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Psychiatric disorders share the same pattern of longitudinal evolution and have courses that tend to be chronic and recurrent. These aspects of chronicity and longitudinal evolution are currently studied under the deficit-oriented neuroprogression framework. Interestingly, considering the plasticity of the brain, it is also necessary to emphasize the bidirectional nature of neuroprogression. We review evidence highlighting alterations of the brain associated with the longitudinal evolution of psychiatric disorders from the framework of neuroplastic adaptation to pathology. This new framework highlights that substantial plasticity and remodeling may occur beyond the classic deficit-oriented neuroprogressive framework, which has been associated with progressive loss of gray matter thickness, decreased brain connectivity, and chronic inflammation. We also integrate the brain economy concept in the neuroplastic adaptation to pathology framework, emphasizing that to preserve its economy, i.e. function, the brain learns how to cope with the disease by adapting its architecture. Neuroplastic adaptation to pathology is a proposition for a paradigm shift to overcome the shortcomings of traditional psychiatric diagnostic boundaries; this approach can disentangle both the specific pathophysiology of psychiatric symptoms and the adaptation to pathology, thus offering a new framework for both diagnosis and treatment.
Here we describe emergent properties of the brain and the key challenges associated with modelling them in vitro. Modeling emergent properties of the brain will provide insights into brain function, development, and disease.
The Amyloid Precursor Protein (APP) is infamous for its proposed pivotal role in the pathogenesis of Alzheimer’s disease (AD). Much research on APP focusses on potential contributions to neurodegeneration, mostly based on mouse models with altered expression or mutated forms of APP. However, cumulative evidence from recent years indicates the indispensability of APP and its metabolites for normal brain physiology. APP contributes to the regulation of synaptic transmission, plasticity, and calcium homeostasis. It plays an important role during development and it exerts neuroprotective effects. Of particular importance is the soluble secreted fragment APPsα which mediates many of its physiological actions, often counteracting the effects of the small APP-derived peptide Aβ. Understanding the contribution of APP for normal functions of the nervous system is of high importance, both from a basic science perspective and also as a basis for generating new pathophysiological concepts and therapeutic approaches in AD. In this article, we review the physiological functions of APP and its metabolites, focusing on synaptic transmission, plasticity, calcium signaling, and neuronal network activity.
Color provides valuable information about the environment, yet the exact mechanisms explaining how colors appear to us remain poorly understood. Retinal signals are processed in the visual cortex through high-level mechanisms that link color perception with top-down expectations and knowledge. Here, we review the neuroimaging evidence about color processing in the brain, and how it is affected by acquired brain lesions in humans. Evidence from patients with brain-damage suggests that high-level color processing may be divided into at least three modules: perceptual color experience, color naming, and color knowledge. These modules appear to be functionally independent but richly interconnected, and serve as cortical relays linking sensory and semantic information, with the final goal of directing object-related behavior. We argue that the relations between colors and their objects are key mechanisms to understand high-level color processing.
Paired associative stimulation (PAS) is a noninvasive neuromodulation method with rare cases of adverse effects for the patients with neurological injuries such as spinal cord injury (SCI). PAS is based on the principles of associative long-term potentiation and depression where the activation of presynaptic and postsynaptic neurons correlated in time is artificially induced. Statistically significant improvement in motor functions after applying PAS has been reported by several research groups. With further standardization of the technique, PAS could be an effective treatment for functional rehabilitation of SCI patients. In this review, we have summarized the methods and findings of PAS on SCI rehabilitation to facilitate the readers to understand the potentials and limitations of PAS for its future clinical use.
Recent clinical evidence has put forward a new region of interest for the treatment of psychiatric disorders. Deep brain stimulation in the bed nucleus of the stria terminalis (BST) significantly attenuates symptoms in patients suffering from severe, treatment-resistant obsessive-compulsive disorder (OCD). The BST is not typically implicated in OCD neuropsychopathology but is certainly not an unknown in the field of emotional learning and memory. Substantial evidence supports its involvement in anxiety responses, particularly to ambiguous threats. This seems consistent with the intolerance of uncertainty and tendency to overestimate danger, which fuel obsessions and compulsions in many patients with OCD. Translational research in rodents can help to obtain a deeper understanding of the effects of high-frequency electrical stimulation in the BST on anxiety, which may be valuable to improve treatment for psychiatric patients.