Current Neuropharmacology - Volume 17, Issue 6, 2019

Visuoperceptive impairments are among the most frequently reported deficits in alcoholuse disorders, but only very few studies have investigated their origin and interactions with other categories of dysfunctions. Besides, these deficits have generally been interpreted in a linear bottom- up perspective, which appears very restrictive with respect to the new models of vision developed in healthy populations. Indeed, new theories highlight the predictive nature of the visual system and demonstrate that it interacts with higher-level cognitive functions to generate top-down predictions. These models notably posit that a fast but coarse visual analysis involving magnocellular pathways helps to compute heuristic guesses regarding the identity and affective value of inputs, which are used to facilitate conscious visual recognition. Building on these new proposals, the present review stresses the need to reconsider visual deficits in alcohol-use disorders as they might have crucial significance for core features of the pathology, such as attentional bias, loss of inhibitory control and emotion decoding impairments. Centrally, we suggest that individuals with severe alcohol-use disorders could present with magnocellular damage and we defend a dynamic explanation of the deficits. Rather than being restricted to high-level processes, deficits could start at early visual stages and then extend and potentially intensify during following steps due to reduced cerebral connectivity and dysfunctional cognitive/emotional regions. A new research agenda is specifically provided to test these hypotheses.

Adolescents’ media use represents a normative need for information, communication, recreation and functionality, yet problematic Internet use has increased. Given the arguably alarming prevalence rates worldwide and the increasingly problematic use of gaming and social media, the need for an integration of prevention efforts appears to be timely. The aim of this systematic literature review is (i) to identify school-based prevention programmes or protocols for Internet Addiction targeting adolescents within the school context and to examine the programmes’ effectiveness, and (ii) to highlight strengths, limitations, and best practices to inform the design of new initiatives, by capitalizing on these studies’ recommendations. The findings of the reviewed studies to date presented mixed outcomes and are in need of further empirical evidence. The current review identified the following needs to be addressed in future designs to: (i) define the clinical status of Internet Addiction (IA) more precisely, (ii) use more current psychometrically robust assessment tools for the measurement of effectiveness (based on the most recent empirical developments), (iii) reconsider the main outcome of Internet time reduction as it appears to be problematic, (iv) build methodologically sound evidence-based prevention programmes, (v) focus on skill enhancement and the use of protective and harm-reducing factors, and (vi) include IA as one of the risk behaviours in multi-risk behaviour interventions. These appear to be crucial factors in addressing future research designs and the formulation of new prevention initiatives. Validated findings could then inform promising strategies for IA and gaming prevention in public policy and education.

Background: The concept of food addiction attracts much interest in the scientific community. Research is mainly based on the Yale Food Addiction Scale (YFAS), a tool developed to assess food addiction. Substance use disorder criteria have been used to develop this scale. Objective: The aim of this paper was to review the clinical significance of food addiction diagnoses made with the YFAS and to discuss the results in light of the current debate on behavioral addictions. Methods: We performed a systematic review of the studies that assessed food addiction with the YFAS published between January 2014 and July 2017 by searching the electronic databases PsycINFO, MEDLINE, and PsycARTICLES. Results: Sixty publications were included in the analysis. Thirty-three studies examined nonclinical samples and 27 examined clinical samples. All studies used YFAS scoring results to define food addiction. The prevalence of food addiction according to the YFAS varied largely by the studied samples. In general, a higher body mass index and the presence of eating disorders (EDs), especially binge eating disorder (BED), were associated with higher YFAS scores. Conclusion: The concept of food addiction has not been established to this day although it can be grouped with other EDs such as BED. More research is needed to understand this behavior and the differences between food addiction and other EDs. The criteria for food addiction should be revisited in light of the concepts currently used to examine behavioral addictions.

Ceruloplasmin (CP) is the major copper transport protein in plasma, mainly produced by the liver. Glycosylphosphatidylinositol-linked CP (GPI-CP) is the predominant form expressed in astrocytes of the brain. A growing body of evidence has demonstrated that CP is an essential protein in the body with multiple functions such as regulating the homeostasis of copper and iron ions, ferroxidase activity, oxidizing organic amines, and preventing the formation of free radicals. In addition, as an acute-phase protein, CP is induced during inflammation and infection. The fact that patients with genetic disorder aceruloplasminemia do not suffer from tissue copper deficiency, but rather from disruptions in iron metabolism shows essential roles of CP in iron metabolism rather than copper. Furthermore, abnormal metabolism of metal ions and oxidative stress are found in other neurodegenerative diseases, such as Wilson’s disease, Alzheimer’s disease and Parkinson’s disease. Brain iron accumulation and decreased activity of CP have been shown to be associated with neurodegeneration. We hypothesize that CP may play a protective role in neurodegenerative diseases. However, whether iron accumulation is a cause or a result of neurodegeneration remains unclear. Further research on molecular mechanisms is required before a consensus can be reached regarding a neuroprotective role for CP in neurodegeneration. This review article summarizes the main physiological functions of CP and the current knowledge of its role in neurodegenerative diseases.

Background: Depression is a widespread phenomenon with varying degrees of pathology in different patients. Various hypotheses have been proposed for the cause and continuance of depression. Some of these include, but not limited to, the monoamine hypothesis, the neuroendocrine hypothesis, and the more recent epigenetic and inflammatory hypotheses. Objective: In this article, we review all the above hypotheses with a focus on the role of mitochondria as the connecting link. Oxidative stress, respiratory activity, mitochondrial dynamics and metabolism are some of the mitochondria-dependent factors which are affected during depression. We also propose exogenous ATP as a contributing factor to depression. Result: Literature review shows that pro-inflammatory markers are elevated in depressive individuals. The cause for elevated levels of cytokines in depression is not completely understood. We propose exogenous ATP activates purinergic receptors which in turn increase the levels of various proinflammatory factors in the pathophysiology of depression. Conclusion: Mitochondria are integral to the function of neurons and undergo dysfunction in major depressive disorder patients. This dysfunction is reflected in all the various hypotheses that have been proposed for depression. Among the newer targets identified, which also involve mitochondria, includes the role of exogenous ATP. The diversity of purinergic receptors, and their differential expression among various individuals in the population, due to genetic and environmental (prenatal) influences, may influence the susceptibility and severity of depression. Identifying specific receptors involved and using patient-specific purinergic receptor antagonist may be an appropriate therapeutic course in the future.

Neurodegenerative diseases are among the most serious health problems affecting millions of people worldwide. Such diseases are characterized by a progressive degeneration and / or death of neurons in the central nervous system. Currently, there are no therapeutic approaches to cure or even halt the progression of neurodegenerative diseases. During the last two decades, much attention has been paid to the neuroprotective and anti-neurodegenerative activities of compounds isolated from natural products with high efficacy and low toxicity. Accumulating evidence indicates that berberine, an isoquinoline alkaloid isolated from traditional Chinese medicinal herbs, may act as a promising anti-neurodegenerative agent by inhibiting the activity of the most important pathogenic enzymes, ameliorating intracellular oxidative stress, attenuating neuroinflammation, triggering autophagy and protecting neurons against apoptotic cell death. This review attempts to summarize the current state of knowledge regarding the therapeutic potential of berberine against neurodegenerative diseases, with a focus on the molecular mechanisms that underlie its effects on Alzheimer’s, Parkinson’s and Huntington’s diseases.