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Although first rank symptoms focus on positive symptoms of psychosis they are shared by a number of psychiatric conditions. The difficulty in differentiating bipolar disorder from schizophrenia with affective features has led to a third category of patients often loosely labeled as schizoaffective. Research in schizophrenia has attempted to render the presence or absence of negative symptoms and their relation to etiology and prognosis more explicit. A dichotomous population is a recurring theme in experimental paradigms. Thus, schizophrenia is defined as process or reactive, deficit or non-deficit and by the presence or absence of affective symptoms. Laboratory tests confirm the clinical impression showing conflicting responses to dexamethasone suppression and clearly defined differences in autonomic responsiveness, but their patho-physiological significance eludes mainstream theory. Added to this is the difficulty in agreeing to what exactly constitutes useful clinical features differentiating, for example, negative symptoms of a true deficit syndrome from features of depression. Two recent papers proposed that the general and specific cognitive features of schizophrenia and major depression result from a monoamine-cholinergic imbalance, the former due to a relative muscarinic receptor hypofunction and the latter, in contrast, to a muscarinic hypersensitivity exacerbated by monoamine depletion. Further development of these ideas will provide pharmacological principles for what is currently an incomplete and largely, descriptive nosology of psychosis. It will propose a dimensional view of affective and negative symptoms based on relative muscarinic integrity and is supported by several exciting intracellular signaling and gene expression studies. Bipolar disorder manifests both muscarinic and dopaminergic hypersensitivity. The greater the imbalance between these two receptor signaling systems, the more the clinical picture will resemble schizophrenia with bizarre, incongruent delusions and increasingly disorganized thought. The capacity for affective expression, by definition a non-deficit syndrome, will remain contingent on the degree of preservation of muscarinic signaling, which itself may be unstable and vary between trait and state examinations. At the extreme end of muscarinic impairment, a deficit schizophrenia subpopulation is proposed with a primary and fixed muscarinic receptor hypofunction.

The genomic profile of bipolar disorder and schizophrenia overlap and both have a common dopaminergic intracellular signaling which is hypersensitive to various stressors. It is proposed that the concomitant muscarinic receptor upregulation differentiates the syndromes, being marked in bipolar disorder and rather less so in schizophrenia. From a behavioral point of view non-deficit syndromes and bipolar disorder appear most proximate and could be reclassified as a spectrum of affective psychosis or schizoaffective disorders. Because of a profound malfunction of the muscarinic receptor, the deficit subgroup cannot express a comparable stress response. None -theless, a convergent principle of psychotic features across psychiatric disorders is a relative monoaminergic-muscarinic imbalance in signal transduction.

The purpose of this paper is to investigate the body-mind problem from a mathematical invariance principle in relation to personality dynamics in the psychological and the biological levels of description.

The relationship between the two mentioned levels of description is provided by two mathematical models as follows: the response model and the bridge model. The response model (an integro-differential equation) is capable to reproduce the personality dynamics as a consequence of a determined stimulus. The invariance principle asserts that the response model can reproduce personality dynamics at the two levels of description. The bridge model (a second-order partial differential equation) can be deduced as a consequence of this principle: it provides the co-evolution of the general factor of personality (GFP) (mind), the it is an immediate early gene (c-fos) and D3 dopamine receptor gene (DRD3) gens and the glutamate neurotransmitter (body).

An application case is presented by setting up two experimental designs: a previous pilot AB pseudo-experimental design (AB) pseudo-experimental design with one subject and a subsequent ABC experimental design (ABC) experimental design with another subject. The stimulus used is the stimulant drug methylphenidate. The response and bridge models are validated with the outcomes of these experiments.

The mathematical approach here presented is based on a holistic personality model developed in the past few years: the unique trait personality theory, which claims for a single personality trait to understand the overall human personality: the GFP.

Noninvasive brain stimulation (NIBS) such a transcranial magnetic stimulation, intermittent theta burst stimulation, transcranial direct current stimulation and electroconvulsive therapy have emerged as an efficacious and well-tolerated therapy for treatment-resistant psychiatric disorders. While novel NIBS techniques are an exciting addition to the current repertoire of neuropsychiatric therapies, their success is somewhat limited by the wide range of treatment responses seen among treated patients.

