Abstract
Amyloid-β (Aβ) peptide accumulation in the brain, leading to amyloid plaques, is considered to be the starting point of Alzheimer's disease. It is believed that these plaques impair cognitive and functional capacities and induce neurodegeneration. Research on uncommon genetic variants that either increase or decrease the quantity of Aβ deposited offers proof that amyloid plaques are involved in the disease's progression. Early-stage amyloid plaque buildup increases the likelihood that moderate cognitive impairment may progress to dementia.Donanemab, a humanized IgG1 antibody, targets an N-terminal pyroglutamate Aβ epitope that is unique to plaques that have already begun to develop. It is specific to this epitope and has no known clinical effect. Furthermore, it doesn't show any off-target binding to neurotransmitters, their receptors, or other Aβ species. In this systematic review, we first collect the necessary information after carefully reviewing four different study articles. After the data is collected, we evaluate it and create a graph to compare those study articles.
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