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MDMA users consistently exhibit memory dysfunction but there is an ongoing debate if these deficits are induced mainly by alterations in the prefrontal or mediotemporal cortex, especially the hippocampus. Thus, we investigated the relation of verbal memory deficits with alterations of regional cerebral brain glucose metabolism rMRGlu in recreational MDMA users. As previously shown, MDMA users showed significant impairment in verbal declarative memory performance. PET scans revealed significantly decreased rMRGlu in the bilateral dorsolateral prefrontal and inferior parietal cortex, bilateral thalamus, right hippocampus, right precuneus, right cerebellum, and pons at the level of raphe nuclei of MDMA users. Among MDMA users, learning and recall were positively correlated with rMRGlu predominantly in bilateral frontal and parietal brain regions, while recognition was additionally related to rMRGlu in the right mediotemporal and bihemispheric lateral temporal cortex. Moreover, cumulative lifetime dose of MDMA was negatively correlated with rMRGlu in the left dorsolateral and bilateral orbital and medial PFC, left inferior parietal and right lateral temporal cortex. Verbal learning and recall deficits of recreational MDMA users are correlated with glucose hypometabolism in prefrontal and parietal cortex, while word recognition was additionally correlated with mediotemporal hypometabolism. We conclude that memory deficits of MDMA users arise from combined fronto-parieto-mediotemporal dysfunction. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Funding: Dr. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing interests: The authors have declared that no competing interests exist. After cannabis and cocaine, MDMA together with other amphetamines are the most commonly used illegal drugs in Europe and worldwide \[3\] , \[4\]. In a recent survey, 5. Numerous animal studies with different species provided compelling evidence for an impairment of the 5-HT system following MDMA exposure \[6\] ,. The human neurotoxicity of MDMA was also supported by the highly consistent finding that at least intense MDMA users display marked verbal and visuo-spatial memory deficits \[19\] — \[27\]. Finally, also electrophysiological studies suggested alterations of the 5-HT system in regular MDMA users \[29\] — \[31\]. Finally, in a large sample of MDMA users, increased glucose metabolism in the ventrolateral frontal cortex Brodman areal \[BA\] 10 was reported as well \[33\]. PET studies using serotonergic radioligands consistently showed globally reduced 5-HTT binding in chronic MDMA users most pronounced in mediotemporal and frontal cortices \[36\] — \[41\]. In this sample, time of abstinence was positively correlated with subcortical, but not cortical, 5-HTT binding, suggesting only a partial neuronal recovery in these subjects. Also investigations of postsynaptic 5-HT receptors revealed rather inconsistent results. Functional magnetic resonance imaging fMRI studies also suggested differences in the activation of the hippocampus between MDMA users and healthy controls during working memory tasks and supported the view of a hippocampal dysfunction in MDMA users \[48\] — \[52\]. However, further functional imaging studies additionally reported abnormalities in the activation of several other brain regions—including frontal, thalamic, striatal, cingulate, temporolateral, parietal, and occipital regions—of MDMA users during working memory tasks \[50\] , \[52\] — \[54\]. Neuropsychological evidence additionally points to an MDMA-related impairment of executive functions such as impulsivity, decision-making, and recall consistency indicating frontal dysfunction \[27\] , \[55\] , \[56\]. Thus, although memory deficits are the most consistent finding in MDMA users \[57\] , their neurobiological basis are unclear so far. Moreover, no study explored cerebral glucose metabolism assessed by PET in relation to MDMA-related memory deficits subdivided into different functions such as learning, recall, and recognition. The neuropsychological pattern already published from this sample suggested that frontal and mediotemporal dysfunction might be involved in the development of memory deficits \[27\]. Thus, we expect to find correlations specifically between decreased rMRGlu in frontal and temporomedial brain regions and diminished memory performance in MDMA users. Both groups did not significantly differ with respect to age, handedness, years of education, and verbal intellectual performance Table 1. The amount of illicit drug use is presented in Table 2. However, MDMA users also revealed a mild to moderate cannabis use. Moreover, MDMA users revealed a slight and non-significant reduction of verbal recognition, showing, however, a medium effect size. Previously, we already demonstrated that several indicators of MDMA use were significantly correlated with memory scores \[27\]. Bilateral frontal hypometabolism ranged from BA 8, 9, and 10 up to the premotor cortex BA 6 , showing slightly stronger effects in the right hemisphere Figure 1 , Table 4. In addition, the bilateral thalamus showed significant hypometabolism primarily in areas connected with the prefrontal cortex PFC \[58\]. The significant cluster including the right thalamus extended to the right hippocampus. A significant decrease of rMRGlu could also be shown in the metencephalon pons and mesencephalon at the level of the rostral raphe nuclei as well as in the right posterior cerebellum of the MDMA users Figure 1. To investigate the impact of cumulative MDMA intake across lifetime on structural alterations of the brain, we only investigated negative correlations between resting rMRGlu and drug dose high consumption corresponding with decreased rMRGlu. Delayed recall was chosen because MDMA users showed the strongest impairment here. Finally, drug intake and delayed recall correlations with rMRGlu overlapped in right inferior parietal cortex BA The aim of this study was to investigate the neurobiological correlates of memory deficits in currently abstinent recreational MDMA users. Using 18 FDG-PET in rest, we demonstrated that MDMA users showed a significant reduction of cerebral glucose metabolism predominantly in the bilateral DLPFC and inferior parietal cortex, as well as the bilateral thalamus, right hippocampus, right precuneus, right cerebellum, and pons at the level of raphe nuclei. In the group of MDMA users, learning and recall parameters were positively correlated with rMRGlu primarily in bilateral frontal and parietal brain regions, while word recognition was additionally related to rMRGlu in the right mediotemporal and bihemispheric lateral temporal cortex. In addition, cumulative lifetime dose of MDMA was negatively correlated with rMRGlu in the left DLPFC, bilateral ventromedial prefrontal and orbitofrontal cortex as well as left inferior parietal and right lateral temporal cortex. Our results are also in line with previous studies showing changes of serotonergic radioligand binding in prefrontal and parietal regions \[39\] — \[41\] , \[44\] , hippocampus \[39\] , and in the thalamus \[37\] , \[59\] of MDMA users. However, our sample might have been underpowered to detect these additional changes. Previous studies demonstrated that regional reduction of cerebral glucose metabolism might result from loss of neuronal connections and projections \[60\] — \[62\]. As such, the reductions of cortical rMRGlu in MDMA users might as well be explained by loss of neuronal connections and projections and thus be interpreted as a direct neurotoxic effect of the drug, as they were shown in many pervious animal studies \[13\] , \[63\]. Interestingly, the thalamic hypometabolism of MDMA users shown here occurred in anatomical areas that are well connected to frontocortical regions presenting also hypometabolism \[58\]. Also the reduction of glucose metabolism at the brain stem level might be explained by lesions of the raphe nuclei as a previous study with non-human primates demonstrated pathological changes specifically in the dorsal raphe nucleus induced by MDMA \[64\]. Crucially, the symmetry of glucose hypometabolism in MDMA users, which occurred bilaterally in several regions such as the thalamus, frontal and prefrontal areas as well as the parietal cortex, confirms the validity and stability of the present results. Furthermore, it supports the argument of neurotoxicity, as neuronal damages would be expected to develop spatially nonspecific, thus equally distributed over both hemispheres \[65\]. Given that we have only investigated current users with a mean duration of abstinence of two to three weeks in a cross-sectional design, it can not be concluded if the reported alterations are lasting or transitory. The results from this study confirm our hypothesis that hypometabolism in the frontal cortex and in the hippocampus is correlated with verbal memory deficits in recreational MDMA users. Within the MDMA group, total learning performance was