The DOI matches its Crossref record; 29 of the 31 references it cites were found in a registry or an index, and 2 are not checked yet.
Neurotrophic and Neurotoxic Effects of Amyloid β Protein: Reversal by Tachykinin Neuropeptides
Abstract
The amyloid β protein is deposited in the brains of patients with Alzheimer's disease but its pathogenic role is unknown. In culture, the amyloid β protein was neurotrophic to undifferentiated hippocampal neurons at low concentrations and neurotoxic to mature neurons at higher concentrations. In differentiated neurons, amyloid β protein caused dendritic and axonal retraction followed by neuronal death. A portion of the amyloid β protein (amino acids 25 to 35) mediated both the trophic and toxic effects and was homologous to the tachykinin neuropeptide family. The effects of the amyloid β protein were mimicked by tachykinin antagonists and completely reversed by specific tachykinin agonists. Thus, the amyloid β protein could function as a neurotrophic factor for differentiating neurons, but at high concentrations in mature neurons, as in Alzheimer's disease, could cause neuronal degeneration.
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“This Aβ peptide fragment contains the biologically active portion of Aβ (Yanker et al., 1990; Takadera et al., 1993).”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Yanker et al., 1990
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Cites
Glenner, G. G., & Wong, C. W. (1984) · Biochemical and Biophysical Research Communications · doi:10.1016/s0006-291x(84)80190-4 · Cited by 5,404
The precursor of Alzheimer's disease amyloid A4 protein resembles a cell-surface receptor
Kang, J., Lemaire, H.-G., Unterbeck, A., Salbaum, J. M., Masters, C. L., Grzeschik, K.-H., Multhaup, G., Beyreuther, K., & Müller-Hill, B. (1987) · Nature · doi:10.1038/325733a0 · Cited by 4,619
Amyloid plaque core protein in Alzheimer disease and Down syndrome.
Masters, C. L., Simms, G., Weinman, N. A., Multhaup, G., McDonald, B. L., & Beyreuther, K. (1985) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.82.12.4245 · Cited by 4,431
The establishment of polarity by hippocampal neurons in culture.
Dotti, C., Sullivan, C., & Banker, G. (1988) · The Journal of Neuroscience · doi:10.1523/jneurosci.08-04-01454.1988 · Cited by 1,862
Glutamate neurotoxicity in cortical cell culture
Choi, D. W., Maulucci-Gedde, M., & Kriegstein, A. (1987) · Journal of Neuroscience · doi:10.1523/jneurosci.07-02-00357.1987 · Cited by 1,506
Rat hippocampal neurons in dispersed cell culture.
Banker, G. A., & Cowan, W. M. (1977) · Brain Research · doi:10.1016/0006-8993(77)90594-7 · Cited by 1,110
Masters, C. L., Multhaup, G., Simms, G., Pottgiesser, J., Martins, R. N., & Beyreuther, K. T. (1985) · The EMBO Journal · doi:10.1002/j.1460-2075.1985.tb04000.x · Cited by 1,048
Neurotoxicity of a Fragment of the Amyloid Precursor Associated with Alzheimer's Disease
Yankner, B. A., Dawes, L. R., Fisher, S., Villa-Komaroff, L., Oster-Granite, M. L., & Neve, R. L. (1989) · Science · doi:10.1126/science.2474201 · Cited by 907
Self-citationOutgrowth-regulating actions of glutamate in isolated hippocampal pyramidal neurons
Mattson, M. P., Dou, P., & Kater, S. B. (1988) · Journal of Neuroscience · doi:10.1523/jneurosci.08-06-02087.1988 · Cited by 557
Maggio, J. E. (1988) · Annual Review of Neuroscience · doi:10.1146/annurev.ne.11.030188.000305 · Cited by 550
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Research works printed but not linked: 2
- Dayhoff, M. O., Atlas of Protein Sequence and Structure 5 3: 345 (1978).
- GLENNER, G, BRANBURY REPORT 15: 137 (1983).
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Li, X., Uemura, K., Hashimoto, T., Nasser-Ghodsi, N., Arimon, M., Lill, C. M., Palazzolo, I., Krainc, D., Hyman, B. T., & Berezovska, O. (2013) · Neurobiology of Disease · doi:10.1016/j.nbd.2012.10.002 · Cited by 38
β-Amyloid Enhances Glial Glutamate Uptake Activity and Attenuates Synaptic Efficacy
Ikegaya, Y., Matsuura, S., Ueno, S., Baba, A., Yamada, M. K., Nishiyama, N., & Matsuki, N. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m203764200 · Cited by 39
Lemmens, M. A. M., Sierksma, A. S. R., Rutten, B. P. F., Dennissen, F., Steinbusch, H. W. M., Lucassen, P. J., & Schmitz, C. (2011) · Brain Structure and Function · doi:10.1007/s00429-011-0305-1 · Cited by 37
Chen, G.-J., Xiong, Z., & Yan, Z. (2013) · Molecular Neurodegeneration · doi:10.1186/1750-1326-8-3 · Cited by 30
Beta-amyloid short- and long-term synaptic entanglement
Lanni, C., Fagiani, F., Racchi, M., Preda, S., Pascale, A., Grilli, M., Allegri, N., & Govoni, S. (2019) · Pharmacological Research · doi:10.1016/j.phrs.2018.11.018 · Cited by 29
Part, K., Künnis-Beres, K., Poska, H., Land, T., Shimmo, R., & Zetterström Fernaeus, S. (2015) · Brain Research · doi:10.1016/j.brainres.2015.09.034 · Cited by 16
Carvalho, K. M., França, M. S. F., Camarão, G. C., & Ruchon, A. F. (1997) · Brazilian Journal of Medical and Biological Research · doi:10.1590/s0100-879x1997001000002 · Cited by 11
Klegeris (1997) · doi:10.1002/(sici)1097-4547(19970715)49:2
Metadata
- Authors
- Yankner, B. A., Duffy, L. K., & Kirschner, D. A.
- Affiliations
- Boston Children's Hospital (US)
- University of Alaska Fairbanks (US)
- Venue
- Science
- Published
- 1990-10-12
- Volume
- 250
- Issue
- 4978
- Pages
- 279-282
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2059214757
- Cited by
- 1,975
- References
- 31
- Citations by year
- 2026: 9 · 2025: 17 · 2024: 15 · 2023: 22 · 2022: 14 · 2021: 29 · 2020: 19 · 2019: 29 · 2018: 32 · 2017: 27 · 2016: 37 · 2015: 44 · 2014: 46 · 2013: 40 · 2012: 40
- FWCI
- 64.80
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (AG08572, R01AG008572)
- National Institute of Neurological Disorders and Stroke (NS01240, K08NS001240)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- amyloid-beta, Alzheimer's disease, neurotoxicity, neurotrophic effects, tachykinin antagonists, hippocampal neurons, neuronal differentiation, neuronal cell death, dendritic retraction, axonal retraction, neurotrophic factors
- MeSH terms
- Amino Acid Sequence, Animals, Cells, Cultured, Embryo, Mammalian, Hippocampus, Molecular Sequence Data, Neurons, Neurotoxins, Peptide Fragments, Tachykinins, Amyloid beta-Peptides, Rats
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