Neuroprogression in Psychiatry

2019 ◽  
Keyword(s):  
Psychiatric Disorders ◽  
Redox Balance ◽  
Therapeutic Approaches ◽  
Cognitive Changes ◽  
Process Understanding ◽  
Cognitive Sequelae ◽  
Brain Changes ◽  
Late Stages ◽  
The Brain ◽  
Cellular Resilience

Psychiatric disorders are characterized by an overlapping set of pathophysiological pathways that include monoamines but also neurotrophins, apoptotic and mitochondrial pathways, epigenetics, and dysregulation of immunity and redox balance, counterbalanced by cellular resilience and defence pathways and the effects of treatment. These conspire in a subset of individuals to cause changes in brain function and, over time, the activity of these pathways in chronic psychiatric disorders can lead to cognitive sequelae and changes in brain structure. This can lead to differences between early and late stages of illness. These biological underpinnings could explain why late-stage patients are more prone to treatment refractoriness, progressive brain changes, and consequent cognitive and functioning impairment. This process is understood under the construct of neuroprogression, which refers to the pathological rewiring of the brain underlying the clinical and cognitive changes that underpin the staged progression of the illness, caused by activities of the aforementioned biological pathways. It is important to note that the brain can adapt to the challenges of the environment and respond to medications to ameliorate this process. Understanding the process of neuroprogression provides a window into the core biology of the disorder and opens the door to therapeutic approaches addressing these pathways. This book is an account of the state of the art in the field of neuroprogression in different psychiatric disorders.

Neuroprogression and accelerated ageing in severe psychiatric disorders

2019 ◽  
pp. 21-34
Author(s):  
Elisa Brietzke ◽  
Ana S. Yamagata ◽  
Pawan K. Maurya ◽  
Lucas B. Rizzo
Keyword(s):  
Bipolar Disorder ◽  
Major Depressive Disorder ◽  
Mental Illnesses ◽  
Accelerated Ageing ◽  
Healthy Controls ◽  
Therapeutic Approaches ◽  
Psychiatric Conditions ◽  
Brain Changes ◽  
Late Stages ◽  
Novel Therapeutic

A convergent body of evidence suggests an overlap between neural, molecular, and functional findings in patients with severe mental illnesses and normative ageing. Patients in late stages of mood disorders and psychosis present brain changes and cognitive decline consistent with a pattern of accelerated ageing. In addition, replicated but heterogeneous findings support the notion that individuals with major depressive disorder, bipolar disorder, and schizophrenia have shorter telomeres compared to age-matched healthy controls. The recognition that severe mental illnesses are associated with premature or accelerated ageing offers new avenues of investigation for really novel therapeutic approaches. The hope is that these interventions will not only treat symptoms but be able to modify the course of these psychiatric conditions.

Neurobiology of psychiatric disorders

2017 ◽  
Author(s):  
Vladimir Maletic ◽  
Bernadette DeMuri
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Anxiety Disorders ◽  
Psychiatric Disorders ◽  
Therapeutic Approaches ◽  
Major Depressive ◽  
Autonomic Changes ◽  
Brain Changes ◽  
Major Factors ◽  
Structural Brain

Recent decades have witnessed a burgeoning multidisciplinary research into the neurobiological underpinning of major psychiatric disorders. Despite recent discoveries, our psychiatric taxonomy, and hence diagnosis, continues to be based on phenomenology. We have summarized some of the major advancements in our understanding of the role that genetics, functional and structural brain changes, alterations in neurotransmission and neuroplasticity, and cytopathology may play in etiopathogenesis of psychiatric disorders, particularly focusing on major depressive disorder and anxiety disorders. Furthermore, recent research has unequivocally implicated peripheral immune, endocrine, and autonomic changes in the pathophysiology of psychiatric disorders, not only as correlates but also as major factors involved in shaping the clinical expression of these conditions. Better understanding of the pathophysiology underlying psychiatric disorders may assist us in developing markers to help identify subtypes of these highly biologically and phenotypically heterogeneous conditions. Additionally, greater knowledge of etiological mechanisms may help us adopt more effective therapeutic approaches.

