hαSyn/hAPP).”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [198]
In the citing paper
“Compared to animals expressing only hαSyn or hAPP, the hαSyn/hAPP animals had marked cholinergic neuron loss, intraneuronal LRP, florid Aβ plaques, exhibited marked motor dysfunction and had significant learning and memory deficits [198].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [198]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D. (2013) · Neurodegenerative Diseases · doi:10.1159/000337230 · Cited by 10,359
Spillantini, M. G., Schmidt, M. L., Lee, V. M.-Y., Trojanowski, J. Q., Jakes, R., & Goedert, M. (1997) · Nature · doi:10.1038/42166 · Cited by 8,382
Mutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease
Polymeropoulos, M. H., Lavedan, C., Leroy, E., Ide, S. E., Dehejia, A., Dutra, A., Pike, B., Root, H., Rubenstein, J., Boyer, R., et al. (1997) · Science · doi:10.1126/science.276.5321.2045 · Cited by 8,240
Alzheimer's Disease: Genes, Proteins, and Therapy
Selkoe, D. J. (2001) · Physiological Reviews · doi:10.1152/physrev.2001.81.2.741 · Cited by 6,063
Terry, R. D., Masliah, E., Salmon, D. P., Butters, N., DeTeresa, R., Hill, R., Hansen, L. A., & Katzman, R. (1991) · Annals of Neurology · doi:10.1002/ana.410300410 · Cited by 4,397
Self-citationMcKeith, I. G., Galasko, D., Kosaka, K., Perry, E. K., Dickson, D. W., Hansen, L. A., Salmon, D. P., Lowe, J., Mirra, S. S., Byrne, E. J., et al. (1996) · Neurology · doi:10.1212/wnl.47.5.1113 · Cited by 3,960
AlaSOPro mutation in the gene encoding α-synuclein in Parkinson's disease
Krüger, R., Kuhn, W., Müller, T., Woitalla, D., Graeber, M., Kösel, S., Przuntek, H., Epplen, J. T., Schols, L., & Riess, O. (1998) · Nature Genetics · doi:10.1038/ng0298-106 · Cited by 3,836
Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein
Games, D., Adams, D., Alessandrini, R., Barbour, R., Borthelette, P., Blackwell, C., Carr, T., Clemens, J., Donaldson, T., Gillespie, F., et al. (1995) · Nature · doi:10.1038/373523a0 · Cited by 2,516
Self-citationA Drosophila model of Parkinson's disease
Feany, M. Β., & Bender, W. W. (2000) · Nature · doi:10.1038/35006074 · Cited by 2,157
Lang, A. E., & Lozano, A. M. (1998) · New England Journal of Medicine · doi:10.1056/nejm199810083391506 · Cited by 2,073
Research works printed but not linked: 3
- R D Terry, R Katzman, K L Bick, S S Sisodia Alzheimer Disease (Lippincott, Philadelphia, 1999).
- A Takeda, M Mallory, M Sundsmo, W Honer, L Hansen, E Masliah Am J Pathol 152, 367–372 (1998).
- D Van Gool, B De Strooper, F Van Leuven, R Dom Dementia 6, 63–68 (1995).