associated with the right premotor cortex, bilateral dorsolateral prefrontal, and the left inferior frontal cortex. Therefore, learning deficits in MDMA users seem to be caused by dysfunction of frontal encoding or recall processes \[69\]. Interestingly, acute MDMA effects also seem to influence middle frontal gyrus BA 10 activity leading to verbal memory encoding impairments \[70\]. Delayed recall performance was positively correlated with the rMRGlu in a prefrontal cluster including the bilateral dorsolateral and ventrolateral PFC and right premotor cortex. Moreover, a parieto-temporal cluster including the right inferior parietal cortex and right superior temporal cortex appeared. Thus, prefrontal and parieto-temporal areas seem to be involved in the dysfunction of delayed recall in MDMA users, indicating disturbed memory formation into—or diminished recall from association cortices, beyond the shown working memory and frontal encoding and recall deficits \[66\]. Corrected recognition performance was associated with rMRGlu in bilateral superior temporal cortices, right orbitofrontal cortex gyrus rectus , left anterior hippocampus and parahippocampal gyrus, and left parieto-occipital part of the angular gyrus. Therefore, particularly reduced recognition performance in MDMA users might be explained by hippocampal dysfunction \[71\]. However, also prefrontal and anterior temporal areas seem to be involved—areas that were previously linked with recognition in several PET studies \[72\]. Notably, most of the areas showing glucose hypometabolism in MDMA users are part of the two core brain networks: the resting-state default mode network DMN; precuneus, lateral temporal cortex and hippocampus \[73\] and its anti-correlated cognitive control network CCN; DLPFC, parietal cortex \[74\]. Taken together, the previously postulated dissociation of prefrontal and hippocampal functions as correlates of memory deficits in MDMA users, resulting from temporal or hippocampal dysfunction alone \[21\] , \[47\] , \[49\] , \[51\] , could not be confirmed. In our sample, verbal learning and recall deficits of MDMA users were correlated with glucose hypometabolism in the prefrontal, frontal and parietal cortex, while word recognition was additionally correlated with mediotemporal hypometabolism. Thus, our imaging data support the neuropsychology-based hypothesis of a combined fronto-parieto-mediotemporal dysfunction in abstinent MDMA users \[27\] , \[55\]. This assumption is in accordance to the results of early animal studies showing that MDMA-induced denervation of 5-HT axons in the frontal cortex and hippocampus display a relatively low regeneration, thus indicating a high susceptibility of these structures for MDMA neurotoxicity \[13\] , \[75\] , \[76\]. The cumulative total dose of MDMA was negatively correlated with rMRGlu in the left dorsolateral and bilateral orbital and ventromedial PFC, left inferior parietal, and right lateral temporal cortex. This finding is largely in line with a recent study showing significant correlation of the severity of MDMA, heroin, alcohol, and cannabis use with rMRGlu in the DLPFC and lateral temporal cortex of polydrug users \[35\]. A limitation of this study is the use of subjective reports for assessing the extent of drug consumption. The reliability of these reports may be questionable, as they depend on memory function and are probably influenced by anticipated social expectancies. A solution of this problem would be a toxicological hair analysis, which was not available for us at that time. In this regard, our urine drug screenings are only of restricted advantage, as water soluble substances such as MDMA can only be analyzed until few days post exposure \[77\]. However, in a study that addressed this problem, a concordance of Collectively, it is a pertinent unsolved problems of neurotoxicological research, that an objective method to determine the cumulative lifetime drug consumption is not available to date \[79\]. Another key issue of human neurotoxicity studies in illicit drug users is the high prevalence of polytoxic drug use in this population. Although, this study included only subjects with a predominant use of MDMA, these participants also used other drugs. A retrospective differentiation of single substance effects is difficult, as the use of the different substances is highly intercorrelated. In addition, potential protective or potentiating effects of substance combinations on neurotoxicity limit the interpretation of such