The Association Between Cingulate Cortex Glutamate Concentration and Delay Discounting Is Mediated by Resting State Functional Connectivity.

The association between cingulate cortex glutamate concentration and delay discounting is mediated by resting state functional connectivity.

Filed under: Addiction Rehab

Brain Behav. 2012 Sep; 2(5): 553-62
Schmaal L, Goudriaan AE, Meer J, Brink W, Veltman DJ

Humans vary in their ability to delay gratification and impulsive decision making is a common feature in various psychiatric disorders. The level of delay discounting is a relatively stable psychological trait, and therefore neural processes implicated in delay discounting are likely to be based on the overall functional organization of the brain (under task-free conditions) in which state-dependent shifts from baseline levels occur. The current study investigated whether delay discounting can be predicted by intrinsic properties of brain functioning. Fourteen healthy male subjects performed a delay discounting task. In addition, resting state functional magnetic resonance imaging (fMRI) and magnetic resonance spectroscopy (¹H MRS) were used to investigate the relationship between individual differences in delay discounting and molecular and regional measures of resting state (baseline) activity of dorsal anterior cingulate cortex (dACC). Results showed that delay discounting was associated with both dACC glutamate concentrations and resting state functional connectivity of the dACC with a midbrain region including ventral tegmental area and substantia nigra. In addition, a neural pathway was established, showing that the effect of glutamate concentrations in the dACC on delay discounting is mediated by functional connectivity of the dACC with the midbrain. The current findings are important to acknowledge because spontaneous intrinsic brain processes have been proposed to be a potential promising biomarker of disease and impulsive decision making is associated with several psychiatric disorders.
HubMed – addiction

 

Methamphetamine reduces human influenza a virus replication.

Filed under: Addiction Rehab

PLoS One. 2012; 7(11): e48335
Chen YH, Wu KL, Chen CH

Methamphetamine (meth) is a highly addictive psychostimulant that is among the most widely abused illicit drugs, with an estimated over 35 million users in the world. Several lines of evidence suggest that chronic meth abuse is a major factor for increased risk of infections with human immunodeficiency virus and possibly other pathogens, due to its immunosuppressive property. Influenza A virus infections frequently cause epidemics and pandemics of respiratory diseases among human populations. However, little is known about whether meth has the ability to enhance influenza A virus replication, thus increasing severity of influenza illness in meth abusers. Herein, we investigated the effects of meth on influenza A virus replication in human lung epithelial A549 cells. The cells were exposed to meth and infected with human influenza A/WSN/33 (H1N1) virus. The viral progenies were titrated by plaque assays, and the expression of viral proteins and cellular proteins involved in interferon responses was examined by Western blotting and immunofluorescence staining. We report the first evidence that meth significantly reduces, rather than increases, virus propagation and the susceptibility to influenza infection in the human lung epithelial cell line, consistent with a decrease in viral protein synthesis. These effects were apparently not caused by meth’s effects on enhancing virus-induced interferon responses in the host cells, reducing viral biological activities, or reducing cell viability. Our results suggest that meth might not be a great risk factor for influenza A virus infection among meth abusers. Although the underlying mechanism responsible for the action of meth on attenuating virus replication requires further investigation, these findings prompt the study to examine whether other structurally similar compounds could be used as anti-influenza agents.
HubMed – addiction

 

Neurochemical biomarkers in Alzheimer’s disease and related disorders.

Filed under: Addiction Rehab

Ther Adv Neurol Disord. 2012 Nov; 5(6): 335-48
Bibl M, Esselmann H, Wiltfang J

Neurochemical biomarkers for diagnosing dementias are currently under intensive investigation and the field is rapidly expanding. The main protagonists and the best defined among them are cerebrospinal fluid levels of A?42, tau and its phosphorylated forms (p-tau). In addition, novel cerebrospinal fluid biomarkers are emerging and their multiparametric assessment seems most promising for increasing the accuracy in neurochemical dementia diagnostics. The combined assessment of A?42 and p-tau has recently shown value for diagnosing prodromal states of Alzheimer’s dementia, that is, mild cognitive impairment. Disease-specific biomarkers for other degenerative dementias are still missing, but some progress has recently been made. As lumbar puncture is an additional burden for the patient, blood-based neurochemical biomarkers are definitely warranted and promising new discoveries have been made in this direction. These diagnostic developments have implicit therapeutic consequences and give rise to new requirements for future neurochemical dementia diagnostics.
HubMed – addiction

 


 

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