Increasing evidence suggests that Ab has a direct influence on cholinergic activity. Acetylcholinesterase activity is Ibrutinib Src-bcr-Abl inhibitor increased in plaques and tangles very early in the process of amyloid deposition. In particular, Ab has been shown to induce the expression of acetylcholinesterase in the brains of CT-100-expressing transgenic mice and in cell culture experiments indicating a link between Ab production and acetylcholinesterase activity. In our study, the results demonstrated that exposure of SK-N-MC cells to Ab resulted in a significant increase in acetylcholinesterase activity indicating cytotoxicity compared to controls. However, ASH plus Ab treated cultures showed protective effects against the cytotoxicity as the levels of acetylcholinesterase activity were comparable with plain and ASH treated controls. It has been reported that Ab enhances acetylcholinesterase activity by increasing calcium entry through Ltype voltage-dependent calcium channels, suggesting that increase may be a consequence of a disturbance of calcium homeostasis. Brain deposition of Ab is a common pathologic feature in HIV positive patients. An increased prevalence of amyloid plaques was observed in cortex of the brains of AIDS patients compared with the age matched controls. Several reports have shown an increase in the amyloid deposition in brains of HIV-1 infected patients. Further, HIV-1 associated neurocognitive disorders in elderly is associated with b-amyloidosis and that the Ab accumulation reflects the clinical outcome of HIV-1 infection. Due to higher survival rates after antiretroviral therapy, several factors including aging, HIV-1 infection, and secondary effects of ART contribute to brain Ab deposition and further to AD. Illicit or drugs of abuse such as Methamphetamine, and Cocaine are powerful psycho-stimulants that are widely abused in USA and all over the world and are significant risk factors for HIV-1 infection and AIDS disease progression. Accordingly, both, HIV-1 infection and drugs of abuse contribute to the amyloid deposition in the brain and associated neurocognitive disorders and impacts in neurodegeneration. In the present study, the levels of MAP2 were significantly increased in cells infected with HIV-1and as well as in cells treated with Cocaine and METH compared with untreated control cells. In plain ASH treated cells the MAP2 levels were significantly less compared to controls. In cells treated with combination of HIV-1+ ASH, Cocaine + ASH, METH + ASH, and as well as HIV-1 + Cocaine + ASH and HIV-1 + METH + ASH, the MAP2 levels were reduced and comparable with controls. It is known that increased levels of MAP2 induces neuronal differentiation and can profoundly affect cell cycle progression and further induce apoptosis and accordingly contribute to neurodegeneration. ASH and its constituents showed various beneficial effects against models of Alzheimer’s disease and spinal cord injury. ASH extracts also showed ameliorative effects against other neurodegenerative disease models such as Parkinson’s disease and Huntington’s disease suggesting that ASH may be useful against various neurodegenerative diseases. The reduction in the levels of MAP2 in ASH treated cells and further decreasing the levels in HIV-1 infected and drugs of abuse treated cells.