Neuroprotective and Neurotrophic Effects of Lithium on Bipolar Disorder

ABSTRACT: Despite the development of other medications with mood-stabilising properties, such as atypical antipsychotics and antiepileptic drugs, lithium still remains the first-line treatment for bipolar disorder (BPD), and there is increasing evidence for the hypothesis of its neuroprotective and...

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Autores:
Vargas Upegui, Cristian David
López Jaramillo, Carlos Alberto
Vieta, Eduard
Tipo de recurso:
Review article
Fecha de publicación:
2013
Institución:
Universidad de Antioquia
Repositorio:
Repositorio UdeA
Idioma:
eng
OAI Identifier:
oai:bibliotecadigital.udea.edu.co:10495/39554
Acceso en línea:
https://hdl.handle.net/10495/39554
Palabra clave:
Trastorno Bipolar
Bipolar Disorder
Litio
Lithium
Factor Neurotrófico Derivado del Encéfalo
Brain-Derived Neurotrophic Factor
https://id.nlm.nih.gov/mesh/D008094
https://id.nlm.nih.gov/mesh/D001714
https://id.nlm.nih.gov/mesh/D019208
Rights
openAccess
License
Derechos reservados - Está prohibida la reproducción parcial o total de esta publicación
Description
Summary:ABSTRACT: Despite the development of other medications with mood-stabilising properties, such as atypical antipsychotics and antiepileptic drugs, lithium still remains the first-line treatment for bipolar disorder (BPD), and there is increasing evidence for the hypothesis of its neuroprotective and neurotrophic effects as key factors for its clinical effects. Methods: A literature research was conducted using the PubMed database without chronological or language limits to August 2012. The following MESH terms were used: Bipolar Disorder and Lithium combined with: Neuroprotective, Neurotrophic, Neurocognitive effects, GSK-3b, bcl-2, BDNF, hippocampal. Original studies and reviews were selected (in vitro, in vivo and clinical studies). Results: We found evidence in basic studies of neuroprotective and neurotrophic molecular pathways like GSK-3b, Bcl-2, BDNF, glutamate excitotoxicity, AP-1, mitochondrial dysfunction and neurosteroids. Several clinical studies in BPD show increased brain areas, reduced neuronal loss, reduced risk of dementia and one study showed improvement in neurocognitive function (verbal memory) associated with increased hippocampal size in lithium- treated groups versus controls, and other medications. The main areas were hippocampus (HC), anterior cingulate and prefrontal cortex (PFC). Functional Studies with N-Acetyl-aspartate (NAA) also support this hypothesis. Conclusions: Despite basic, structural and functional evidence that shows neurotrophic and neuroprotective effect of lithium, longitudinal studies are needed to clarify the clinical relevance of these findings and their correlation with cognitive performance, which seems to be directly related with functional outcome.