Evaluation of the Effect of Low Dose of Methamphetamine on the Human Astrocyte Cell Cycle Exposed to Amyloid Beta

Astrocytes are the most important and abundant cells helping neurons. They are involved in the neural survival, ionic, and osmotic homeostasis, as well as in the formation of synapses and growth of the axons and dendrites. Activating markers of the cell cycle increased in Alzheimer’s disease. Cyclin dependent kinase 1(Cdk1) and cyclin E2 (CE2) are among the cell cycle markers. Besides, methamphetamine in non-toxic dose reduces the automatic division capacity and leads to cell differentiation. In this study, the human astrocytes exposed to amyloid beta (Aβ) and treated with low doses of methamphetamine (METH) and the cell cycle arrest and expression of the Cdk1 and CE2 were assessed in all groups. Five groups were used: 1- The cells expose to Aβ, 2- The cells exposed to METH, 3- The cells exposed to Aβ and then METH, 4- the cells exposed to METH and then Aβ, 5- The control group. Each group was repeated three times. Cdk1 gene expression decreased in group 3, treatment group, but increased in group 4, prevention group. The CE2 gene expression decreased in both groups. Furthermore, the cell cycle arrest in G1, G2, and S were assessed. In the Group 3, treatment group, G2 decreased; but in group 4, prevention group, it increased. Changes in the cell cycle are the early symptoms of Alzheimer’s disease. The low dose of METH can reduce cell cycle activating markers as well as reducing cell division and leading the cells to death.