Cited by
Sorted by citations
Neuropathological alterations in Alzheimer disease
Serrano-Pozo, A., Frosch, M. P., Masliah, E., & Hyman, B. T. (2011) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a006189 · Cited by 3,345
Self-citationAlzheimer Mechanisms and Therapeutic Strategies
Huang, Y., & Mucke, L. (2012) · Cell · doi:10.1016/j.cell.2012.02.040 · Cited by 1,758
Self-citationMolecular Pathways of Neurodegeneration in Parkinson's Disease
Dawson, T. M., & Dawson, V. L. (2003) · Science · doi:10.1126/science.1087753 · Cited by 1,674
Neuronal 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
MOLECULAR PATHOPHYSIOLOGY OF PARKINSON'S DISEASE
Moore, D. J., West, A. B., Dawson, V. L., & Dawson, T. M. (2005) · Annual Review of Neuroscience · doi:10.1146/annurev.neuro.28.061604.135718 · Cited by 1,304
Inflammation in Neurodegenerative Disease—A Double-Edged Sword
Wyss-Coray, T., & Mucke, L. (2002) · Neuron · doi:10.1016/s0896-6273(02)00794-8 · Cited by 1,235
Self-citationImaging β-amyloid burden in aging and dementia
Rowe, C. C., Ng, S., Ackermann, U., Gong, S. J., Pike, K., Savage, G., Cowie, T. F., Dickinson, K. L., Maruff, P., Darby, D., et al. (2007) · Neurology · doi:10.1212/01.wnl.0000261919.22630.ea · Cited by 1,104
α-synuclein toxicity in neurodegeneration: mechanism and therapeutic strategies
Wong, Y. C., & Krainc, D. (2017) · Nature Medicine · doi:10.1038/nm.4269 · Cited by 897
Parkinson's disease dementia: convergence of α-synuclein, tau and amyloid-β pathologies
Irwin, D. J., Lee, V. M. ‐., & Trojanowski, J. Q. (2013) · Nature reviews. Neuroscience · doi:10.1038/nrn3549 · Cited by 909
Three dimensions of the amyloid hypothesis: time, space and 'wingmen'
Musiek, E. S., & Holtzman, D. M. (2015) · Nature Neuroscience · doi:10.1038/nn.4018 · Cited by 662
Epilepsy and Cognitive Impairments in Alzheimer Disease
Palop, J. J. (2009) · Archives of Neurology · doi:10.1001/archneurol.2009.15 · Cited by 684
Protein 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
Bharali, D. J., Klejbor, I., Stachowiak, E. K., Dutta, P., Roy, I., Kaur, N., Bergey, E. J., Prasad, P. N., & Stachowiak, M. K. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0504926102 · Cited by 622
Amyloid oligomers: formation and toxicity of Aβ oligomers
Sakono, M., & Zako, T. (2010) · FEBS Journal · doi:10.1111/j.1742-4658.2010.07568.x · Cited by 633
Kirkitadze, M. D., Bitan, G., & Teplow, D. B. (2002) · Journal of Neuroscience Research · doi:10.1002/jnr.10328 · Cited by 589
Lewy- and Alzheimer-type pathologies in Parkinson's disease dementia: which is more important?
Compta, Y., Parkkinen, L., O’Sullivan, S. S., Vandrovcová, J., Holton, J. L., Collins, C., Lashley, T., Kallis, C., Williams, D. R., de Silva, R., et al. (2011) · Brain · doi:10.1093/brain/awr031 · Cited by 603
Clinton, L. K., Blurton-Jones, M., Myczek, K., Trojanowski, J. Q., & LaFerla, F. M. (2010) · The Journal of Neuroscience · doi:10.1523/jneurosci.0490-10.2010 · Cited by 576
Half a century of amyloids: past, present and future
Ke, P. C., Zhou, R., Serpell, L. C., Riek, R., Knowles, T. P. J., Lashuel, H. A., Gazit, E., Hamley, I. W., Davis, T. P., Fändrich, M., et al. (2020) · Chemical Society Reviews · doi:10.1039/c9cs00199a · Cited by 571
Effects of α-Synuclein Immunization in a Mouse Model of Parkinson’s Disease
Masliah, E., Rockenstein, E., Adame, A., Alford, M., Crews, L., Hashimoto, M., Seubert, P., Lee, M., Goldstein, J., Chilcote, T., et al. (2005) · Neuron · doi:10.1016/j.neuron.2005.05.010 · Cited by 542
Self-citationHashimoto, M., Rockenstein, E. M., Crews, L. A., & Masliah, E. (2003) · NeuroMolecular Medicine · doi:10.1385/nmm:4:1-2:21 · Cited by 507
