Alzheimer's disease (AD), a neurodegenerative disorder characterized by the the loss of cognition and memory, dysfunction in mental abilities, personality changes, difficulties in judgement, language, calculation and most importantly dementia. Among all age-associated neurodegenerative disorders, Alzheimer's disease has been proven to be the most devastating one (McKhann G, 1984). Senile plaques, one of the hallmarks of AD, are composed of an extracellular deposition of 40 to 43 amino acid polypeptides in which the 42-residue amyloid peptides (AB1-42)is the major form (Roher, 1993). Increasing number of reports revealed that (AB 1-42) can accumulate within the neurons and plays an important role in AD pathology (Gouras, 2000). The accumulation of (AB1-42) within the neurons is now termed Amyloid Beta Toxicity. Amyloid Beta toxicity has been postulated to initiate synaptic loss and subsequent neuronal degeneration seen in Alzheimer's disease (Wu, 2006). The confirmation of this hypothesis has yet to be finalized.

The standard Ginkgo biloba leaf extract EGb 761 has been given as a prescription drug in many countries, and as a dietary supplement in the United States, for Alzheimer's dementia (Christen and Maxient, 2002). Donepezil Hydrochloride (Aricept) on the other hand is a widely used prescribed drug used for patients in any stages of Alzheimer's disease (Atcha, 2010). In 2008, a report written by the Institute for Quality and Efficiency in Health Care (IQWiG) in Germany concludes that there are indications for cognitive function improvements in Alzheimer's disease patients taking a high-dose (240 mg daily) of Ginkgo extract EGb 761 (QWiG, Germany, 2008). Two of its major constituents, flavonoids (24%) and terpenoids (6%), have been widely investigated for their neuroprotective properties.

This study seeks to investigate the compatibility of introducing Ginkgo Biloba Extract as one of the prominent drug in the treatment of Alzheimer's disease. By comparing the effects of Ginkgo Biloba Extract against the effects of Donepezil Hydrochloride on Amyloid Beta Toxicity in transgenic C.elegans (CL4176), the study strives to show evidence that Ginkgo Biloba Extract is capable of becoming one of AD's prescribed drug. Transgenic C.elegan (CL4176) is chosen to be the model of organism in the study because this species is genetically engineered to generate and accumulate amyloid-beta protein after 20 hours of temperature upshift from 16 degree Celsius to 25 degree Celsius. And as a result of the continuous accumulation of Amyloid-beta protein, the worms will eventually become paralyzed. The accumulation of Amyloid-beta protein is a process that also takes place in the brains of AD patients; therefore, the result of Amyloid-beta accumulation in CL4176 (paralysis) is analogous to the result of the same process in humans (dementia).

Data shows that at a low concentration, Ginkgo biloba extract has a more significant effect on the delaying of the paralysis in CL4176 than does both levels of Donepezil Hydrochloride have on the delaying of paralysis. However, at a high concentration (100ug/ml), Ginkgo biloba extract has the same effects as both high and low concentration of Donepezil Hydrochloride, as further statistical analysis illustrates that there is no significant difference between the three data values. Future studies of the same study will seek to investigate the effects of the combination of Ginkgo biloba and Donepezil Hydrochloride on the delaying of CL4176 paralysis.