Abstract
Alzheimer's disease (AD) is characterized by the presence of two types of protein deposits in the brain, amyloid plaques and neurofibrillary tangles. The first one are dense deposits of beta amyloid protein, the second one are dense deposits of the protein tau. These proteins are present in all of our brains, but in AD they act unusually, leading to neuronal degeneration. This review will provide an overview of the AD, including the role of amyloid beta and tau, and mechanisms that lead to the formation of plaques and tangles. The review will also cover the existing researches that have focused on the inhibition of amyloid beta formation, cholinesterase, tau hyperphosphorylation, the pathogenic mechanisms of apoE4, and GSK-3 as a solution that could be used to slow or prevent the disease.
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