Lessons From the Neural Bases of Speech and Voice

2011 ◽  
Vol 21 (1) ◽  
pp. 5-14
Author(s):  
Christy L. Ludlow
Keyword(s):  
Brain Networks ◽  
Neural Substrates ◽  
Voice Behavior ◽  
Therapeutic Approaches ◽  
Neural Bases ◽  
Sound Foundation ◽  
The Brain ◽  
Normal Speech

The premise of this article is that increased understanding of the brain bases for normal speech and voice behavior will provide a sound foundation for developing therapeutic approaches to establish or re-establish these functions. The neural substrates involved in speech/voice behaviors, the types of muscle patterning for speech and voice, the brain networks involved and their regulation, and how they can be externally modulated for improving function will be addressed.

Morphological Changes in the Brain of Acutely Ill and Weight-Recovered Patients with Anorexia Nervosa

2014 ◽  
Vol 42 (1) ◽  
pp. 7-18 ◽  
Author(s):  
Jochen Seitz ◽  
Katharina Bühren ◽  
Georg G. von Polier ◽  
Nicole Heussen ◽  
Beate Herpertz-Dahlmann ◽  
...  
Keyword(s):  
Anorexia Nervosa ◽  
Cognitive Deficits ◽  
Time Course ◽  
Morphological Changes ◽  
Meta Analysis ◽  
Short Term ◽  
Clinical Prognosis ◽  
Qualitative Review ◽  
Brain Changes ◽  
The Brain

Objective: Acute anorexia nervosa (AN) leads to reduced gray (GM) and white matter (WM) volume in the brain, which however improves again upon restoration of weight. Yet little is known about the extent and clinical correlates of these brain changes, nor do we know much about the time-course and completeness of their recovery. Methods: We conducted a meta-analysis and a qualitative review of all magnetic resonance imaging studies involving volume analyses of the brain in both acute and recovered AN. Results: We identified structural neuroimaging studies with a total of 214 acute AN patients and 177 weight-recovered AN patients. In acute AN, GM was reduced by 5.6% and WM by 3.8% compared to healthy controls (HC). Short-term weight recovery 2–5 months after admission resulted in restitution of about half of the GM aberrations and almost full WM recovery. After 2–8 years of remission GM and WM were nearly normalized, and differences to HC (GM: –1.0%, WM: –0.7%) were no longer significant, although small residual changes could not be ruled out. In the qualitative review some studies found GM volume loss to be associated with cognitive deficits and clinical prognosis. Conclusions: GM and WM were strongly reduced in acute AN. The completeness of brain volume rehabilitation remained equivocal.

Redox State in Atrial Fibrillation Pathogenesis and Relevant Therapeutic Approaches

2019 ◽  
Vol 26 (5) ◽  
pp. 765-779 ◽  
Author(s):  
Alexios S. Antonopoulos ◽  
Athina Goliopoulou ◽  
Evangelos Oikonomou ◽  
Sotiris Tsalamandris ◽  
Georgios-Angelos Papamikroulis ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Clinical Studies ◽  
Redox State ◽  
Redox Balance ◽  
Therapeutic Approaches ◽  
Critical Determinant ◽  
Electrophysiological Properties ◽  
Antioxidant Agents ◽  
Clinical Benefits

Background: Myocardial redox state is a critical determinant of atrial biology, regulating cardiomyocyte apoptosis, ion channel function, and cardiac hypertrophy/fibrosis and function. Nevertheless, it remains unclear whether the targeting of atrial redox state is a rational therapeutic strategy for atrial fibrillation prevention. Objective: To review the role of atrial redox state and anti-oxidant therapies in atrial fibrillation. Method: Published literature in Medline was searched for experimental and clinical evidence linking myocardial redox state with atrial fibrillation pathogenesis as well as studies looking into the role of redoxtargeting therapies in the prevention of atrial fibrillation. Results: Data from animal models have shown that altered myocardial nitroso-redox balance and NADPH oxidases activity are causally involved in the pathogenesis of atrial fibrillation. Similarly experimental animal data supports that increased reactive oxygen / nitrogen species formation in the atrial tissue is associated with altered electrophysiological properties of atrial myocytes and electrical remodeling, favoring atrial fibrillation development. In humans, randomized clinical studies using redox-related therapeutic approaches (e.g. statins or antioxidant agents) have not documented any benefits in the prevention of atrial fibrillation development (mainly post-operative atrial fibrillation risk). Conclusion: Despite strong experimental and translational data supporting the role of atrial redox state in atrial fibrillation pathogenesis, such mechanistic evidence has not been translated to clinical benefits in atrial fibrillation risk in randomized clinical studies using redox-related therapies.

