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Kraepelin Revisited: Schizophrenia from Degeneration to Failed Regeneration

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Kraepelin Revisited: Schizophrenia from Degeneration to Failed Regeneration Molecular Psychiatry (2015) 20, 671–676 © 2015 Macmillan Publishers Limited All rights reserved 1359-4184/15 www.nature.com/mp REVIEW Kraepelin revisited: schizophrenia from degeneration to failed regeneration P Falkai1, MJ Rossner1,2, TG Schulze3, A Hasan1, MM Brzózka1, B Malchow1, WG Honer4 and A Schmitt1,5 One hundred years after its conceptual definition as ‘Dementia Praecox’ by Emil Kraepelin, schizophrenia is still a serious psychiatric illness that affects young adults and leads to disability in at least half of patients. The key treatment issue is partial or non-response, especially of negative symptoms. The illness is also associated with different degrees of cognitive dysfunction, particularly in verbal and working memory; the resulting functional impairment may lead to unemployment and an inability to maintain stable relationships. Patients’ cognitive dysfunction led Kraepelin to the assumption that schizophrenia is a form of juvenile dementia caused by a degenerative process of the human brain. Postmortem studies and a plethora of imaging studies do not support the notion of a degenerative process, but such a process is supported by the recently published, largest genome-wide association study on schizophrenia. More than a 100 hits were described, converging on pathways that have a significant role in dopamine metabolism in immune modulation, calcium signalling and synaptic plasticity. This review suggests that research should focus on animal models based on risk genes like transcription factor 4 and study the effects of exposure to environmental stressors relevant for schizophrenia. The use of relevant end points like pre-pulse inhibition or cognitive dysfunction will allow us to gain an understanding of the molecular pathways in schizophrenia and consequently result in improved treatment options, especially for the disabling aspects of this illness. Molecular Psychiatry (2015) 20, 671–676; doi:10.1038/mp.2015.35; published online 31 March 2015 INTRODUCTION In the 6th edition of his textbook ‘Psychiatrie’,1 published in More than 100 years after its conceptual definition as ‘Dementia 1899, Kraepelin (Figure 1) grouped most of the insanities into two Praecox’ by Emil Kraepelin, schizophrenia is still a serious large categories: Dementia Praecox and manic-depressive illness psychiatric illness. The introduction of antipsychotic drugs in (the so-called Kraepelinian dichotomy). Dementia Praecox was 1953 helped improve outcome significantly; however, since then characterised by the following features: there have been only limited developments in long-term out- come. Paralleling human studies and animal experiments may ● It was primarily a disorder of intellectual functioning, whereas lead to a deeper understanding of the pathophysiology of manic-depressive illness was primarily a disorder of affect schizophrenia and subsequently to causal treatment options for or mood. patients. This review, written by a group of researchers from the ● It had a deteriorating course and a poor prognosis, whereas Department of Psychiatry at the University Hospital in Munich, manic-depressive illness had a course of acute exacerbations once chaired by E Kraepelin himself (1903–1922), puts its focus on followed by complete remissions. cognition, and thus offers a conceptual framework of schizo- phrenia from ethological factors through brain mechanisms and functional consequences in patients to related animal models. ALOIS ALZHEIMER: DEMENTIA PRAECOX AS A DEGENERATIVE DISORDER E KRAEPLIN: ‘DEMENTIA PRAECOX’ AND COGNITIVE E Kraepelin categorised patients with a major psychiatric illness on DYSFUNCTION the basis of their long-term course. At admission, a score sheet The term Dementia Praecox, which refers to ‘premature dementia’ (‘Zählkarte’) was compiled for each patient that contained all the or ‘precocious madness’, was first used in this Latin form in 1891 necessary information to allow Kraepelin and his team to classify by Arnold Pick (1851–1924), a professor of psychiatry at the patients at the end of the hospital stay and in the years of follow- German branch of Charles University in Prague. It was popularised up. In addition to his work on classifying mental illness to identify by E Kraepelin in his textbooks published in 1893, 1896 and 1899, aetiological subgroups, Kraepelin encouraged talented young in which he referred to a chronic, deteriorating psychotic illness people to come to the department in Munich and supported their characterised by rapid cognitive disintegration, usually beginning research on mental disorders. In addition to Franz Nissl (1860– in the late teens or early adulthood. 