ISSN: 2474-9214
Authors: Mbah Chika John*
Alzheimers disease (AD) is a neurodegenerativedisorder (brain disorder) that is irreversible, progressive and gradually destroys memory, thinking skills and ultimately the ability to carry out the minimal activities [1]. It is the most frequent type of dementia among elderly people. Dementia is characterized by the loss of cognitive functioning such as thinking, remembering, reasoning and behavioral abilities. Neuronal degeneration in Alzheimers disease could be as a result of deposition of I²-amyloid protein (AI²) in the form of senile plaques,intraneuronal neurofibrillary tangles, protein tau(I) hyperphosphorylation, oxidative stress and inflammation [2]. The neurochemical changes in Alzheimers disease form the basis for the symptomatic treatment with drugs like donepezil, galantamine, memantine, rivastigmine and tacrine. They are used orally in the treatment of mild to moderate Alzheimers disease. These drugs are competitive and reversible cholinesterase inhibitors (AChEI) inhibiting the activity of enzyme cholmesterase and increasing the level of acetylcholine in brain. A dysfunction of glutamatergic neurotransmission is also considered to be involved in the etiology of the disease. Memantine, an N-methyl D-aspartate antagonist (NMDA) acts on the glutamatergic system by blocking NMDA glutamate receptors and is utilized to treat moderate to severe form of the disease. Similarly, donepezil is the most widely used cholinesterase inhibitor probably due to its 100% bioavailability and ability to cross the bloodbrain barrier.
Keywords:
