Group items tagged

Dysfunctional cortico-limbic brain activity associated with anger may be normalized by nicotine. Cortico-limbic brain activity associated with anger may be susceptible to nicotine and, thus, may contribute to smoking initiation and nicotine addiction. Functional imaging studies on regional brain activity in response to nicotine and smoking have documented the involvement of cortico-limbic structures such as the prefrontal cortex (including the dorsolateral prefrontal cortex, inferior frontal, medial frontal, and orbitofrontal gyri), cingulate, thalamus, and amygdala

Primary source: Gehricke JG, et al "Nicotine-induced brain metabolism associated with anger provocation" Behav Brain Func 2009; DOI: 10.1186/1744-9081-5-19.

Professor Fuchs from the Clinical Neurobiology Laboratory, German Primate Center in Goettingen, will present the latest findings on how brain cells can be adversely affected by stress and depression. He will explain how the adult brain is generating new cells and which impact these findings will have on the development of novel antidepressant drugs. Contact: Sonja Mak s.mak@update.europe.at 43-140-55734 European College of Neuropsychopharmacology Source:Eurekalert (2008)

This article discusses new Duke University research showing a highly significant correlation (p = 0.007) between higher vitamin D intake and MRI brain lesions (http://www.fasebj.org/cgi/content/meeting_abstract/21/6/A1072), as well as the potential for lesion reversal. These lesions have been associated with cognitive impairment, stroke, psychiatric disorders and mortality. This article also discusses the levels of vitamin D and calcium needed to avoid osteoporosis and vascular calcification in the light of new research on blockage of the vitamin D receptor due to bacterial products and elevated 25D.

New findings in rodents and human brain shed light on the mechanisms of major depressive disorder (MDD), uncovering over-expression of MKP-1 (mitogen-activated protein kinase [MAPK] phosphatase-1)...and identifying a new therapeutic target. MKP-1, also known as dual-specificity phosphatase-1 (DUSP1), is a member of a family of proteins that dephosphorylate both threonine and tyrosine residues and thereby serves as a key negative regulator of the MAPK cascade4, a major signaling pathway involved in neuronal plasticity, function and survival This study identifies MKP-1 as a key factor in MDD pathophysiology, and as a new target for therapeutic interventions.f Here we use whole-genome expression profiling of postmortem tissue and show significantly increased expression of mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1, encoded by DUSP1, but hereafter called MKP-1) in the hippocampal subfields of subjects with MDD compared to matched controls. MKP-1, also known as dual-specificity phosphatase-1 (DUSP1), is a member of a family of proteins that dephosphorylate both threonine and tyrosine residues and thereby serves as a key negative regulator of the MAPK cascade4, a major signaling pathway involved in neuronal plasticity, function and survival. We tested the role of altered MKP-1 expression in rat and mouse models of depression and found that increased hippocampal MKP-1 expression, as a result of stress or viral-mediated gene transfer, causes depressive behaviors. Conversely, chronic antidepressant treatment normalizes stress-induced MKP-1 expression and behavior, and mice lacking MKP-1 are resilient to stress. These postmortem and preclinical studies identify MKP-1 as a key factor in MDD pathophysiology and as a new target for therapeutic interventions.

"new research demonstrates that ingested vitamin D is immunosuppressive and that low blood levels of vitamin D may be actually a result of the disease process. Supplementation may make the disease worse. "