Background: The recent literature frequently represents schizophrenia as a deteriorating neurocognitive process similar to organic degenerative dementia.
Methods: This study addresses the following questions: (1) Did the classic authors equate degenerative dementia with schizophrenia? (2) Is there empirical evidence pointing to a close similarity between schizophrenia and organic dementia? (3) Does empirical evidence support the view that intellectual impairment and/or more specific neuropsychological dysfunctions are core features of schizophrenia? The classic authors agreed that the intellectual dysfunctions were most likely a consequence rather than a primary, causal factor in the manifestation of schizophrenia despite their consensus on the assumption of its neurobiological origins. Rather, they considered impairments of intelligence and neurocognition as an expression of pseudodementia, i.e. a dementia-like clinical picture caused by a weakening of motivation.
Results: The empirical data from the draft, high-risk birth cohort and clinical samples show a low IQ and a variety of neurocognitive dysfunctions in schizophrenia. These findings are far from universal since substantial proportions of patients do not show deficits. In addition, the empirical morphological and neuropathological evidence does not support any close analogy of schizophrenia with neurodegenerative dementia. Moreover, neurocognitive dysfunctions cannot be considered a core feature of schizophrenia if core is understood as 'essential', i.e. constitutive of a diagnosis, or as 'generative', i.e. symptom producing. In the phenomenological psychopathological tradition, schizophrenia is seen as a progressive condition marked by autism, which is a profound alteration in the structures (frameworks) of subjectivity (consciousness), manifest in self-relation (self-disorders) and in the relation to the world (lack of natural evidence) and to others (eccentricity, solipsism and isolation).
Conclusion: It is suggested that the neurodevelopmental model should integrate interactions between emerging psychological structures and genetic and environmental factors.
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http://dx.doi.org/10.1159/000318814 | DOI Listing |
Geroscience
December 2024
Laboratory of Neurodegenerative Diseases, Center for Interdisciplinary Research and Innovation, Aristotle University of Thessaloniki (CIRI-AUTh), 54124, Thessaloniki, Greece.
The accurate diagnosis of aging-related neurocognitive disorders as early as possible, even in a phase that is characterized by the absence of clinical symptoms, is nowadays the holy grail of the neurosciences. R4Alz-R is a novel cognitive tool designed to objectively detect the subtle cognitive changes that emerge as the very first result of the aging processes and could be developed and broadened in a continuum from healthy aging to subjective cognitive impairment (SCI) and mild cognitive impairment (MCI), before reaching some type of dementia. The goal of the present study was to examine whether the R4Alz-R battery has the potential to detect these subtle changes.
View Article and Find Full Text PDFBrain Commun
December 2024
NeuroScape@NeuroTech Lab, Service Universitaire de Neuroréhabilitation (SUN), Département des Neurosciences Cliniques, Centre Hosoitalier Universitaire Vaudois (CHUV), Institution de Lavigny, University of Lausanne, 1011 Lausanne, Switzerland.
Neurocognitive impairment (NCI) is present in around 40% of people with HIV and substantially affects everyday life, adherence to combined antiretroviral therapy (cART) and overall life expectancy. Suboptimal therapy regimen, opportunistic infections, substance abuse and highly prevalent psychiatric co-morbidities contribute to NCI in people with HIV. In this review, we highlight the need for efficacious treatment of HIV-related NCI through pharmacological approaches and cognitive neurorehabilitation, discussing recent randomized controlled trials in this domain.
View Article and Find Full Text PDFNat Neurosci
December 2024
Laboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Wako, Japan.
Tau pathology is a hallmark of several neurodegenerative diseases, including frontotemporal dementia and Alzheimer's disease. However, the sequence of events and the form of tau that confers toxicity are still unclear, due in large part to the lack of physiological models of tauopathy initiation and progression in which to test hypotheses. We have developed a series of targeted mice expressing frontotemporal-dementia-causing mutations in the humanized MAPT gene to investigate the earliest stages of tauopathy.
View Article and Find Full Text PDFNEJM Evid
January 2025
TIMI Study Group, Division of Cardiovascular Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston.
Background: Concerns persist regarding the cognitive safety of achieving very low levels of low-density lipoprotein (LDL) cholesterol. Although short-term studies are reassuring, the long-term cognitive effects of sustained exposure to very low LDL cholesterol levels through combined proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibition and statin therapy remain unknown.
Methods: This prospective study enrolled a subset of adults with atherosclerotic cardiovascular disease who had completed a neurocognitive substudy (EBBINGHAUS) of a placebo-controlled randomized trial of evolocumab (FOURIER) and were eligible for a long-term open-label extension.
Front Neurol
December 2024
Students Research Committee, Ardabil University of Medical Sciences, Ardabil, Iran.
Background And Aim: Neurodegenerative disorders (e.g., Alzheimer's, Parkinson's) lead to neuronal loss; neurocognitive disorders (e.
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