Abstract:
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder, accounting for ap-
proximately 60-80% of all dementia cases, with an estimated 24 million patients worldwide [1].
The disease affects cognitive function, resulting in memory, language, and behavioral deficits
and an inability to perform basic daily activities [1]. Although the exact mechanism surrounding
the development of AD is not well understood, one major hypothesis is that neuronal loss is sub-
sequent to neuroinflammation, following deposition of amyloid-β (Aβ) plaques and the genera-
tion of neurofibrillary tangles (which is a result of abnormal tau protein phosphorylation) [2]. Aβ plaques are created following
the cleavage of amyloid precursor protein (APP) by β- and γ-secretases into insoluble Aβ peptides. The aggregates of Aβ have
multiple neurotoxic mechanisms including binding to Ca2+ channels (which increases intracellular Ca 2+ levels and induces exci-
totoxicity apoptosis), producing oxidative stress (via increasing levels of reactive oxygen species) and initiating the formation
of neurofibrillary tangles (which produce neuronal death due to a communication disruption between neurons) [3]. Currently,
the only approved drugs for the treatment of AD are used for symptomatic relief and do not prevent disease progression [4].
