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Therapeutic use of serotoninergic hallucinogens: A review of the evidence and of the biological and psychological mechanisms.
Dos Santos, RG, Hallak, JEC
Neuroscience and biobehavioral reviews. 2020;:423-434
Abstract
Serotoninergic hallucinogens include drugs such as lysergic acid diethylamide (LSD), dimethyltryptamine (DMT) and psilocybin. Recent trials with single/few doses of these compounds show that they induce rapid and sustained antidepressive, anxiolytic, and antiaddictive effects. These effects are also observed in religious groups using the DMT-containing brew ayahuasca. The agonist action of these substances on 5-HT2A receptors expressed in frontal and limbic areas increase glutamatergic transmission and neuroplasticity. These neurochemical effects are associated with acute alterations on self-perception and increases in introspection and positive mood, and with subacute and long-term decreases in psychiatric symptoms, increases in some personality traits such as openness, improvements in emotional processing, and increases in empathy. These are preliminary but promising results that should be further explored in controlled trials with larger sample sizes, especially considering that these compounds could be beneficial in the treatment of treatment-resistant psychiatric disorders.
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Effects of Noninvasive Brain Stimulation on Food Cravings and Consumption: A Meta-Analytic Review.
Lowe, CJ, Vincent, C, Hall, PA
Psychosomatic medicine. 2017;(1):2-13
Abstract
OBJECTIVE The primary aim of this review was to evaluate the effectiveness of noninvasive brain stimulation to the dorsolateral prefrontal cortex (dlPFC) for modulating appetitive food cravings and consumption in laboratory (via meta-analysis) and therapeutic (via systematic review) contexts. METHODS Keyword searches of electronic databases (PubMed, Scopus, Web of Science, PsychoInfo, and EMBASE) and searches of previous quantitative reviews were used to identify studies (experimental [single-session] or randomized trials [multi-session]) that examined the effects of neuromodulation to the dlPFC on food cravings (n = 9) and/or consumption (n = 7). Random-effects models were employed to estimate the overall and method-specific (repetitive transcranial magnetic stimulation [rTMS] and transcranial direct current stimulation [tDCS]) effect sizes. Age and body mass index were examined as potential moderators. Two studies involving multisession therapeutic stimulation were considered in a separate systematic review. RESULTS Findings revealed a moderate-sized effect of modulation on cravings across studies (g, -0.516; p = .037); this effect was subject to significant heterogeneity (Q, 33.086; p < .001). Although no statistically significant moderators were identified, the stimulation effect on cravings was statistically significant for rTMS (g, -0.834; p = .008) but not tDCS (g, -0.252; p = .37). There was not sufficient evidence to support a causal effect of neuromodulation and consumption in experimental studies; therapeutic studies reported mixed findings. CONCLUSIONS Stimulation of the dlPFC modulates cravings for appetitive foods in single-session laboratory paradigms; when estimated separately, the effect size is only significant for rTMS protocols. Effects on consumption in laboratory contexts were not reliable across studies, but this may reflect methodological variability in delivery of stimulation and assessment of eating behavior. Additional single- and multi-session studies assessing eating behavior outcomes are needed.
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LRRK2 detection in human biofluids: potential use as a Parkinson's disease biomarker?
Taymans, JM, Mutez, E, Drouyer, M, Sibran, W, Chartier-Harlin, MC
Biochemical Society transactions. 2017;(1):207-212
Abstract
Leucine-rich repeat kinase 2 (LRRK2) is a complex signalling protein that is a key therapeutic target, particularly in Parkinson's disease (PD). In addition, there is now evidence showing that LRRK2 expression and phosphorylation levels have potential as markers of disease or target engagement. Indeed, reports show increases in LRRK2 protein levels in the prefrontal cortex of PD patients relative to controls, suggesting that increase in total LRRK2 protein expression is correlated with disease progression. LRRK2 phosphorylation levels are reduced in experimental systems for most disease mutants, and LRRK2 is also rapidly dephosphorylated upon LRRK2 inhibitor treatment, considered potential therapeutics. Recently, the presence of LRRK2 was confirmed in exosomes from human biofluids, including urine and cerebrospinal fluid. Moreover, phosphorylation of LRRK2 at phosphosites S910, S935, S955 and S973, as well as at the autophosphoryation site S1292, was found in urinary exosomes. In this review, we summarize knowledge on detection of LRRK2 in human biofluids and the relevance of these findings for the development of PD-related biomarkers.
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Transcranial magnetic stimulation of medial prefrontal cortex modulates implicit attitudes towards food.
Mattavelli, G, Zuglian, P, Dabroi, E, Gaslini, G, Clerici, M, Papagno, C
Appetite. 2015;:70-6
Abstract
The medial prefrontal cortex (mPFC) is known to be associated with food representation and monitoring of eating behaviour, but the neural mechanisms underlying attitudes towards food are still unclear. Transcranial magnetic stimulation (TMS) was used in combination with the implicit association test (IAT) to investigate the causal role of mPFC in controlling implicit food evaluation in healthy volunteers. Participants performed an IAT on tasty and tasteless food to test TMS interaction with food evaluation. Moreover, IATs assessing self-related concepts and attitude towards flowers and insects were carried out to control whether TMS could also affect self-representation or, more in general, the cognitive mechanisms required by the IAT. TMS was applied over mPFC; the left parietal cortex (lPA) was also stimulated as control site. Results revealed that mPFC-TMS selectively affected IAT on food, increasing implicit preference for tasty than tasteless food, only in a subgroup of participants who did not show extreme explicit evaluation for tasty and tasteless food. This demonstrates that mPFC has a critical causal role in monitoring food preference and highlights the relevance of considering individual differences in studying food representation and neural mechanisms associated with eating behaviour.
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The addictive dimensionality of obesity.
Volkow, ND, Wang, GJ, Tomasi, D, Baler, RD
Biological psychiatry. 2013;(9):811-8
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Abstract
Our brains are hardwired to respond and seek immediate rewards. Thus, it is not surprising that many people overeat, which in some can result in obesity, whereas others take drugs, which in some can result in addiction. Though food intake and body weight are under homeostatic regulation, when highly palatable food is available, the ability to resist the urge to eat hinges on self-control. There is no homeostatic regulator to check the intake of drugs (including alcohol); thus, regulation of drug consumption is mostly driven by self-control or unwanted effects (i.e., sedation for alcohol). Disruption in both the neurobiological processes that underlie sensitivity to reward and those that underlie inhibitory control can lead to compulsive food intake in some individuals and compulsive drug intake in others. There is increasing evidence that disruption of energy homeostasis can affect the reward circuitry and that overconsumption of rewarding food can lead to changes in the reward circuitry that result in compulsive food intake akin to the phenotype seen with addiction. Addiction research has produced new evidence that hints at significant commonalities between the neural substrates underlying the disease of addiction and at least some forms of obesity. This recognition has spurred a healthy debate to try and ascertain the extent to which these complex and dimensional disorders overlap and whether or not a deeper understanding of the crosstalk between the homeostatic and reward systems will usher in unique opportunities for prevention and treatment of both obesity and drug addiction.
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Brain structure and function in borderline personality disorder.
O'Neill, A, Frodl, T
Brain structure & function. 2012;(4):767-82
Abstract
The spotlight on borderline personality disorder (BPD) has been growing in recent years, with the number of papers discussing potential causes and triggers of the disorder rapidly on the increase. Also on the increase, though still lacking sufficient numbers to produce well-supported hypotheses, are studies employing neuroimaging techniques as investigative tools in BPD. In this review, we investigate the current state and findings of neuroimaging studies in BPD, focusing in particular, on the studies examining structural, functional, and neurometabolic abnormalities in the disorder. Some suspected trends in the data are highlighted, including reductions in the hippocampi and amygdalae of BPD patients compared to healthy controls, exaggerated amygdala activity in BPD patients when confronted with emotion-related stimulus, and negative correlations between increases in left amygdalar creatine and reductions in amygdalar volume, reductions in absolute N-acetylaspartate concentration in the dorsolateral prefrontal cortex of BPD patients, and increases in glutamate concentration in the anterior cingulate cortices of BPD patients. We also discuss the limitations of some of the current studies including hindrances due to sample effects and techniques used and the potential of future neuroimaging research in BPD.