In this study, the authors will review the studies on relevant genetic polymorphisms and discuss the role of RNA genotyping in personalizing NIBS.

Genome studies have revealed several genetic polymorphisms that may contribute for the heterogeneity of treatment response to NIBS where the presence of certain single nucleotide polymorphisms (SNPs) are associated with responders versus nonresponders.

Historically, mental illnesses have been arguably some of the most challenging disorders to study and to treat because of the degree of biological variability across affected individuals, the role of genetic and epigenetic modifications, the diversity of clinical symptomatology and presentations and the interplay with environmental factors. In lieu of these challenges, there has been a push for personalized medicine in psychiatry that aims to optimize treatment response based on one’s unique characteristics.

Purpose – This chapter offers an integrative review of psychological and neurobiological differences between younger and older adults that might impact economic behavior. Focusing on key health economic challenges facing the elderly, it offers perspectives on how these psychological and neurobiological factors may influence decision-making over the life course and considers future interdisciplinary research directions.

Methodology/approach – We review relevant literature from three domains that are essential for developing a comprehensive science of decision-making and economic behavior in aging (psychology, neuroscience, and economics), consider implications for prescription drug coverage and long-term care (LTC) insurance, and highlight future research directions.

Findings – Older adults face many complex economic decisions that directly affect their health and well-being, including LTC insurance, prescription drug plans, and end of life care. Economic research suggests that many older Americans are not making cost-effective and economically rational decisions. While economic models provide insight into some of the financial incentives associated with these decisions, they typically do not consider the roles of cognition and affect in decision-making. Research has established that older age is associated with predictable declines in many cognitive functions and evidence is accumulating that distinct social motives and affect-processing profiles emerge in older age. It is unknown how these age differences impact the economic behaviors of older people and implies opportunities for path-breaking interdisciplinary research.

Originality/value of the chapter – Our chapter looks to develop interdisciplinary research to better understand the causes and consequences of age-related changes in economic decision-making and guide interventions to improve public programs and overall social welfare.

The purpose of this study was to evaluate the increase in sensitivity of a single risperidone administration in relation to energy intake of Wistar rats treated with cafeteria diet from birth to adulthood (119 days).

During the lactation period, six litters of Wistar rats (dam + 8 pups each litter) were fed one of the following two diets: Control (n = 3) or Cafeteria (n = 3) diets and water ad libitum. After weaning, the males were placed in individual cages, receiving the same diet offered to their respective dams (Control = 18; or Cafeteria = 18) until adulthood (119 postnatal days). The following parameters were evaluated: food and energy intake; macronutrient intake; weight gain; adipose tissue relative weight; sucrose preference; food intake after an administration of risperidone (0.1 mg/kg body weight).

The Cafeteria group showed a higher energy intake in relation to the Control group (p < 0.001). The consumption of energy beyond the individual needs can be understood as a hyperphagic condition. Also, the Cafeteria group reported greater weight gain (p = 0.048) and accumulation of adipose tissue (p < 0.001) with respect to the Control group. These results indicate that the cafeteria diet generated obesity in animals. The Cafeteria group showed reduced sucrose preference (p = 0.031), which is associated with the development of anhedonia-like behavior. In the food intake test, risperidone showed a greater sensitivity in Cafeteria animals, promoting a decrease in their energy intake in relation to the Control group that received risperidone (p = 0.040).

The cafeteria diet promoted hyperphagia, anhedonia-like behavior and obesity in animals. Acute risperidone administration showed greater sensitivity in the Cafeteria group, with a decrease in energy intake. The reported effects may be related to a downregulation of the dopaminergic system in the NAc region.

Classical definitions of motivation typically involve two main components: direction and activation. Motivated behavior is directed toward or away from particular stimuli (i.e., appetitive and aversive motivation). Furthermore, activational aspects of motivation refer to the observation that motivated behavior is characterized by substantial activity, vigor, persistence, and exertion of effort in both the initiation and maintenance of behavior. Although separate neural systems direct organisms toward distinct motivational stimuli (e.g., food, water, sex), there appears to be a common circuitry regulating behavioral activation and the exertion of effort. Mesolimbic dopamine is one of the brain systems mediating activational aspects of motivation and exertion of effort. This system integrates aspects of motivation and motor control functions involved in the instigation of action. Research on the neurobiology of effort has contributed to our understanding of the pathophysiology of neurological and psychiatric disorders that are characterized by motivational dysfunction.

Motivation significantly influences learning and memory. While a long history of research has focused on simple forms of associative learning, such as Pavlovian conditioning, recent research is beginning to characterize how motivation influences episodic memory. In this chapter we synthesize findings across behavioral, cognitive, and educational neuroscience to characterize motivation’s influence on memory. We provide evidence that neural systems underlying motivation, namely the mesolimbic dopamine system, interact with and facilitate activity within systems underlying episodic memory, centered on the medial temporal lobes. We focus on two mechanisms of episodic memory enhancement: encoding and consolidation. Together, the reviewed research supports an adaptive model of memory in which an individual’s motivational state (i.e., learning under states of reward or punishment) shapes the nature of memory representations in service of future goals. The impact of motivation on learning and memory, therefore, has very clear implications for and applications to educational settings.

This paper aims to depict the mechanistic role of vitamin D on dementia prevention, relief of the severity and the complication of the disease. All papers indexed in scientific databases, including Scopus, Elsevier, PubMed, Embase and Google Scholar between 2000 and 2021 were extracted and discussed. To present the mechanistic role of vitamin D in declining the severity of dementia, keywords including dementia, vitamin D, oxidative stress, inflammation, amyloid beta-Peptides were used.

Dementia is a prevalent cognitive disorder worldwide, especially in elderly people, which is accompanied by serious disabilities. Besides genetic, biological and lifestyle factors are involved in the incidence of dementia. An unhealthy diet along with micronutrient deficiencies are among modifiable factors. Vitamin D is one of the important micronutrients in brain health. Besides the involvement in gene expression, bone mineralization, apoptosis, inflammation, skeletal maturation, neurotropic action and hemostasis of phosphate and calcium, vitamin D also exerts neuroprotective effects via genomic and non-genomic pathways.

Vitamin D up-regulates the expression of various genes involved in dementia incidence via various mechanisms. Decreasing oxidative stress and the neuro-inflammatory cytokines levels, regulation of the expression of alternated Proteins including Tau and Amyloid-ß, calcium homeostasis in the central nervous system and also vascular are considered main mechanisms.

Considering the importance of diet in preventing dementia, adherence to a healthy diet that provides essential nutrients to brain function seems to be urgent. Controlling serum levels of vitamin D periodically and providing vitamin D by related sources or supplements, if there is a deficiency, is recommended. Future studies are needed to clarify other related mechanisms.

This review provides an overview of recent advances in electrochemical sensors for analyte detection in saliva, highlighting their potential applications in diagnostics and health care. The purpose of this paper is to summarize the current state of the field, identify challenges and limitations and discuss future prospects for the development of saliva-based electrochemical sensors.

The paper reviews relevant literature and research articles to examine the latest developments in electrochemical sensing technologies for saliva analysis. It explores the use of various electrode materials, including carbon nanomaterial, metal nanoparticles and conducting polymers, as well as the integration of microfluidics, lab-on-a-chip (LOC) devices and wearable/implantable technologies. The design and fabrication methodologies used in these sensors are discussed, along with sample preparation techniques and biorecognition elements for enhancing sensor performance.

Electrochemical sensors for salivary analyte detection have demonstrated excellent potential for noninvasive, rapid and cost-effective diagnostics. Recent advancements have resulted in improved sensor selectivity, stability, sensitivity and compatibility with complex saliva samples. Integration with microfluidics and LOC technologies has shown promise in enhancing sensor efficiency and accuracy. In addition, wearable and implantable sensors enable continuous, real-time monitoring of salivary analytes, opening new avenues for personalized health care and disease management.

This review presents an up-to-date overview of electrochemical sensors for analyte detection in saliva, offering insights into their design, fabrication and performance. It highlights the originality and value of integrating electrochemical sensing with microfluidics, wearable/implantable technologies and point-of-care testing platforms. The review also identifies challenges and limitations, such as interference from other saliva components and the need for improved stability and reproducibility. Future prospects include the development of novel microfluidic devices, advanced materials and user-friendly diagnostic devices to unlock the full potential of saliva-based electrochemical sensing in clinical practice.