Bringing Advocacy, Hope and Cure for Metabolic and Mental Disorders.

The European Mental and Metabolism Association (EMMA) is a non-profit, non-governmental organization founded in 1996 and officialised in June 2005. The scope of this essentially European, but also International, Association is to advocate reliable, valid and independent biomedical research, and bring the hope for a cure, in the field of Mental and Metabolic diseases.

"Synaptic plasticity and adaptive behaviors are likely dependent on the capacity of neurons to meet the energy demands for neuronal activity, imposed by daily environmental challenges. In case of excessive pressure, neuronal energy metabolism may get overwhelmed. Then, depressed mood, tiredness, low-energy feelings, and listlessness are the most common symptoms associated with such a mental fatigue."   

Evolved Minds shall : concentrate onto a goal, filter distracting stimuli, evaluate the input against a cognitive map, elaborate and evaluate responses, perform planned activities, inhibit all other inappropriate drives. In challenging situations, such "decision-making" may become difficult, and individuals may be tempted to choose impulsively, or to gamble. Any failure of energy metabolism in brain areas subserving these functions likely results in a failure of behavior, often called "symptom", and in mental disorder. As far as the final behavioral output - in conditions of challenging choice - cannot be foreseen a priori and inequivocally, there is room for what we call "Free Will" and the individual is claimed to be morally responsible for any decision. Conversely, if the behavioral output is set a priori - because of potent overwhelming drives like "impulses, compulsions" - with little or no room for cognitive inhibitory control (i.e. what we call "Madness, Crazyness"), the individual cannot be claimed as morally responsible for the actions deriving from such a non-decision !!!  

 To follow the ongoing campaign(s) supported by EMMA as well as its own goals, click here.

 A major and ultimate goal of EMMA is to foster Behavioral Science, the scientific study of behavior how it is, as well as Ethical Phylosophy, the study of behavior how it should be.  

Human Behavior vs Animal Behavior : merging Psychology to Ethology. Neural Bases of Behavior and Free Will: merging Science to Philosophy.   

The applied research on animal behavior (and its modulation by environmental influences and/or innovative biomedical agents) implies testing alive animals. Please sign the petition for sustaining the need of laboratory research with animals (as ruled by Law and for the sake of Human Health).  

LATEST NEWS & SCIENTIFIC DISCOVERIES, "ADHD" 

Sept 4, 2009.

"Carboxylesterase 1 gene polymorphism and methylphenidate response in ADHD" by Nemoda Z, Angyal N, Tarnok Z, Gadoros J, Sasvari-Szekely M on the journal "Neuropharmacology".

Abstract: Methylphenidate (MPH) is the most frequently prescribed drug in the treatment of attention deficit hyperactivity disorder (ADHD). Several pharmacogenetic studies suggested that catecholamine candidate genes influence individual MPH-responses, but these results are mostly contradictory. Genetic analyses of MPH metabolizing carboxylesterase 1 enzyme (CES1) have not been carried out, whereas, meta-analysis of CYP2D6 genetic variants has been already indicated significant pharmacogenetic differences in atomoxetine treatment. Here we present an association analysis of the CES1 Gly143Glu functional polymorphism in a Hungarian ADHD group (n = 173). The genotype frequencies were similar to that of the general population (5.8% vs 4.1% of Gly/Glu heterozygote). Pharmacogenetic analysis was conducted among 122 ADHD children treated with MPH. Neither the categorical analysis comparing 90 responders vs 32 non-responders, nor the dimensional analysis of Inattention and Hyperactivity-Impulsivity score reduction showed a significant main genotype effect. However, analyzing the daily dose, we observed an association with the rare 143Glu-variant: 5 patients in the responder group carrying the Glu-allele required lower doses of MPH for symptom reduction (0.410 +/- 0.127 vs 0.572 +/- 0.153 mg/kg, t(1,88) = 2.33, p = 0.022). This result warrants for further investigations of the CES1 gene in larger ADHD samples.
 

 May 12, 2009 — NARSAD (Great Neck, N.Y.) — Young Investigator Tracie Paine, Ph.D., was the lead author of a study by Harvard neuroscientists that identified a new link between a brain enzyme and attention deficits and hyperactivity, two key symptoms of attention deficit / hyperactivity disorder (ADHD). The research, performed at McLean Hospital and published online on April 22 by the journal Neuropsychopharmacology, suggests that an enzyme called protein kinase-A (PKA) plays an important role in keeping these symptoms in check.

  All NEWS before May 2009 can be found in our CLINICAL-CARE NEWS ARCHIVE.    

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Working toward a neurobiological account of ADHD: Commentary on Gail Tripp and Jeff Wickens, Dopamine transfer deficit

by Jonathan Williams, Gatsby Computational Neuroscience Unit, University College London, UK 

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Evidence of Developmental Alterations in Cortical and Subcortical Regions of Children With Attention-Deficit / Hyperactivity Disorder. Multivoxel In Vivo Phosphorus 31 Spectroscopy. Arch Gen Psychiatry. 2008;65(12):1419-1428.

An interesting paper on 31-P MRS as diagnostic tool (click to read)

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OTHER NEWS & DISCOVERIES:

Feb 25, 2009 : Behav Brain Funct. 2009 ; 5:11.

Evaluation of animal models of neuro-behavioral disorders. By van der Staay FJ, Arndt SS, Nordquist RE.

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 May 6, 2009. Biol Psychiatry. 2009 [Epub ahead of print]

Changes in the Developmental Trajectories of Striatum in Autism. By Langen M, et al.

 The effect of 5-HTT gene promoter polymorphism on impulsivity depends on family relations ...

 Anti-N-methyl-D-aspartate receptor antibodies, cognitive dysfunction, and depression ...