This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Short Report
Vanessa de Paula
Universidade de Sao Paulo Instituto de Psiquiatria
Corresponding Author
ORCiD: https://orcid.org/0000-0002-2054-6356
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This work is licensed under a CC BY 4.0 License. Read Full License
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 (Aβ)-induced toxicity and telomere length in neurons.
Methods
Cortical neurons were treated with lithium chloride at therapeutic and subtherapeutic concentrations (2mM, 0.2mM and 0.02mM) for seven days. Amyloid toxicity was induced 24 hours before the end of lithium treatment.
Results
Lithium resulted in 120% (2mM), 180% (0.2mM) and 140% (0.02mM) increments in telomere length as compared to untreated controls. Incubation with Aβ1-42 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 Aβ fibrils.
Keywords
telomere, lithium, cortical neurons, amyloid-beta, Alzheimer’s disease
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Developmental Neuroscience
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Short Report
Vanessa de Paula
Universidade de Sao Paulo Instituto de Psiquiatria
Corresponding Author
ORCiD: https://orcid.org/0000-0002-2054-6356
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 03 Mar, 2021
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Developmental Neuroscience
License:
This work is licensed under a CC BY 4.0 License. Read Full License
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 (Aβ)-induced toxicity and telomere length in neurons.
Methods
Cortical neurons were treated with lithium chloride at therapeutic and subtherapeutic concentrations (2mM, 0.2mM and 0.02mM) for seven days. Amyloid toxicity was induced 24 hours before the end of lithium treatment.
Results
Lithium resulted in 120% (2mM), 180% (0.2mM) and 140% (0.02mM) increments in telomere length as compared to untreated controls. Incubation with Aβ1-42 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 Aβ fibrils.
Figure 1
Figure 2
This is a list of supplementary files associated with this preprint. Click to download.
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