Abstract

The most sensible and scientific way to control Alzheimer’s disease (AD) is to diagnose and treat it early and change lifestyle and diet, so diagnostic modalities rely primarily on imaging analysis of biomarkers and examination and evaluation of serum and cerebrospinal fluid to determine AD type and disease progression in patients by several characteristic biomarkers (e.g., protein dysfunction, oxidative stress, metal ion vascular disease, mitochondrial population changes). However, there are preferences for different biomarkers in the aspect of inspection cost and patient type. As one of the signature pathologies of AD, β-site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1) plays a crucial role in diagnosis and treatment. The difficult transmission of neurotransmitters in the synaptic gap caused by Aβ deposition is the breakthrough point for treatment and detection, which also means that detecting Aβ’s specific PET ligand in cerebrospinal fluid is more meaningful. For treatments, APP-making BACE1 becomes the key point in the AD clinical treatment. The review summarizes the diagnosis and treatment of AD based on BACE1’s mechanism and the process that causes AD.

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