Self-citationA Hundred Years of Alzheimer's Disease Research
Hardy, J. (2006) · Neuron · doi:10.1016/j.neuron.2006.09.016 · Cited by 467
Suh, Y.-H., & Checler, F. (2002) · Pharmacological Reviews · doi:10.1124/pr.54.3.469 · Cited by 476
Braak, H., Sastre, M., & Del Tredici, K. (2007) · Acta Neuropathologica · doi:10.1007/s00401-007-0244-3 · Cited by 462
Neuropathology of sporadic Parkinson's disease: Evaluation and changes of concepts
Jellinger, K. A. (2011) · Movement Disorders · doi:10.1002/mds.23795 · Cited by 480
Alzheimer disease models and human neuropathology: similarities and differences
Duyckaerts, C., Potier, M.-C., & Delatour, B. (2008) · Acta Neuropathologica · doi:10.1007/s00401-007-0312-8 · Cited by 375
Mhyre, T. R., Boyd, J. T., Hamill, R. W., & Maguire‐Zeiss, K. A. (2012) · Sub-cellular biochemistry/Subcellular biochemistry · doi:10.1007/978-94-007-5416-4_16 · Cited by 461
Recent Advances in the Genetics of Parkinson's Disease
Martin, I., Dawson, V. L., & Dawson, T. M. (2011) · Annual Review of Genomics and Human Genetics · doi:10.1146/annurev-genom-082410-101440 · Cited by 451
Interactions of pathological proteins in neurodegenerative diseases
Spires‐Jones, T. L., Attems, J., & Thal, D. R. (2017) · Acta Neuropathologica · doi:10.1007/s00401-017-1709-7 · Cited by 435
Genetics and Pathogenesis of Parkinson's Syndrome
Ye, H., Robak, L. A., Yu, M., Cykowski, M. D., & Shulman, J. M. (2022) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev-pathmechdis-031521-034145 · Cited by 488
Masliah, E., Rockenstein, E. M., Mante, M., Crews, L. A., Spencer, B. J., Adame, A., Patrick, C., Trejo, M., Ubhi, K. K., Rohn, T. T., et al. (2011) · PLoS ONE · doi:10.1371/journal.pone.0019338 · Cited by 422
Self-citationRetractedα-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
β-Synuclein Inhibits α-Synuclein Aggregation
Hashimoto, M., Rockenstein, E., Mante, M., Mallory, M., & Masliah, E. (2001) · Neuron · doi:10.1016/s0896-6273(01)00462-7 · Cited by 398
Self-citationAthauda, D., & Foltynie, T. (2016) · Drug Discovery Today · doi:10.1016/j.drudis.2016.01.013 · Cited by 383
Dementia with Lewy bodies: an update and outlook
Outeiro, T. F., Koss, D. J., Erskine, D., Walker, L., Kurzawa-Akanbi, M., Burn, D., Donaghy, P., Morris, C., Taylor, J.-P., Thomas, A., et al. (2019) · Molecular Neurodegeneration · doi:10.1186/s13024-019-0306-8 · Cited by 381
Amyloid Imaging with18F-Florbetaben in Alzheimer Disease and Other Dementias
Villemagne, V. L., Ong, K. T., Mulligan, R. S., Holl, G., Pejoska, S., Jones, G. R., O'Keefe, G. J., Ackerman, U., Tochon‐Danguy, H., Chan, J. G., et al. (2011) · Journal of Nuclear Medicine · doi:10.2967/jnumed.111.089730 · Cited by 378
Crews, L. A., Spencer, B. J., Desplats, P., Patrick, C., Paulino, A., Rockenstein, E. M., Hansen, L. A., Adame, A., Galasko, D. R., & Masliah, E. (2010) · PLoS ONE · doi:10.1371/journal.pone.0009313 · Cited by 379
Self-citationRetractedKang, J. (2013) · JAMA Neurology · doi:10.1001/jamaneurol.2013.3861 · Cited by 366
Alzheimer Disease With Amygdala Lewy Bodies: A Distinct Form of α-Synucleinopathy
Uchikado, H., Lin, W.-L., DeLucia, M. W., & Dickson, D. W. (2006) · Journal of Neuropathology and Experimental Neurology · doi:10.1097/01.jnen.0000225908.90052.07 · Cited by 359
Neumann, M., Kahle, P. J., Giasson, B. I., Ozmen, L., Borroni, E., Spooren, W. P. J. M., Müller, V., Odoy, S., Fujiwara, H., Hasegawa, M., et al. (2002) · Journal of Clinical Investigation · doi:10.1172/jci15777 · Cited by 363
Neuropathological spectrum of synucleinopathies
Jellinger, K. A. (2003) · Movement Disorders · doi:10.1002/mds.10557 · Cited by 345
Insulin resistance and Parkinson’s disease: A new target for disease modification?
