Abstract
About 60% to 70% of people with dementia have Alzheimer's Disease (AD), a neurodegenerative illness. One reason for this disorder is the misfolding of naturally occurring proteins in the human brain, specifically β-amyloid (Aβ) and tau. Certain diagnostic imaging techniques, such as amyloid PET imaging, tau PET imaging, Magnetic Resonance Imaging (MRI), Computerized Tomography (CT), and others, can detect biomarkers in blood, plasma, and cerebral spinal fluids, like an increased level of β-amyloid, plaques, and tangles. In order to create new pharmacotherapeutics for Alzheimer's disease, researchers must have a thorough and detailed knowledge of amyloid beta misfolding and other related aspects. Donepezil, rivastigmine, galantamine, and other acetylcholinesterase inhibitors are among the medications now used to treat Alzheimer's disease. Another medication that can temporarily alleviate dementia symptoms is memantine, which blocks the N-methyl-D-aspartate (NMDA) receptor. However, it is not able to halt or reverse the progression of the disease. Medication now on the market can only halt its advancement, not reverse it. Interventions to alleviate behavioral and psychological symptoms, exhibit anti- neuroinflammation and anti-tau effects, induce neurotransmitter alteration and cognitive enhancement, and provide other targets have recently been developed. For some Alzheimer's patients, the FDA-approved monoclonal antibody, aducanumab, is an option; for others, phase 3 clinical studies are underway for drugs, like lecanemab and donanemab, which have demonstrated potential in eliminating amyloid protein. However, additional study is required to identify and address these limitations in order to reduce the likelihood of side effects and maximize the therapeutic efficacy.
Graphical Abstract
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