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Introduction Chronic use of methamphetamine induces neuropsychological deficits and neurochemical changes in frontostriatal regions. This study aimed to examine the relationship between brain metabolites alterations in frontostriatal regions and neuropsychological deficits in patients with methamphetamine use disorder. Method A total of 30 methamphetamine users and 20 control participants were selected and a battery of standardized executive function, attention, and memory tasks, including the Wisconsin Card Sorting Test, Stroop Test, and Wechsler Memory Scale, was administered to them. Proton-Magnetic resonance spectroscopy (H-MRS) of N-Acetylaspartate/Creatine (NAA/Cr), Choline/Creatine (Cho/Cr), and glutamate + glutamine/creatine (Glx/Cr) in dorsolateral prefrontal cortex (DLPFC), anterior cingulate cortex (ACC), and basal ganglia (BG) were also undertaken. Results Current findings indicated that there were significant differences between two groups in metabolite ratios including NAA/Cr, Cho/Cr, and Glx/Cr in three areas, except for Glx/Cr in BG. Moreover, compared to healthy controls, methamphetamine users showed poorer performance in all neuropsychological tests. Finally, a significant relationship was found between regional metabolites alterations, particularly in the ACC, and neuropsychological deficits in methamphetamine users. Conclusions In addition to neurochemical changes and neuropsychological deficits in patients with methamphetamine use disorder, current results highlighted the relationship between these changes in DLPFC, ACC, and BG with cognitive deficits in methamphetamine users. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a neurodegenerative disorder, in which amyloid precursor protein (APP) misprocessing and tau protein hyperphosphorylation are well-established pathogenic cascades. Despite extensive considerations, the central mediator of neuronal cell death upon AD remains under debate. Therefore, we examined the direct interplay between tauopathy and amyloidopathy processes. We employed primary culture neurons and examined pathogenic P-tau and Aβ oligomers upon hypoxia treatment by immunofluorescence and immunoblotting. We observed both tauopathy and amyloidopathy processes upon the hypoxia condition. We also applied Aβ1–42 or P-tau onto primary cultured neurons. We overexpressed P-tau in SH-SY5Y cells and found Aβ accumulation. Furthermore, adult male rats received Aβ1–42 or pathogenic P-tau in the dorsal hippocampus and were examined for 8 weeks. Learning and memory performance, as well as anxiety behaviors, were assessed by Morris water maze and elevated plus-maze tests. Both Aβ1–42 and pathogenic P-tau significantly induced learning and memory deficits and enhanced anxiety behavior after treatment 2 weeks. Aβ administration induced robust tauopathy distribution in the cortex, striatum, and corpus callosum as well as CA1. On the other hand, P-tau treatment developed Aβ oligomers in the cortex and CA1 only. Our findings indicate that Aβ1–42 and pathogenic P-tau may induce each other and cause almost identical neurotoxicity in a time-dependent manner, while tauopathy seems to be more distributable than amyloidopathy. [ABSTRACT FROM AUTHOR]