Athauda, D. S., & Foltynie, T. (2016) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2016.10.001 · Cited by 340
Games, D., Valera, E., Spencer, B. J., Rockenstein, E. M., Mante, M., Adame, A., Patrick, C., Ubhi, K. K., Nuber, S., Sacayon, P., et al. (2014) · Journal of Neuroscience · doi:10.1523/jneurosci.5314-13.2014 · Cited by 329
Self-citationBeta-amyloid deposition in chronic traumatic encephalopathy
Stein, T. D., Montenigro, P. H., Alvarez, V. E., Xia, W., Crary, J. F., Tripodis, Y., Daneshvar, D. H., Mez, J., Solomon, T., Meng, G., et al. (2015) · Acta Neuropathologica · doi:10.1007/s00401-015-1435-y · Cited by 291
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
Self-citationRetractedGötz, J., Streffer, J. R., David, D. C., Schild, A., Hoerndli, F. J., Pennanen, L., Kurosinski, P., & Chen, F. (2004) · Molecular Psychiatry · doi:10.1038/sj.mp.4001508 · Cited by 284
The ongoing pursuit of neuroprotective therapies in Parkinson disease
Athauda, D. S., & Foltynie, T. (2014) · Nature Reviews Neurology · doi:10.1038/nrneurol.2014.226 · Cited by 280
Prevalence and impact of vascular and Alzheimer pathologies in Lewy body disease
Jellinger, K. A., & Attems, J. (2008) · Acta Neuropathologica · doi:10.1007/s00401-008-0347-5 · Cited by 267
Dementia with Lewy bodies and Parkinson’s disease-dementia: current concepts and controversies
Jellinger, K. A. (2017) · Journal of Neural Transmission · doi:10.1007/s00702-017-1821-9 · Cited by 277
Part II: α-synuclein and its molecular pathophysiological role in neurodegenerative disease
Dev, K. K. (2003) · Neuropharmacology · doi:10.1016/s0028-3908(03)00140-0 · Cited by 265
Interface between tauopathies and synucleinopathies: A tale of two proteins
Galpern, W. R., & Lang, A. E. (2006) · Annals of Neurology · doi:10.1002/ana.20819 · Cited by 267
Interleukin-1 mediates Alzheimer and Lewy body pathologies
Griffin, W. S. T., Liu, L., Li, Y., Mrak, R. E., & Barger, S. W. (2006) · Journal of Neuroinflammation · doi:10.1186/1742-2094-3-5 · Cited by 267
Cognitive impairment and dementia in Parkinson's disease
Pagonabarraga, J., & Kulisevsky, J. (2012) · Neurobiology of Disease · doi:10.1016/j.nbd.2012.03.029 · Cited by 272
Shults, C. W., Rockenstein, E., Crews, L., Adame, A., Mante, M., Larrea, G., Hashimoto, M., Song, D., Iwatsubo, T., Tsuboi, K., et al. (2005) · The Journal of Neuroscience · doi:10.1523/jneurosci.3527-05.2005 · Cited by 254
Self-citationBassil, F., Brown, H. J., Pattabhiraman, S., Iwasyk, J. E., Maghames, C. M., Meymand, E. S., Cox, T. O., Riddle, D. M., Zhang, B., Trojanowski, J. Q., et al. (2019) · Neuron · doi:10.1016/j.neuron.2019.10.010 · Cited by 246
Molecular mechanisms of α-synuclein neurodegeneration
Waxman, E. A., & Giasson, B. I. (2008) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2008.09.013 · Cited by 247
Cognitive dysfunction and dementia in Parkinson disease
Caballol, N. S., Martı́, M. J., & TOLOSA, E. S. (2007) · Movement Disorders · doi:10.1002/mds.21677 · Cited by 242
A decade of modeling Alzheimer's disease in transgenic mice
MCGOWAN, E., ERIKSEN, J., & HUTTON, M. (2006) · Trends in Genetics · doi:10.1016/j.tig.2006.03.007 · Cited by 287
Mandler, M., Valera, E., Rockenstein, E. M., Weninger, H., Patrick, C., Adame, A., Santic, R., Meindl, S., Vigl, B., Smrzka, O. W., et al. (2014) · Acta Neuropathologica · doi:10.1007/s00401-014-1256-4 · Cited by 239
Self-citationThe Role of Insulin/IGF-1/PI3K/Akt/GSK3β Signaling in Parkinson's Disease Dementia
