Methamphetamine-induced cognitive impairment: Evaluation of amyloid beta 40 and phosphorylated tau protein 217 in male users

Abstract

Methamphetamine (METH) addiction is one of the most illegal substances use disorder worldwide, resulting in social, medical, and psychological consequences. This stimulant of the central nervous system (CNS) has been linked with different physiological effects that lead to the onset of multiple health disorders. This study aimed to investigate cognitive impairment in individuals with METH addiction by analyzing levels of amyloid β 40 (Aβ40) and phosphorylated tau protein at threonine 217 (p-tau 217), as key biomarkers associated with neurodegeneration. Two groups of adult males were assigned in this study, one containing 75 males with no previous history of addiction, non-medical use of any type of drugs, and no history of neurodegenerative diseases. The other group contained 75 males confirmed with METH addiction (1–10 years), Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA) and the Mini-Mental State Examination (MMSE). Among the METH group, 44 % exhibited cognitive impairment based on these assessments. The levels of Amβ 40 and p-tau 217 protein increased significantly (p < 0.001) in individuals with METH addiction compared to non-addicts’ group. Also, Amβ 40 and p-tau 217 protein were correlated positively (r = 0.443, p < 0.001), as well as p-tau 217 and albumin (r = 0.346, p = 0.002). Moreover, Amβ 40 has shown significant impact as risk factor for cognitive impairment in individuals with METH addiction with OR of 1.074 (1.035–1.115 95 % CI). Thus, abusing METH may stimulate dysfunction in the memory, resulting in elevation of Amβ 40 and p-tau 217 protein which leads to hypomnesia, and ultimately may increase the risk of neurodegenerative pathology.