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  1.  63
    Genes can disconnect the social brain in more than one way.André Aleman & René S. Kahn - 2004 - Behavioral and Brain Sciences 27 (6):855-855.
    Burns proposes an intriguing hypothesis by suggesting that the “schizophrenia genes” might not be regulatory genes themselves, but rather closely associated with regulatory genes directly involved in the proper growth of the social brain. We point out that this account would benefit from incorporating the effects of localized lesions and aberrant hemispheric asymmetry on cortical connectivity underlying the social brain. In addition, we argue that the evolutionary framework is superfluous.
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  2.  36
    Top-down modulation, emotion, and hallucination.André Aleman & René S. Kahn - 2002 - Behavioral and Brain Sciences 25 (5):578-578.
    We argue that the pivotal role assigned by Northoff to the principle of top-down modulation in catatonia might successfully be applied to other symptoms of schizophrenia, for example, hallucinations. Second, we propose that Northoff's account would benefit from a more comprehensive analysis of the cognitive level of explanation. Finally, contrary to Northoff, we hypothesize that “top-down modulation” might play as important a role as “horizontal modulation” in affective-behavioral alterations.
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  3.  77
    Underconstrained perception or underconstrained theory?André Aleman, Edward H. F. de Haan & René S. Kahn - 2004 - Behavioral and Brain Sciences 27 (6):787-788.
    Although the evidence remains tentative at best, the conception of hallucinations in schizophrenia as being underconstrained perception resulting from intrinsic thalamocortical resonance in sensory areas might complement current models of hallucination. However, in itself, the approach falls short of comprehensively explaining the neurogenesis of hallucinations in schizophrenia, as it neglects the role of external attributional biases, mental imagery, and a disconnection between frontal and temporal areas.
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  4.  6
    Diminished Feedback Evaluation and Knowledge Updating Underlying Age-Related Differences in Choice Behavior During Feedback Learning.Tineke de Haan, Berry van den Berg, Marty G. Woldorff, André Aleman & Monicque M. Lorist - 2021 - Frontiers in Human Neuroscience 15.
    In our daily lives, we continuously evaluate feedback information, update our knowledge, and adapt our behavior in order to reach desired goals. This ability to learn from feedback information, however, declines with age. Previous research has indicated that certain higher-level learning processes, such as feedback evaluation, integration of feedback information, and updating of knowledge, seem to be affected by age, and recent studies have shown how the adaption of choice behavior following feedback can differ with age. The neural mechanisms underlying (...)
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  5.  27
    Mental imagery: In search of my theory.Edward de Haan & André Aleman - 2002 - Behavioral and Brain Sciences 25 (2):188-189.
    We argue that the field has moved forward from the old debate about “analogical” versus “symbolic” processing. First, it is questionable that there is a strong a priori argument for assuming a common processing mode. Second, we explore the possibility that imagery is not a unitary mental function. Finally, we discuss the empirical basis of the involvement of primary areas.
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  6.  29
    Neural correlates of reward processing in healthy siblings of patients with schizophrenia.Esther Hanssen, Jorien van der Velde, Paula M. Gromann, Sukhi S. Shergill, Lieuwe de Haan, Richard Bruggeman, Lydia Krabbendam, André Aleman & Nienke van Atteveldt - 2015 - Frontiers in Human Neuroscience 9.
  7.  38
    Psychosis and autism as two developmental windows on a disordered social brain.Sophie van Rijn, Hanna Swaab & André Aleman - 2008 - Behavioral and Brain Sciences 31 (3):280-281.
    With regard to social-cognitive deficits in autism and psychosis, Crespi & Badcock's (C&B's) theory does not incorporate the developmental context of the disorders. We propose that there is significant overlap in social-cognitive impairments, but that the exact manifestation of social-cognitive deficits is highly dependent on the dynamics of cognitive development and hence different in autism as compared to psychosis.
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