Yang, L., Wang, H., Liu, L., & Xie, A. (2018) · Frontiers in Neuroscience · doi:10.3389/fnins.2018.00073 · Cited by 236
Alves, G. W., Brønnick, K., Aarsland, D., Blennow, K., Zetterberg, H., Ballard, C. G., Kurz, M. W., Andréasson, U., Tysnes, O., Larsen, J. O., et al. (2010) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp.2009.199950 · Cited by 221
Mahul‐Mellier, A., Fauvet, B., Gysbers, A. M., Dikiy, I., Oueslati, A., Georgeon, S., Lamontanara, A. J., Bisquertt, A., Eliezer, D., Masliah, E., et al. (2014) · Human Molecular Genetics · doi:10.1093/hmg/ddt674 · Cited by 225
Self-citationMandal, 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
Self-citationMorales, R., Moreno‐González, I., & Soto, C. A. (2013) · PLoS Pathogens · doi:10.1371/journal.ppat.1003537 · Cited by 225
Cross‐seeding effects of amyloid β‐protein and α‐synuclein
Ono, K., Takahashi, R., Ikeda, T., & Yamada, M. (2012) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2012.07847.x · Cited by 222
Aβ deposition is associated with enhanced cortical α-synuclein lesions in Lewy body diseases
Pletniková, O., West, N. C., Lee, M. K., Rudow, G. L., Skolasky, R. L., Dawson, T. M., Marsh, L., & Troncoso, J. C. (2004) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2004.10.006 · Cited by 210
Smailagic, N., Vacante, M., Hyde, C., Martin, S., Ukoumunne, O. C., & Sachpekidis, C. (2015) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd010632.pub2 · Cited by 235
Pedrós, I., Petrov, D., Allgaier, M., Sureda, F. X., Barroso, E., Beas‐Zárate, C., Auladell, C., Pallàs, M., Vázquez‐Carrera, M., Casadesús, G., et al. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2014.05.025 · Cited by 211
Bharadwaj, P., Wijesekara, N., Liyanapathirana, M., Newsholme, P., Ittner, L. M., Fraser, P. E., & Verdile, G. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-161192 · Cited by 209
Ngolab, J., Trinh, I., Rockenstein, E., Mante, M., Florio, J., Trejo, M., Masliah, D., Adame, A., Masliah, E., & Rissman, R. A. (2017) · Acta Neuropathologica Communications · doi:10.1186/s40478-017-0445-5 · Cited by 200
Self-citationRetractedDual-phenotype GABA/glutamate neurons in adult preoptic area: sexual dimorphism and function
Ottem, E. N., Godwin, J. G., Krishnan, S., & Petersen, S. L. (2004) · The Journal of Neuroscience · doi:10.1523/jneurosci.2267-04.2004 · Cited by 201
Regional Multiple Pathology Scores Are Associated with Cognitive Decline in L ewy Body Dementias
Howlett, D. R., Whitfield, D., Johnson, M. A., Attems, J., O'Brien, J. T., Aarsland, D., Lai, M. K. P., Lee, J. H., Chen, C., Ballard, C. G., et al. (2014) · Brain Pathology · doi:10.1111/bpa.12182 · Cited by 199
Confluence of α-Synuclein, Tau, and β-Amyloid Pathologies in Dementia With Lewy Bodies
Colom‐Cadena, M., Gelpí, E., Charif, S., Belbin, O., Blesa, R., Martí, M. J., Clarimón, J., & Lleó, A. (2013) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0000000000000018 · Cited by 188
In vivo alpha-synuclein overexpression in rodents: A useful model of Parkinson's disease?
Chesselet, M. (2007) · Experimental Neurology · doi:10.1016/j.expneurol.2007.08.006 · Cited by 193
Buttini, M., Yu, G.-Q., Shockley, K., Huang, Y., Jones, B., Masliah, E., Mallory, M., Yeo, T., Longo, F. M., & Mucke, L. (2002) · The Journal of Neuroscience · doi:10.1523/jneurosci.22-24-10539.2002 · Cited by 183
“In the presence of murine apoE (Hsia et al., 1999; Mucke et al., 2000; Masliah et al., 2001) or human apoE (this study), A clearly did affect the integrity or function of presynaptic terminals and cholinergic neurons.”