Reflex Epilepsy with Hot Water: Clinical and EEG Findings, Treatment, and Prognosis in Childhood

2020 ◽  
Vol 51 (05) ◽  
pp. 336-340 ◽  
Author(s):  
Fatma Hanci ◽  
Sevim Türay ◽  
Paşa Balci ◽  
Nimet Kabakuş
Keyword(s):  
Seizure Control ◽  
Hot Water ◽  
Reflex Epilepsy ◽  
Therapeutic Approaches ◽  
Water Age ◽  
Epileptiform Discharges ◽  
Neurology Clinic ◽  
Neuromuscular Development ◽  
The Brain ◽  
International League

AbstractHot water epilepsy (HWE) is a subtype of reflex epilepsy in which seizures are triggered by the head being immersed in hot water. Hot water or bathing epilepsy is the type of reflex epilepsy most frequently encountered in our clinic. We describe our patients with HWE and also discuss the clinical features, therapeutic approaches, and prognosis. Eleven patients (10 boys, 1 girl), aged 12 months to 13 years, admitted to the pediatric neurology clinic between January 2018 and August 2019, and diagnosed with HWE or bathing epilepsy based on International League Against Epilepsy (ILAE)-2017, were followed up prospectively for ∼18 months. Patients' clinical and electroencephalography (EEG) findings and treatment details were noted. All 11 patients' seizures were triggered by hot water. Age at first seizure was between 2 months and 12 years. Seizure types were generalized motor seizures, absence, and atonic. EEG was normal in two patients, but nine patients had epileptiform discharges. Magnetic resonance imaging of the brain was performed and reported as normal (except in one case). Histories of prematurity were present in two patients, unprovoked seizures in one, and low birth weight and depressed birth in the other. Patients with HWE have normal neuromuscular development and neurological examination results, together with prophylaxis or seizure control with a single antiepileptic drug, suggesting that it is a self-limited reflex epilepsy.

scholarly journals Metabolism in the Zebrafish Retina

2021 ◽  
Vol 9 (1) ◽  
pp. 10
Author(s):  
Natalia Jaroszynska ◽  
Philippa Harding ◽  
Mariya Moosajee
Keyword(s):  
Pigment Epithelium ◽  
Retinal Pigment ◽  
The Body ◽  
Therapeutic Approaches ◽  
Retinal Photoreceptors ◽  
Sufficient Energy ◽  
Metabolic Products ◽  
Sight Loss ◽  
Choroidal Vasculature ◽  
The Brain

Retinal photoreceptors are amongst the most metabolically active cells in the body, consuming more glucose as a metabolic substrate than even the brain. This ensures that there is sufficient energy to establish and maintain photoreceptor functions during and after their differentiation. Such high dependence on glucose metabolism is conserved across vertebrates, including zebrafish from early larval through to adult retinal stages. As the zebrafish retina develops rapidly, reaching an adult-like structure by 72 hours post fertilisation, zebrafish larvae can be used to study metabolism not only during retinogenesis, but also in functionally mature retinae. The interplay between rod and cone photoreceptors and the neighbouring retinal pigment epithelium (RPE) cells establishes a metabolic ecosystem that provides essential control of their individual functions, overall maintaining healthy vision. The RPE facilitates efficient supply of glucose from the choroidal vasculature to the photoreceptors, which produce metabolic products that in turn fuel RPE metabolism. Many inherited retinal diseases (IRDs) result in photoreceptor degeneration, either directly arising from photoreceptor-specific mutations or secondary to RPE loss, leading to sight loss. Evidence from a number of vertebrate studies suggests that the imbalance of the metabolic ecosystem in the outer retina contributes to metabolic failure and disease pathogenesis. The use of larval zebrafish mutants with disease-specific mutations that mirror those seen in human patients allows us to uncover mechanisms of such dysregulation and disease pathology with progression from embryonic to adult stages, as well as providing a means of testing novel therapeutic approaches.

scholarly journals Delivery of Thyronamines (TAMs) to the Brain: A Preliminary Study

