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[A potential neuroprotective and synaptic plasticity mechanism induced by estradiol through PI3K/GSK3beta in cerebral
A A Barrera-Ocampo1, A E Céspedes-Rubio, G P Cardona-Gómez
1Grupo de Neurociencias, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia.
Aim:
To review the basic molecular mechanisms that are triggered by neuroactive steroids related to protection and plasticity, and their possible therapeutic application in cases of cerebral ischaemia.
Development:
The term 'neuroprotection' embraces a series of strategies and effects that are aimed at preventing, impeding or delaying anomalies in the functioning of the central nervous system. The neuroactive steroids, and particularly estradiol, have been widely reported owing to their neuroprotective action because they give rise to a wide range of cell signals and generate effects in genes by means of canonical pathways or through non-conventional mechanisms that are involved in neuronal survival, dendritogenesis and synapse remodelling. Thus, neuroactive steroids become an important long-term protective therapeutic alternative due to the fact that such effects converge on neuronal plasticity.
Conclusions:
Further work needs to be carried out to study the mechanisms of action of neuroactive steroids, especially the non-conventional ones, which involve proteins such as GSK-3beta and beta-catenin. These proteins are involved in the functions of synaptic plasticity and survival, and play a crucial role in maintaining and recovering the functional integrity of the brain after the appearance of the lesions caused by cerebral ischaemia.
Insights
Neuroactive steroids, like estradiol, offer neuroprotection and promote brain plasticity by influencing cell signals and gene expression. Further research into their mechanisms could lead to new therapies for cerebral ischemia.
Area of Science:
- Neuroscience
- Molecular Biology
- Pharmacology
Background:
- Neuroprotection involves strategies to prevent or delay central nervous system dysfunction.
- Neuroactive steroids, particularly estradiol, demonstrate significant neuroprotective effects.
- These steroids modulate cell signaling and gene expression via canonical and non-conventional pathways.
Purpose of the Study:
- To review the molecular mechanisms of neuroactive steroids in neuroprotection and plasticity.
- To explore their therapeutic potential in cerebral ischemia.
Main Methods:
- Review of literature on neuroactive steroids and their effects on neuronal survival, dendritogenesis, and synapse remodeling.
- Focus on both conventional and non-conventional signaling pathways.
- Investigation of the role of specific proteins like GSK-3beta and beta-catenin.
Main Results:
- Neuroactive steroids activate diverse cell signaling cascades.
- They influence gene expression related to neuronal survival and plasticity.
- Estradiol is highlighted for its broad neuroprotective actions.
Conclusions:
- Neuroactive steroids represent a promising therapeutic avenue for long-term neuroprotection.
- Further investigation of non-conventional mechanisms involving GSK-3beta and beta-catenin is warranted.
- These pathways are critical for brain functional integrity post-ischemia.
