Lithium Prevents Telomere Shortening in Cortical Neurons in Amyloid-Beta Induced Toxicity

Nenhuma Miniatura disponível
Citações na Scopus
Tipo de produção
article
Data de publicação
2023
DOI
Web of Science
Título da Revista
ISSN da Revista
Título do Volume
Editora
MDPI
Autores
Citação
NEUROSCI, v.4, n.1, p.1-8, 2023
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background: There is consistent evidence of the potential benefits of lithium attenuating mechanisms of neurodegeneration, including those related to the pathophysiology of Alzheimer's disease (AD), and facilitating neurotrophic and protective responses, including maintenance of telomere length. The aim was to investigate the protective effect of the pre-treatment with lithium on amyloid-beta (A beta)-induced toxicity and telomere length in neurons. Methods: Cortical neurons were treated with lithium chloride at therapeutic and subtherapeutic concentrations (2 mM, 0.2 mM and 0.02 mM) for seven days. Amyloid toxicity was induced 24 h before the end of lithium treatment. Results: Lithium resulted in 120% (2 mM), 180% (0.2 mM) and 140% (0.02 mM) increments in telomere length as compared to untreated controls. Incubation with A beta 1-42 was associated with significant reductions in MTT uptake (33%) and telomere length (83%) as compared to controls. Conclusions: Lithium prevented loss of culture viability and telomere shortening in neuronal cultures challenged with A beta fibrils.
Palavras-chave
telomere, lithium, cortical neurons, amyloid-beta, Alzheimer's disease
URI
https://observatorio.fm.usp.br/handle/OPI/58019
Referências
  1. Alberts B., 2014, Molecular Biology of the Cell, V6th ed., P254
  2. Apel C, 2009, J NEURAL TRANSM, V116, P71, DOI 10.1007/s00702-008-0135-3
  3. Boccardi V, 2015, AGEING RES REV, V22, P1, DOI 10.1016/j.arr.2015.04.003
  4. Cai ZY, 2013, NEUROMOL MED, V15, P25, DOI 10.1007/s12017-012-8207-9
  5. Cardillo GD, 2018, J ALZHEIMERS DIS, V63, P93, DOI 10.3233/JAD-170838
  6. Cuello AC, 2019, FRONT PHARMACOL, V10, DOI 10.3389/fphar.2019.00189
  7. De-Paula VJ, 2022, N-S ARCH PHARMACOL, V395, P105, DOI 10.1007/s00210-021-02171-6
  8. De-Paula VD, 2015, MOLECULES, V20, P19878, DOI 10.3390/molecules201119663
  9. De-Paula VJ, 2021, METAB BRAIN DIS, V36, P193, DOI 10.1007/s11011-020-00638-8
  10. De-Paula VJ, 2016, BIPOLAR DISORD, V18, P692, DOI 10.1111/bdi.12449
  11. De-Paula VJ, 2016, CURR ALZHEIMER RES, V13, P848, DOI 10.2174/1567205013666160219112612
  12. Forlenza OV, 2014, ACS CHEM NEUROSCI, V5, P443, DOI 10.1021/cn5000309
  13. Forlenza OV, 2019, BRIT J PSYCHIAT, V215, P668, DOI 10.1192/bjp.2019.76
  14. Forlenza OV, 2012, DRUG AGING, V29, P335, DOI 10.2165/11599180-000000000-00000
  15. Forlenza OV, 2011, BRIT J PSYCHIAT, V198, P351, DOI 10.1192/bjp.bp.110.080044
  16. Gherardelli C, 2022, INT J MOL SCI, V23, DOI 10.3390/ijms23158733
  17. Huang WJ, 2016, BIOMED REP, V4, P519, DOI 10.3892/br.2016.630
  18. Jakobsson E, 2017, J MEMBRANE BIOL, V250, P587, DOI 10.1007/s00232-017-9998-2
  19. Liu M, 2020, NEUROREPORT, V31, P943, DOI 10.1097/WNR.0000000000001499
  20. Nunes MA, 2013, CURR ALZHEIMER RES, V10, P104
  21. Quiroz JA, 2010, NEUROPSYCHOBIOLOGY, V62, P50, DOI 10.1159/000314310
  22. Rocha NKR, 2020, FRONT NEUROSCI-SWITZ, V14, DOI 10.3389/fnins.2020.579984
  23. Spilsbury A, 2015, J NEUROSCI, V35, P1659, DOI 10.1523/JNEUROSCI.2925-14.2015
  24. Wang JS, 2015, J AM CHEM SOC, V137, P1213, DOI 10.1021/ja511030s
  25. Zhang Y, 2012, J BIOL CHEM, V287, P32494, DOI 10.1074/jbc.M112.368282

Coleções
Artigos e Materiais de Revistas Científicas - FM/MPS
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - LIM/23
Artigos e Materiais de Revistas Científicas - LIM/27