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HTTLPR functional polymorphism in schizophrenia: executive functions vs. sustained attention dissociation.
Marta Bosia1, Simona Anselmetti, Adele Pirovano
1Department of Clinical Neurosciences, San Raffaele Universitary Scientific Institute Hospital, Via Stamira d'Ancona 20, 20127 Milano, Italy. bosia.marta@hsr.it
The serotonin transporter gene polymorphism (5-HTTLPR) influences cognitive functions in schizophrenia patients. The long allele (L) is linked to better executive function but poorer attention.
Area of Science:
- Neuroscience
- Psychiatry
- Genetics
Background:
- Serotonin (5-HT) plays a crucial role in cognitive functions.
- Genetic variations in serotonin neurotransmission regulators, like the serotonin transporter gene polymorphism (5-HTTLPR), can impact cognition.
- Cognitive impairments are a hallmark of schizophrenia, suggesting potential therapeutic targets in serotonergic pathways.
Purpose of the Study:
- To investigate the association between the 5-HTTLPR polymorphism and specific cognitive functions in schizophrenia patients.
- To determine if genetic variations in serotonin transporter influence executive functions and attention.
Main Methods:
- 223 schizophrenia patients were genotyped for the 5-HTTLPR polymorphism.
- Cognitive flexibility was assessed using the Wisconsin Card Sorting Test (WCST).
- Sustained attention was evaluated with the Continuous Performance Test (CPT).
Main Results:
- A significant association was found between the 5-HTTLPR polymorphism and executive functions.
- The presence of the high-activity long (L) allele in homozygosis predicted better executive performances.
- Conversely, the L allele homozygosis was associated with poorer sustained attention.
Conclusions:
- Serotonin availability, influenced by genetic factors like 5-HTTLPR, plays a specific role in cognitive processes.
- These findings suggest complex modulations of cognitive components by serotonergic system variations.
- Understanding these genetic influences may inform novel treatment strategies for cognitive deficits in schizophrenia.
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