1919), who invented the cell staining method now bearing his 1Department of Psychiatry and Psychotherapy; Ludwig-Maximilians-University, Munich, Germany; 2Max-Planck-Institute of Experimental Medicine, Goettingen, Germany; 3Institute for Psychiatric Phenomics and Genomics; Ludwig-Maximilians-University, Munich, Germany; 4Department of Psychiatry; University of British Columbia, Canada and 5Laboratory of Neuroscience (LIM27), Institute of Psychiatry, University of Sao Paulo, Sao Paulo, Brazil. Correspondence: Professor P Falkai, Department of Psychiatry and Psychotherapy, Ludwig-Maximilians-University (LMU), Nussbaumstrasse 7, München 80336, Germany. E-mail: [email protected] Received 26 September 2014; revised 11 February 2015; accepted 24 February 2015; published online 31 March 2015 Kraepelin revisited P Falkai et al 672 affectivity and ambivalence) and that the biological disease was much more prevalent in the population than previously assumed because of its ‘simple’ and especially ‘latent’ forms. SCHIZOPHRENIA TODAY: STILL A COGNITIVE DISORDER WITH AN UNFAVOURABLE OUTCOME? More than a 100 years after Kraepelin popularised the term Dementia Praecox, schizophrenia still has an unfavourable prognosis. The worldwide prevalence is 1% and the first onset is usually in young adults aged between 20 and 35.5,6 Only 20% of patients are employed in the primary labour market and only 30% are able to maintain a stable relationship.7 The introduction of antipsychotics by Delay and Deniker in 1953 significantly helped to improve the severity of acute symptoms and prevent relapses in many patients. Nevertheless, 60 years later 450% of patients still do not show remission but have residual syndromes of significant functional relevance.8,9 After reconstruct- ing the prodromal stages of first-episode schizophrenia and performing a systematic follow-up, Häfner and an der Heiden were able to show that patients who develop the illness between the ages of 36 and 59 demonstrate a significant loss of their ability to maintain unsheltered work years before their first admission (‘social prognosis’). Treating these patients improved the social prognosis to some extent; however, in the end only ~ 30% were able to maintain unsheltered work, compared with 80% at the beginning of the illness.7 This study showed clearly that negative symptoms, consisting of affective and cognitive domains, contribute substantially to this unfavourable long-term outcome. The stability of the cognitive deficits, particularly episodic and verbal memory, was convincingly shown in 5- and 10-year follow- up studies of first-episode schizophrenia.10 UNDERSTANDING COGNITIVE DYSFUNCTION IN Figure 1. Emil Kraepelin, 1921 at the Department of Psychiatry, SCHIZOPHRENIA: HUMAN STUDIES Munich. As outlined above, cognitive dysfunction is one key to the unfavourable outcome in schizophrenia and may be independent name, it was A Alzheimer who systematically investigated the of the long-term course of both positive and negative fi postmortem brains of patients with Dementia Praecox. In his rst symptoms.11,12,13 Recent studies suggest that cognitive distur- publication he described the thinning of the neocortical layers, 2 bance in schizophrenia contributes to relapses and also has a role which he interpreted as a sign of a destructive process. These and in the likelihood of remission. Understanding the underlying other investigations brought E Kraepelin in 1913 to the following neurobiology of cognitive dysfunction is critical to improve ‘ conclusions: These considerations force us to draw the direct outcome, and parallel investigations of patients and animal models conclusion that there must be a manifest destruction of the cortex. form the best strategy to improve such understanding (Figure 2). In those cases that have been investigated more closely by reliable Family and adoption studies show that the risk to develop means, regular alterations have actually been demonstrated for schizophrenia has a large genetic contribution of up to 80%. In which there is no other explanation. [....]. We therefore reach the recent years, large-scale collaborative genome-wide association conclusion that in Dementia Praecox there is severe damage to or studies have identified well over 100 genes that may contribute to destruction of the nervous cortical elements, which may be the pathophysiology of schizophrenia.14 Interestingly, these genes compensated for in individual cases, but which mostly results in a converge on pathways that have a significant role in immune ’ 3 peculiar, persistent impairment of the psyche . modulation (major histocompatibility complex), calcium signalling (CACNA1C and CACNB) and regulating neuronal plasticity and adult EUGEN BLEULER: THE SCHIZOPHRENIAS AND COGNITIVE neurogenesis (microRNA MIR137 (which codes for miR-137)and IMPAIRMENT transcription factor 4, TCF4), both of which are components
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