Serotoninergic antidepressants positively affect platelet ADAM10 expression in patients with Alzheimer's disease.
Int Psychogeriatr
; 28(6): 939-44, 2016 06.
Article
em En
| MEDLINE
| ID: mdl-26555131
BACKGROUND: Studies have demonstrated a decreased platelet ADAM10 expression in patients with Alzheimer's Disease (AD), classifying this protein as a blood-based AD biomarker. About 50% of the patients with AD are diagnosed with depression, which is commonly treated with tricyclic and tetracyclic antidepressants, monoaminoxidade (MAO) inhibitors and, more preferably, with selective serotonin reuptake inhibitors (SSRIs). Considering that a large proportion of patients with AD takes antidepressant medications during the course of the disease we investigated the influence of this medication on the expression of platelet ADAM10, which is considered the main α-secretase preventing beta-amyloid (ßA) formation. METHODS: Blood was collected for protein extraction from platelets. ADAM10 was analyzed by using western blotting and reactive bands were measured using ß-actin as endogenous control. RESULTS: Platelet ADAM10 protein expression in patients with AD was positively influenced by serotoninergic medication. CONCLUSION: More studies on the positive effects of serotonergic antidepressants on ADAM10 platelet expression should be performed in order to understand its biological mechanisms and to verify whether these effects are reflected in the central nervous system. This work represents an important advance for the study of AD biomarkers, as well as for more effective pharmacological treatment of patients with AD and associated depression.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Plaquetas
/
Inibidores Seletivos de Recaptação de Serotonina
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Doença de Alzheimer
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Proteína ADAM10
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Antidepressivos
Limite:
Female
/
Humans
País/Região como assunto:
America do sul
/
Brasil
Idioma:
En
Revista:
Int Psychogeriatr
Assunto da revista:
GERIATRIA
/
PSIQUIATRIA
Ano de publicação:
2016
Tipo de documento:
Article
País de afiliação:
Brasil
País de publicação:
Reino Unido