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It affects tens of millions of people worldwide, and this number is rising dramatically.
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These prospects include agents acting on Aβ, its receptors and tau protein, such as small molecules, vaccines and antibodies against Aβ inhibitors or modulators of β- and γ-secretase Aβ-degrading proteases tau protein inhibitors and vaccines amyloid dyes and microRNAs.Īlzheimer's disease is the most common type of dementia. Finally, we will report on the progress in searching for novel, potentially effective agents as well as selected promising strategies for the treatment of Alzheimer's disease. Additionally, we summarize the therapeutic developments and recent advances of different strategies for treating Alzheimer's disease. We also discuss the potential receptors that interact with Aβ and mediate Aβ intake, clearance, and metabolism. In this paper, we review the structures, biological functions, and neurotoxicity role of Aβ. Moreover, there are no efficient drugs to stop or reverse the progression of Alzheimer's disease. Currently, it is unclear what the physiological and pathological forms of Aβ are and by what mechanism Aβ causes dementia. Aβ accumulation in the brain is proposed to be an early toxic event in the pathogenesis of Alzheimer's disease, which is the most common form of dementia associated with plaques and tangles in the brain. Amyloid beta peptide (Aβ) is produced through the proteolytic processing of a transmembrane protein, amyloid precursor protein (APP), by β- and γ-secretases.