Current Drug Treatments And Its Effects - 804 Words

Current drug treatments are limited to those which only offer symptomatic relief that may not be seen in all patients rather than treatments which target and slow disease progression (Anand, Gill Mahdi 2014; Nelson Tabet 2015). Only two types of drugs have been approved for the symptomatic treatment of AD, acetylcholine esterase inhibitors (AChEIs) and  ¬N-methyl-D-asparate (NMDA) receptor antagonists (Anand, Gill Mahdi 2014; Nelson Tabet 2015). There are three approved AChEIs, Donepezil (Aricept), Rivastigmine (Exelon) and Galantamine (Razadyne), along with a fourth cholinesterase inhibitor Tacrine which is no longer readily used due to hepatotoxicity (Watkins et al. 1994) and one NMDA, Memantine (Namenda) (Nelson Tabet 2015).†¦show more content†¦However, these treatments have so far only proved effective throughout the initial stages of the disease; as once the disease has progressed further the drugs no longer offer adequate symptomatic relief (Rogers Friedhoff 1996; Small et al. 2005; Wilkinson Murray 2001). More recently the first NMDA drug uncompetitive receptor antagonist, memantine was approved for clinical use in management and treatment of moderate-to-severe AD (Anand, Gill Mahdi 2014). It is currently the only approved drug for the treatment of moderate-to-severe AD; and a review conducted by (Revett et al. 2013) concluded that meantime had a significant effect on slowing cognitive decline and on the ability of patient to complete every day activities. It seemed to have no effect on patients with mild AD (Schneider et al. 2014) and displayed inconsistent results when used in conjunction with existing AChEI treatments (Nelson Tabet 2015). Memantine aims to prevent the occurrence of increased pathological influx of Ca2+ ions, during temporal and spatial convergent activation of glutamatergic synapses throughout learning and memory process (Danysz Parsons 2012). As previously stated glutamatergic neurons are affected towards the later stages of AD, and results in an accumulation of glutamate and increase NMDA receptor activity resulting in excitotoxicity; inadvertently causing the death of central neurons (Revett et al. 2013). Anand, R, Gill, KD Mahdi, AA