Ranjini Garani

Bio: Ranjini Garani is an academic researcher from Centre for Addiction and Mental Health. The author has contributed to research in topics: Cannabinoid receptor & Bipolar disorder. The author has an hindex of 1, co-authored 1 publications receiving 5 citations.

Endocannabinoid system in psychotic and mood disorders, a review of human studies.

Abstract: Despite widespread evidence of endocannabinoid system involvement in the pathophysiology of psychiatric disorders, our understanding remains rudimentary. Here we review studies of the endocannabinoid system in humans with psychotic and mood disorders. Postmortem, peripheral, cerebrospinal fluid and in vivo imaging studies provide evidence for the involvement of the endocannabinoid system in psychotic and mood disorders. Psychotic disorders and major depressive disorder exhibit alterations of brain cannabinoid CB1 receptors and peripheral blood endocannabinoids. Further, these changes may be sensitive to treatment status, disease state, and symptom severity. Evidence from psychotic disorder extend to endocannabinoid metabolizing enzymes in the brain and periphery, whereas these lines of evidence remain poorly developed in mood disorders. A paucity of studies examining this system in bipolar disorder represents a notable gap in the literature. Despite a growing body of productive work in this field of research, there is a clear need for investigation beyond the CB1 receptor in order to more fully elucidate the role of the endocannabinoid system in psychotic and mood disorders.

Country-level gender inequality is associated with structural differences in the brains of women and men

Abstract: Significance Gender inequality is associated with worse mental health and academic achievement in women. Using a dataset of 7,876 MRI scans from healthy adults living in 29 different countries, we here show that gender inequality is associated with differences between the brains of men and women: cortical thickness of the right hemisphere, especially in limbic regions such as the right caudal anterior cingulate and right medial orbitofrontal, as well as the left lateral occipital, present thinner cortices in women compared to men only in gender-unequal countries. These results suggest a potential neural mechanism underlying the worse outcome of women in gender-unequal settings, as well as highlight the role of the environment in the brain differences between women and men.

Biological hypotheses, risk factors, and biomarkers of schizophrenia

Abstract: Both the discovery of biomarkers of schizophrenia and the verification of biological hypotheses of schizophrenia are an essential part of the process of understanding the etiology of this mental disorder. Schizophrenia has long been considered a neurodevelopmental disease whose symptoms are caused by impaired synaptic signal transduction and brain neuroplasticity. Both the onset and chronic course of schizophrenia are associated with risk factors-induced disruption of brain function and the establishment of a new homeostatic setpoint characterized by biomarkers. Different risk factors and biomarkers can converge to the same symptoms of schizophrenia, suggesting that the primary cause of the disease can be highly individual. Schizophrenia-related biomarkers include measurable biochemical changes induced by stress (elevated allostatic load), mitochondrial dysfunction, neuroinflammation, oxidative and nitrosative stress, and circadian rhythm disturbances. Here is a summary of selected valid biological hypotheses of schizophrenia formulated based on risk factors and biomarkers, neurodevelopment, neuroplasticity, brain chemistry, and antipsychotic medication. The integrative neurodevelopmental-vulnerability-neurochemical model is based on current knowledge of the neurobiology of the onset and progression of the disease and the effects of antipsychotics and psychotomimetics and reflects the complex and multifactorial nature of schizophrenia.

A honokiol-enriched Magnolia officinalis Rehder & E.H. Wilson. bark extract possesses anxiolytic-like activity with neuroprotective effect through the modulation of CB1 receptor.

Abstract: Objectives The exposure of neurons to an excessive excitatory stimulation induces the alteration of the normal neuronal function. Mood disorders are among the first signs of alterations in the central nervous system function. Magnolia officinalis bark extract has been extensively used in the traditional medicine systems of several countries, showing several pharmacological activities. Honokiol, the main constituent of M. officinalis, is a GABA modulator and a CB1 agonist, which is deeply investigated for its role in modulating mood disorders. Methods Thus, we evaluated the possible neuroprotective effect of a standardized M. officinalis bark extract (MOE), enriched in honokiol, and its effect on animal mood behavioural tests and in an in vitro model of excitotoxicity. Key findings MOE showed neuroprotective effect using SH-SY5Y cells, by normalizing brain-derived neurotrophic factor release. Then, we tested the effect of MOE in different behavioural tests evaluating anxiety and depression and we observed a selective anxiolytic-like effect. Finally, we confirmed the involvement of CB1 in the final effect of MOE by the co-administration of the CB1 antagonist, AM251. Conclusion These results suggest that MOE could be considered an effective and safe anxiolytic candidate with neuroprotective activity.