BackgroundSelf-citationAmyloid is linked to cognitive decline in patients with Parkinson disease without dementia
Gomperts, S. N., Locascio, J. J., Rentz, D. M., Santarlasci, A., Marquié, M., Johnson, K. A., & Growdon, J. H. (2012) · Neurology · doi:10.1212/wnl.0b013e31827b1a07 · Cited by 189
Genes, proteins, and neurotoxins involved in Parkinson’s disease
Halbach, O. V. B. U., Schober, A., & KRIEGLSTEIN, K. G. (2004) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2004.05.002 · Cited by 180
Alzheimer's disease pattern of brain atrophy predicts cognitive decline in Parkinson's disease
Weintraub, D. A., Dietz, N., Duda, J. E., Wolk, D. A., Doshi, J. J., Xie, S. X., Davatzikos, C. A., Clark, C. M., & Siderowf, A. D. (2011) · Brain · doi:10.1093/brain/awr277 · Cited by 185
Burré, J., Sharma, M., & Südhof, T. C. (2012) · Journal of Neuroscience · doi:10.1523/jneurosci.3545-12.2012 · Cited by 188
Gómez‐Isla, T., Irizarry, M. C., Mariash, A., Cheung, B. S., Soto, O., Schrump, S. E., Sondel, J., Kotilinek, L., Day, J., Schwarzschild, M. A., et al. (2002) · Neurobiology of Aging · doi:10.1016/s0197-4580(02)00091-x · Cited by 181
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 181
Beagle, A. J., Darwish, S. M., Ranasinghe, K. G., La, A. L., Karageorgiou, E., & Vossel, K. A. (2017) · Journal of Alzheimer's Disease · doi:10.3233/jad-170031 · Cited by 173
Lashley, T., Holton, J. L., Gray, E., Kirkham, K., O’Sullivan, S. S., Hilbig, A., Wood, N. W., Lees, A. J., & Révész, T. (2008) · Acta Neuropathologica · doi:10.1007/s00401-007-0336-0 · Cited by 172
Biological links between traumatic brain injury and Parkinson’s disease
Delic, V., Beck, K. D., Pang, K. C. H., & Citron, B. A. (2020) · Acta Neuropathologica Communications · doi:10.1186/s40478-020-00924-7 · Cited by 165
In vivo amyloid imaging in autopsy-confirmed Parkinson disease with dementia
Burack, M. A., Hartlein, J. M., Flores, H., Taylor-Reinwald, L., Perlmutter, J. S., & Cairns, N. J. (2009) · Neurology · doi:10.1212/wnl.0b013e3181c7da8e · Cited by 165
Genome‐Wide Association Studies of Cognitive and Motor Progression in Parkinson's Disease
Tan, M. M. X., Lawton, M., Jabbari, E., Reynolds, R. H., Iwaki, H., Blauwendraat, C., Kanavou, S., Pollard, M. I., Hubbard, L., Malek, N., et al. (2020) · Movement Disorders · doi:10.1002/mds.28342 · Cited by 163
Development of an α-synuclein positron emission tomography tracer for imaging synucleinopathies
Xiang, J., Tao, Y., Xia, Y., Luo, S., Zhao, Q., Li, B., Zhang, X., Sun, Y., Xia, W., Zhang, M., et al. (2023) · Cell · doi:10.1016/j.cell.2023.06.004 · Cited by 163
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
Interactions of Pathological Hallmark Proteins
Oláh, J., Vincze, O., Virók, D., Simon, D., Bozsó, Z., Tőkési, N., Horváth, I., Hlavanda, E., Kovács, J., Magyar, A., et al. (2011) · Journal of Biological Chemistry · doi:10.1074/jbc.m111.243907 · Cited by 137
Combined dementia-risk biomarkers in Parkinson's disease: A prospective longitudinal study
Compta, Y., Pereira, J. B., Ríos, J., Ibarretxe‐Bilbao, N., Junqué, C., Bargalló, N., Cámara, A., Buongiorno, M., Fernández, M., Pont‐Sunyer, C., et al. (2013) · Parkinsonism & Related Disorders · doi:10.1016/j.parkreldis.2013.03.009 · Cited by 163
Nuber, S., Harmuth, F., Kohl, Z., Adame, A., Trejo, M., Schönig, K., Zimmermann, F., Bauer, C. C., Casadei, N., Giel, C., et al. (2013) · Brain · doi:10.1093/brain/aws358 · Cited by 161