Molecules ◽  
2021 ◽  
Vol 26 (6) ◽  
pp. 1616
Author(s):  
Nicoletta di Leo ◽  
Stefania Moscato ◽  
Marco Borso' ◽  
Simona Sestito ◽  
Beatrice Polini ◽  
...  
Keyword(s):  
High Performance ◽  
In Vitro Model ◽  
New Drugs ◽  
Therapeutic Approaches ◽  
Neuroprotective Effects ◽  
Pharmacological Response ◽  
Preliminary Study ◽  
Vitro Model ◽  
The Brain

Recent reports highlighted the significant neuroprotective effects of thyronamines (TAMs), a class of endogenous thyroid hormone derivatives. In particular, 3-iodothyronamine (T1AM) has been shown to play a pleiotropic role in neurodegeneration by modulating energy metabolism and neurological functions in mice. However, the pharmacological response to T1AM might be influenced by tissue metabolism, which is known to convert T1AM into its catabolite 3-iodothyroacetic acid (TA1). Currently, several research groups are investigating the pharmacological effects of T1AM systemic administration in the search of novel therapeutic approaches for the treatment of interlinked pathologies, such as metabolic and neurodegenerative diseases (NDDs). A critical aspect in the development of new drugs for NDDs is to know their distribution in the brain, which is fundamentally related to their ability to cross the blood–brain barrier (BBB). To this end, in the present study we used the immortalized mouse brain endothelial cell line bEnd.3 to develop an in vitro model of BBB and evaluate T1AM and TA1 permeability. Both drugs, administered at 1 µM dose, were assayed by high-performance liquid chromatography coupled to mass spectrometry. Our results indicate that T1AM is able to efficiently cross the BBB, whereas TA1 is almost completely devoid of this property.

scholarly journals Stress Responses in Down Syndrome Neurodegeneration: State of the Art and Therapeutic Molecules

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 266
Author(s):  
Chiara Lanzillotta ◽  
Fabio Di Domenico
Keyword(s):  
Down Syndrome ◽  
Stress Response ◽  
Stress Responses ◽  
Redox Balance ◽  
Antioxidant Response ◽  
Chromosome 21 ◽  
Therapeutic Approaches ◽  
Genomic Disorder ◽  
Therapeutic Molecules ◽  
Early Alzheimer’S Disease

Down syndrome (DS) is the most common genomic disorder characterized by the increased incidence of developing early Alzheimer’s disease (AD). In DS, the triplication of genes on chromosome 21 is intimately associated with the increase of AD pathological hallmarks and with the development of brain redox imbalance and aberrant proteostasis. Increasing evidence has recently shown that oxidative stress (OS), associated with mitochondrial dysfunction and with the failure of antioxidant responses (e.g., SOD1 and Nrf2), is an early signature of DS, promoting protein oxidation and the formation of toxic protein aggregates. In turn, systems involved in the surveillance of protein synthesis/folding/degradation mechanisms, such as the integrated stress response (ISR), the unfolded stress response (UPR), and autophagy, are impaired in DS, thus exacerbating brain damage. A number of pre-clinical and clinical studies have been applied to the context of DS with the aim of rescuing redox balance and proteostasis by boosting the antioxidant response and/or inducing the mechanisms of protein re-folding and clearance, and at final of reducing cognitive decline. So far, such therapeutic approaches demonstrated their efficacy in reverting several aspects of DS phenotype in murine models, however, additional studies aimed to translate these approaches in clinical practice are still needed.

Event-Related Potentials in Psychiatry: Approaches to Research and Clinical Applications

1983 ◽  
Vol 17 (4) ◽  
pp. 307-318 ◽  
Author(s):  
H. G. Stampfer
Keyword(s):  
Information Processing ◽  
Psychiatric Disorders ◽  
Rapid Development ◽  
Event Related Potentials ◽  
Clinical Applications ◽  
Direct Access ◽  
Practical Application ◽  
Clinical Methods ◽  
Related Potentials ◽  
The Brain

This article suggests that the potential usefulness of event-related potentials in psychiatry has not been fully explored because of the limitations of various approaches to research adopted to date, and because the field is still undergoing rapid development. Newer approaches to data acquisition and methods of analysis, combined with closer co-operation between medical and physical scientists, will help to establish the practical application of these signals in psychiatric disorders and assist our understanding of psychophysiological information processing in the brain. Finally, it is suggested that psychiatrists should seek to understand these techniques and the data they generate, since they provide more direct access to measures of complex cerebral processes than current clinical methods.

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