Alzheimer’s disease (AD) is a complex multifactorial disorder that poses a substantial burden on patients, caregivers, and society. Considering the increased aging population and life expectancy, the incidence of AD will continue to rise in the following decades. However, the molecular pathogenesis of AD remains controversial, superior blood-based biomarker candidates for early diagnosis are still lacking, and effective therapeutics to halt or slow disease progression are urgently needed. As powerful genetic regulators, microRNAs (miRNAs) are receiving increasing attention due to their implications in the initiation, development, and theranostics of various diseases, including AD. In this review, we summarize miRNAs that directly target microtubule-associated protein tau (MAPT), amyloid precursor protein (APP), and β-site APP-cleaving enzyme 1 (BACE1) transcripts and regulate the alternative splicing of tau and APP. We also discuss related kinases, such as glycogen synthase kinase (GSK)-3β, cyclin-dependent kinase 5 (CDK5), and death-associated protein kinase 1 (DAPK1), as well as apolipoprotein E, that are directly targeted by miRNAs to control tau phosphorylation and amyloidogenic APP processing leading to Aβ pathologies. Moreover, there is evidence of miRNA-mediated modulation of inflammation. Furthermore, circulating miRNAs in the serum or plasma of AD patients as noninvasive biomarkers with diagnostic potential are reviewed. In addition, miRNA-based therapeutics optimized with nanocarriers or exosomes as potential options for AD treatment are discussed.

Trophoblast cell surface antigen 2 (TROP2) overexpression has been demonstrated in several tumor types, including breast cancer (BC). Circulating tumor cells (CTCs) offer a non-invasive, dynamic and real-time detection method. The detection of TROP2 expression in CTCs is significant for predicting BC progression, prognosis and the efficacy of targeted therapy. A quantitative analysis method for TROP2 of CTCs was established using our established TUMORFISHER detection platform based on epithelial cell adhesion molecule (EpCAM), and a new magnetic nanoparticle with TROP2 as the trapping target was developed, named TROP2@MNPs. The developed quantitative analysis of TROP2 was an effective method for accurately identifying the expression of TROP2 in BC cells and CTCs from BC patients, which was consistent with the data obtained by immunohistochemical (IHC) analysis. The established TROP2@MNPs could specifically capture TROP2-positive BC cells, and the capture efficiency was closely related to the expression of TROP2 in CTCs. Notably, the TROP2-based enrichment strategy was found to capture TROP2-expressing CTCs that were missed by the EpCAM-based enrichment strategy. The TROP2-targeting CTC capture platform, TROP2@MNPs, could serve as a liquid biopsy of TROP2 expression in BC patients, providing an important reference for further research on CTC-related diagnosis and individualised treatment employing TROP2-targeting drugs.