results. Moreover, tobacco use was significantly more pronounced in MDMA users compared to controls. Given, that nicotine has considerable effects on brain networks and cognitive functions \[80\] , \[81\] , the modulating effect of nicotine on our results is not entirely clear although introduction of smoking as a covariate into the group comparisons did not change the main results. Finally, the abstinence duration from the different drugs was highly variable between subjects; however, the abstinence duration of MDMA, cannabis, cocaine, amphetamine and hallucinogens was not systematically correlated with rMRGlu in the user group. The availability of biological markers for the central serotonergic system such as 5-HT or 5-HIAA CSF or plasma concentrations would have been of advantage for the interpretation of our study results. However, to date such markers have only low validity and reliability \[82\]. Using a specific serotonergic radioligand might have been of additional interest, as alterations of the cerebral glucose metabolism only reflect global functioning of neuronal tissue. Also in this case, the reliability and specificity of in particular 5-HTT PET ligands seem questionable, as they are not able to reflect global serotonergic functioning \[83\] , \[84\]. Recently, we developed a novel method employing 18 F-altanserin PET in combination with a dexfenfluramine challenge in order to measure 5-HT release capacity \[85\] , which now provides the first functional measure for the 5-HT system in humans. Our 18 FDG PET and neuropsychological data show that verbal memory deficits are correlated with glucose hypometabolism in dorsolateral prefrontal and parietal areas of the brains of abstinent MDMA users. This is especially true for global learning performance and delayed recall, while recognition is additionally associated with mediotemporal hypometabolism. Frontal and parietal areas show the highest overlap of glucose hypometabolism with impaired memory function and cumulative drug intake. In conclusion, memory deficits of MDMA users seem to arise from combined fronto-parieto-mediotemporal dysfunction. After being informed of the aim of the study by written and oral description, all participants gave written informed-consent statements. The study has been conducted according to the principles expressed in the Declaration of Helsinki. Nineteen male, chronic but currently abstinent users of MDMA and 19 subjects with no history of illicit drug use were studied all of Caucasian ethnicity. All participants were recruited by advertisements in a techno music magazine. In addition, the use of MDMA clearly had to dominate the consumption of any other psychotropic drug and participants should especially have no substantial previous use of other amphetamine derivatives e. PET scans and neuropsychological assessments were carried out when participants were abstinent for at least three days. Inclusion criteria for both groups included negative drug urine toxicology. Exclusion criteria for both groups included use of any psychotropic medication, a present psychiatric disorder, a family history of psychiatric disorders, as well as a severe somatic disease. None of the participants reported a history of migraine, epilepsy, or craniocerebral trauma. On the first day the neuropsychological test battery was assessed in the afternoon 2 p. For the estimation of verbal intellectual performance, the Mehrfachwahl-Wortschatz-Intelligenztest was used \[86\]. Drug history and present pattern of psychotropic drug consumption was assessed by the Interview for Psychotropic Drug Consumption \[30\]. The whole battery took about minutes; including breaks as needed, and was generally well tolerated by the participants. During the psychiatric and neuropsychological assessment, the subjects could ask for a break at any time. In brief, the instrument consists of a word list A of 15 nouns learning list , a second word list B of 15 different nouns interference list and a third list C of 50 nouns which includes all words of lists A and B as well as 20 new, but semantically- and phonetically-related words recognition list. This was followed by a five-minute transmission scan using 68 germanium. Image reconstruction was performed due to filtered back projection using a Hannig-Filter cut-off frequency of 0. Blood glucose levels were assessed anterior to the injection of the tracer. Arterialized blood sampling was used to measure 18 FDG in plasma. Subjects were scanned once, under resting conditions light