Self-citationMikolaenko, I., Pletniková, O., Kawas, C. H., O’Brien, R., Resnick, S. M., Crain, B. J., & Troncoso, J. C. (2005) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/64.2.156 · Cited by 163
Molecular motors implicated in the axonal transport of tau and α-synuclein
Utton, M. A., Noble, W. J., Hill, J. E., Anderton, B. H., & Hanger, D. P. (2005) · Journal of Cell Science · doi:10.1242/jcs.02558 · Cited by 158
CSF Aβ 42 predicts early-onset dementia in Parkinson disease
Alves, G. W., Lange, J., Blennow, K., Zetterberg, H., Andréasson, U., Førland, M. G. G., Tysnes, O., Larsen, J. O., & Pedersen, K. F. (2014) · Neurology · doi:10.1212/wnl.0000000000000425 · Cited by 158
Ivanova, M. I., Lin, Y., Lee, Y., Zheng, J., & Ramamoorthy, A. (2020) · Biophysical Chemistry · doi:10.1016/j.bpc.2020.106507 · Cited by 155
Ihara, M., Tomimoto, H., Kitayama, H., Morioka, Y., Akiguchi, I., Shibasaki, H., Noda, M., & Kinoshita, M. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m301352200 · Cited by 151
Parkinson's Disease and Related α‐Synucleinopathies Are Brain Amyloidoses
Trojanowski, J. Q., & LEE, V. M. ‐. (2003) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2003.tb07468.x · Cited by 150
Amyloid imaging of Lewy body‐associated disorders
Foster, E. R., Campbell, M. C., Burack, M. A., Hartlein, J. M., Flores, H. P., Cairns, N. J., Hershey, T. G., & Perlmutter, J. S. (2010) · Movement Disorders · doi:10.1002/mds.23393 · Cited by 147
Bouchard, T. P., Malykhin, N. V., Martin, W. R. W., Hanstock, C. C., Emery, D. J., Fisher, N., & Camicioli, R. M. (2007) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2007.02.002 · Cited by 152
Luo, J., Wärmländer, S. K. T. S., Gräslund, A., & Abrahams, J. P. (2016) · Journal of Biological Chemistry · doi:10.1074/jbc.r116.714576 · Cited by 142
The fate of the brain cholinergic neurons in neurodegenerative diseases
Pepeu, G., & Giovannini, M. G. (2017) · Brain Research · doi:10.1016/j.brainres.2017.06.023 · Cited by 144
Metadata
- Authors
- Masliah, E., Rockenstein, E., Veinbergs, I., Sagara, Y., Mallory, M., Hashimoto, M., & Mucke, L.
- Affiliations
- University of California, San Francisco (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2001-09-25
- Volume
- 98
- Issue
- 21
- Pages
- 12245-12250
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC59799
- OpenAlex
- W2131710583
- Cited by
- 607
- References
- 56
- Citations by year
- 2026: 8 · 2025: 26 · 2024: 17 · 2023: 23 · 2022: 17 · 2021: 17 · 2020: 39 · 2019: 26 · 2018: 25 · 2017: 23 · 2016: 24 · 2015: 26 · 2014: 44 · 2013: 29 · 2012: 24
- FWCI
- 15.14
- Type
- journal article
- Language
- en
- Update notices
- correction (2025-05-22)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Alzheimer's Association
- National Institutes of Health (AG5131, 5r29ag010869-05, AG‐18440, AG11385, AG10869)
- National Institute on Aging (AG-11385, R37AG018440, R37AG011385, R01AG018440, P50AG005131, AG-5131, AG 18440, AG10869, R01AG011385)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- amyloid-beta, alpha-synuclein, Alzheimer's disease, Parkinson's disease, Lewy body disease, transgenic mice, neuronal inclusions, alpha-synuclein aggregation, cholinergic neuron degeneration, motor impairment, learning and memory impairment, presynaptic terminals
- MeSH terms
- Age Factors, Alzheimer Disease, Animals, Cell Line, Disease Models, Animal, Female, Humans, Learning Disabilities, Male, Memory Disorders, Mice, Transgenic, Nerve Tissue Proteins, Neurons, Parkinson Disease, Gene Expression, Amyloid beta-Peptides, Mice, Synucleins, alpha-Synuclein
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
