عنوان انگلیسی مقاله:
Reinforcement learning as an intermediate phenotype in psychosis? Deficits sensitive to illness stage but not associated with polygenic risk of schizophrenia in the general population
ترجمه فارسی عنوان مقاله:
یادگیری تقویتی به عنوان یک فنوتیپ متوسط در روان پریشی؟ کمبودهای حساس به مرحله بیماری اما با خطر پلی ژنیک اسکیزوفرنی در جمعیت عمومی ارتباط ندارد
Sciencedirect - Elsevier - Schizophrenia Research, Corrected proof. doi:10.1016/j.schres.2020.04.022
Marcella Montagnese a, Franziska Knolle a, Joost Haarsma a, Juliet D. Griffin a, Alex Richards h, Petra E. Vertes a, Beatrix Kiddle a, Paul C. Fletcher a,b,f, Peter B. Jones a,f, Michael J. Owen h, Peter Fonagy g, Edward T. Bullmore a,c,f, Raymond J. Dolan d,e,NSPN Consortium , Michael Moutoussis d,e, Ian M. Goodyer a,f, Graham K. Murray
Background: Schizophrenia is a complex disorder in which the causal relations between risk genes and observed
clinical symptoms are not well understood and the explanatory gap is too wide to be clarified without considering
an intermediary level. Thus, we aimed to test the hypothesis of a pathway frommolecular polygenic influence
to clinical presentation occurring via deficits in reinforcement learning.
Methods: We administered a reinforcement learning task (Go/NoGo) that measures reinforcement learning and
the effect of Pavlovian bias on decision making. We modelled the behavioural data with a hierarchical Bayesian
approach (hBayesDM) to decompose task performance into its underlying learning mechanisms. Study 1 included
controls (n = 29, F|M = 0.81), At Risk Mental State for psychosis (ARMS, n = 23, F|M= 0.35) and FEP
(First-episode psychosis, n = 26, F|M = 0.18). Study 2 included healthy adolescents (n = 735, F|M = 1.06),
390 of whom had their polygenic risk scores for schizophrenia (PRSs) calculated.
Results: Patients with FEP showed significant impairments in overriding Pavlovian conflict, a lower learning rate
and a lower sensitivity to both reward and punishment. Less widespread deficits were observed in ARMS. PRSs
did not significantly predict performance on the task in the general population, which only partially correlated
with measures of psychopathology.
Conclusions: Reinforcement learning deficits are observed in first episode psychosis and, to some extent, in those
at clinical risk for psychosis, and were not predicted by molecular genetic risk for schizophrenia in healthy individuals.
The study does not support the role of reinforcement learning as an intermediate phenotype in psychosis.
Keywords: Psychosis | Schizophrenia | PRS | Bayesian | Reinforcement learning | Go/NoGo task | Computational psychiatry