dimmed, subjects lying, and eyes closed during and a. The normalized and smoothed images were adjusted by a proportional scaling mean to 50, threshold masking 0. For voxel-wise comparisons, t-test for independent samples was used. Voxel-wise correlations were performed to assess the relationship between changes in rMRGlu and changes in individual cognitive performance within each group. We are grateful to Dr. Irene Daum and Dr. Reinhard Heun for earlier comments to the present data and their advice. The authors would like to express their gratitude to the staff of the Department of Nuclear Medicine of the University of Bonn supporting the study and to Lea M. Hulka for critical comments to the manuscript. None of the authors reported biomedical financial interests or potential conflicts of interest with respect to the present study. Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field. Results As previously shown, MDMA users showed significant impairment in verbal declarative memory performance. Conclusions Verbal learning and recall deficits of recreational MDMA users are correlated with glucose hypometabolism in prefrontal and parietal cortex, while word recognition was additionally correlated with mediotemporal hypometabolism. Sensi, University G. Results Demographics and drug use Both groups did not significantly differ with respect to age, handedness, years of education, and verbal intellectual performance Table 1. Download: PPT. Table 1. Table 2. Pattern and amount of illegal drug use: results of the Psychotropic Drug Interview means and standard deviations in parentheses. Table 3. Figure 1. Table 4. Correlations of brain metabolism with verbal memory deficits To investigate the relation of decreased resting rMRGlu with memory impairment we only investigated positive correlations between rMRGlu and memory performance low performance in conjunction with decreased rMRGlu in MDMA users Figure 2 and Table 5. Figure 2. Table 5. Delayed recall. Recall consistency. Figure 3. Figure 4. Table 6. Discussion The aim of this study was to investigate the neurobiological correlates of memory deficits in currently abstinent recreational MDMA users. Furthermore, MDMA users showed a correlation of recall consistency with rMRGlu in the right DLPFC, which is in line with the view the recall consistency represents an aspect of executive functions related to the DLPFC \[68\] , Within the MDMA group, total learning performance was associated with the right premotor cortex, bilateral dorsolateral prefrontal, and the left inferior frontal cortex. Conclusion Our 18 FDG PET and neuropsychological data show that verbal memory deficits are correlated with glucose hypometabolism in dorsolateral prefrontal and parietal areas of the brains of abstinent MDMA users. Participants Nineteen male, chronic but currently abstinent users of MDMA and 19 subjects with no history of illicit drug use were studied all of Caucasian ethnicity. Procedure On the first day the neuropsychological test battery was assessed in the afternoon 2 p. Acknowledgments We are grateful to Dr. References 1. Christophersen AS Amphetamine designer drugs-an overview and epidemiology. Toxicol Lett — — View Article Google Scholar 2. J Psychopharmacol — View Article Google Scholar 3. Vienna: United Nations. View Article Google Scholar 6. Pharmacol Rev — View Article Google Scholar 7. Curr Neuropharmacol 9: 91— View Article Google Scholar 8. Neuropharmacology — View Article Google Scholar 9. 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Nat Rev Neurosci 4: — Neuropsychologia — Behav Brain Sci —; discussion — Hippocampus 9: 71— Ann N Y Acad Sci 1— Cogn Affect Behav Neurosci — Ensslin HK, Kovar KA, Maurer HH Toxicological detection of the designer drug 3,4-methylenedioxyethylamphetamine MDE, 'Eve' and its metabolites in urine by gas chromatography-mass spectrometry and fluorescence polarization immunoassay. J Chromatogr B Biomed Appl — Neuro Endocrinol Lett — An overview of evidence and of methodological problems in research. Neuropsychobiology 34— Biochem Pharmacol — Neuroimage 73— Pharmacol Biochem Behav — Kish SJ How strong is the evidence that brain serotonin neurons are damaged in human users of ecstasy? Neuroimage — Balingen View Article Google Scholar Rey A L'examen de Clinique en Psychologie. Paris: Presses Universitaire de France. The Clinical Neuropsychologist 5: — London: J. Vul E, Pashler H Voodoo and circularity errors. View Article Google Scholar.

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