Analysis of information sources in references of the Wikipedia article "MDMA" in Italian language version.
[...]Decreased FA and increased ADC in the thalamus may reflect ecstasy-induced axonal damage, because axonal cell membranes are known to be responsible for most of the restriction of water diffusion and axonal damage lead to decreased FA and increased ADC. This finding of ecstasy-induced brain pathology in the thalamus corroborates findings from previous studies showing decreased thalamic SERT densities in (heavy) ecstasy users, most probably reflecting damage to terminals of serotonergic axons
[...]These findings suggest sustained effects of ecstasy on brain microvasculature, white matter maturation and possibly axonal damage due to low dosages of ecstasy. Although we do not know yet whether these effects are reversible or not, we cannot exclude that ecstasy even in low doses is neurotoxic to the brain.»• The effects of chronic MDMA use have been analysed in various neurocognitive domains such as working memory, episodic memory, semantic memory, visual stimulation, motor function and impulsivity. Structural neuroimaging in MDMA users has shown reduction in brain 5-HT transporter (5-HTT) and 5-HT2a receptor levels using positron emission tomography (PET) or single photon emission computed tomography (SPECT) and reduced grey matter density in various brain regions using voxel based morphometry method (VBM). Chemical Neuroimaging, assaying the levels of myoinositol (MI) and N-acetylaspartate (NAA) in the brains of MDMA users using proton magnetic resonance spectroscopy (MRS), has not revealed any consistent results. Functional magnetic resonance imaging (fMRI) studies have shown task evoked differences in regional brain activation, measured as blood oxygen level dependent (BOLD) signal intensity and/or spatial extent of activation, in MDMA users and controls. Neurocognitive studies, in MDMA users, have consistently revealed dose related memory and learning problems.
Serotonergic innervation is known to regulate the cerebral microvasculature. Chronic MDMA use results in serotonin toxicity, therefore MDMA users are expected to have altered regional blood flow detectable in fMRI. Animal data has suggested that MDMA is selectively more toxic to the axons more distal to the brainstem cell bodies, that is, those present mainly in the occipital cortesemente.
Also, human PET and SPECT studies have revealed significant reductions in serotonin transporter binding, most evident in the occipital cortex. The effects of poly-drug exposure may result in additive neurotoxicity or mutual neuro-protection. MDMA is known to induce hyperthermia which is a prooxidant neurotoxic condition.Hyperthermia is known to accentuate the neurotoxic potential of MDMA as well as methamphetamine. On the other hand, lowering of the core body temperature has been shown to have a neuroprotective effect."»
[...]Decreased FA and increased ADC in the thalamus may reflect ecstasy-induced axonal damage, because axonal cell membranes are known to be responsible for most of the restriction of water diffusion and axonal damage lead to decreased FA and increased ADC. This finding of ecstasy-induced brain pathology in the thalamus corroborates findings from previous studies showing decreased thalamic SERT densities in (heavy) ecstasy users, most probably reflecting damage to terminals of serotonergic axons
[...]These findings suggest sustained effects of ecstasy on brain microvasculature, white matter maturation and possibly axonal damage due to low dosages of ecstasy. Although we do not know yet whether these effects are reversible or not, we cannot exclude that ecstasy even in low doses is neurotoxic to the brain.»