The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
Lithium, a Common Drug for Bipolar Disorder Treatment, Regulates Amyloid-β Precursor Protein Processing
Abstract
Lithium is one of the most widely used mood-stabilizing agents for the treatment of bipolar disorder. Although the underlying mechanism(s) of this mood stabilizer remains controversial, recent evidence linking lithium to neurotrophic/neuroprotective effects (Choi and Sung (2000) 1475, 225-230; Davies et al. (2000) 351, 95-105) suggests novel benefits of this drug in addition to mood stabilization. Here, we report that both lithium as well as valproic acid (VPA) inhibit beta-amyloid peptide (Abeta) production in HEK293 cells stably transfected with Swedish amyloid precursor protein (APP)(751) and in the brains of the PDAPP (APP(V717F)) Alzheimer's disease transgenic mouse model at clinically relevant plasma concentrations. Both lithium and VPA are known to be glycogen synthase kinase-3 (GSK3) inhibitors. Our studies reveal that GSK3beta is a potential downstream kinase, which modulates APP processing because inhibition of GSK3 activity by either a dominant negative GSK3beta kinase-deficient construct or GSK3beta antisense oligonucleotide mimics lithium and VPA effects. Moreover, lithium treatment abolished GSK3beta-mediated Abeta increase in the brains of GSK3beta transgenics and reduced plaque burden in the brains of the PDAPP (APP(V717F)) transgenic mice.
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Citations
Cites
The Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics
Hardy, J., & Selkoe, D. J. (2002) · Science · doi:10.1126/science.1072994 · Cited by 13,864
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
Specificity and mechanism of action of some commonly used protein kinase inhibitors
DAVIES, S. P., REDDY, H., CAIVANO, M., & COHEN, P. (2000) · Biochemical Journal · doi:10.1042/bj3510095 · Cited by 3,132
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
A molecular mechanism for the effect of lithium on development.
Klein, P. S., & Melton, D. A. (1996) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.93.16.8455 · Cited by 2,301
Isolation and quantification of soluble Alzheimer's β-peptide from biological fluids
Seubert, P., Vigo-Pelfrey, C., Esch, F., Lee, M., Dovey, H., Davis, D., Sinha, S., Schiossmacher, M., Whaley, J., Swindlehurst, C., et al. (1992) · Nature · doi:10.1038/359325a0 · Cited by 1,731
The multifaceted roles of glycogen synthase kinase 3β in cellular signaling
Grimes, C. A., & Jope, R. S. (2001) · Progress in Neurobiology · doi:10.1016/s0301-0082(01)00011-9 · Cited by 1,423
Lithium inhibits glycogen synthase kinase-3 activity and mimics wingless signalling in intact cells
Stambolic, V., Ruel, L., & Woodgett, J. R. (1996) · Current Biology · doi:10.1016/s0960-9822(02)70790-2 · Cited by 1,321
GSK-3α regulates production of Alzheimer's disease amyloid-β peptides
Phiel, C. J., Wilson, C. A., Lee, V. M.-Y., & Klein, P. S. (2003) · Nature · doi:10.1038/nature01640 · Cited by 1,196
Hallcher, L. M., & Sherman, W. R. (1980) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(19)70391-3 · Cited by 1,101
Cited by
Blennow, K., de Leon, M. J., & Zetterberg, H. (2006) · The Lancet · doi:10.1016/s0140-6736(06)69113-7 · Cited by 3,134
Glycogen synthase kinase-3 (GSK3): Inflammation, diseases, and therapeutics
Jope, R. S., Yuskaitis, C. J., & Beurel, E. (2007) · Neurochemical Research · doi:10.1007/s11064-006-9128-5 · Cited by 774
History and progress of hypotheses and clinical trials for Alzheimer’s disease
Liu, P.-P., Xie, Y., Meng, X.-Y., & Kang, J.-S. (2019) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-019-0063-8 · Cited by 723
Rajmohan, R., & Reddy, P. H. (2017) · Journal of Alzheimer’s Disease · doi:10.3233/jad-160612 · Cited by 688
Multiple roles of HDAC inhibition in neurodegenerative conditions
Chuang, D.-M., Leng, Y., Marinova, Z., Kim, H.-J., & Chiu, C.-T. (2009) · Trends in Neurosciences · doi:10.1016/j.tins.2009.06.002 · Cited by 676
Metadata
- Authors
- Su, Y., Ryder, J., Li, B., Wu, X., Fox, N., Solenberg, P., Brune, K., Paul, S., Zhou, Y., Liu, F., & Ni, B.
- Venue
- Biochemistry
- Publisher
- American Chemical Society (ACS)
- Published
- 2004-05-12
- Volume
- 43
- Issue
- 22
- Pages
- 6899-6908
- ISSN
- 0006-2960 (ISSN-L)
- 1520-4995
- OpenAlex
- W2054183594
- Cited by
- 296
- References
- 41
- FWCI
- 8.36
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: Lithium, a Common Drug for Bipolar Disorder Treatment, Regulates Amyloid-β Precursor Protein Processing. https://app.cochat.ai/papers/10.1021/bi035627j
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- Su, Y., Ryder, J., Li, B., Wu, X., Fox, N., Solenberg, P., Brune, K., Paul, S., Zhou, Y., Liu, F., & Ni, B. (2004). Lithium, a Common Drug for Bipolar Disorder Treatment, Regulates Amyloid-β Precursor Protein Processing. Biochemistry. https://doi.org/10.1021/bi035627j
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