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Biological and social influences on cognitive control processes dependent on prefrontal cortex.
Diamond, A
Progress in brain research. 2011;:319-39
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Cognitive control functions ("executive functions" [EFs] such as attentional control, self-regulation, working memory, and inhibition) that depend on prefrontal cortex (PFC) are critical for success in school and in life. Many children begin school lacking needed EF skills. Disturbances in EFs occur in many mental health disorders, such as ADHD and depression. This chapter addresses modulation of EFs by biology (genes and neurochemistry) and the environment (including school programs) with implications for clinical disorders and for education. Unusual properties of the prefrontal dopamine system contribute to PFC's vulnerability to environmental and genetic variations that have little effect elsewhere. EFs depend on a late-maturing brain region (PFC), yet they can be improved even in infants and preschoolers, without specialists or fancy equipment. Research shows that activities often squeezed out of school curricula (play, physical education, and the arts) rather than detracting from academic achievement help improve EFs and enhance academic outcomes. Such practices may also head off problems before they lead to diagnoses of EF impairments, including ADHD. Many issues are not simply education issues or health issues; they are both.
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Event perception: a mind-brain perspective.
Zacks, JM, Speer, NK, Swallow, KM, Braver, TS, Reynolds, JR
Psychological bulletin. 2007;(2):273-93
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People perceive and conceive of activity in terms of discrete events. Here the authors propose a theory according to which the perception of boundaries between events arises from ongoing perceptual processing and regulates attention and memory. Perceptual systems continuously make predictions about what will happen next. When transient errors in predictions arise, an event boundary is perceived. According to the theory, the perception of events depends on both sensory cues and knowledge structures that represent previously learned information about event parts and inferences about actors' goals and plans. Neurological and neurophysiological data suggest that representations of events may be implemented by structures in the lateral prefrontal cortex and that perceptual prediction error is calculated and evaluated by a processing pathway, including the anterior cingulate cortex and subcortical neuromodulatory systems.
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Neuroanatomical circuits modulating fear and anxiety behaviors.
Charney, DS
Acta psychiatrica Scandinavica. Supplementum. 2003;(417):38-50
Abstract
OBJECTIVE Our understanding of the neurobiology of anxiety disorders, although not complete, has advanced significantly with the development and application of genetic, neuroimaging and neurochemical approaches. METHOD The neuroanatomical basis of anxiety disorders is reviewed with particular focus on the amygdala and the temporal and prefrontal cortex. The functional anatomical correlates of anxiety disorders such as panic disorder, specific phobias and post-traumatic stress disorder are also discussed. RESULTS Functional neuroimaging studies in patients with anxiety disorders have shown neurophysiological abnormalities during symptom provocation tests, implicating the limbic, paralimbic and sensory association regions. The involvement of neurotransmitters such as serotonin and norepinephrine in depressive disorders is well established. Antidepressants that affect these neurotransmitter systems have also been shown to be useful in the treatment and management of patients with anxiety disorders. The role of serotonin and norepinephrine in the pathophysiology of anxiety disorders is reviewed. In addition, the involvement of the stress hormone corticotropin-releasing hormone, the peptide cholecystokinin and the amino acid transmitter gamma-amino butyric acid in anxiety disorders is reviewed. CONCLUSION The inconsistency in the results of biologic investigations of anxiety disorders highlights the importance of addressing the neurobiologic heterogeneity inherent within criteria-based, psychiatric diagnoses. Understanding of this heterogeneity will be facilitated by the continued development and application of genetic, neuroimaging and neurochemical approaches that can refine anxiety disorder phenotypes and elucidate the genotypes associated with these disorders. Application of these experimental approaches will also facilitate research aimed at clarifying the mechanisms of anti-anxiety therapies.