Gallium 68–labeled fibroblast-activation protein inhibitor PET/CT may outperform fluorine 18–labeled fluorodeoxyglucose PET/CT in staging lung cancer, particularly in the detection of metastasis to... Background Gallium 68 (68Ga)–labeled fibroblast-activation protein inhibitor (FAPI) has recently been introduced as a promising tumor imaging agent. Purpose To compare 68Ga-FAPI PET/CT with fluorin...

Alzheimer’s disease (AD) is the most common neurodegenerative disease. The accumulation of amyloid beta (Aβ) is the main pathology of AD. Metformin, a well-known antidiabetic drug, has been reported to have AD-protective effect. However, the mechanism is still unclear. In this study, we tried to figure out whether metformin could activate insulin-degrading enzyme (IDE) to ameliorate Aβ-induced pathology. Morris water maze and Y-maze results indicated that metformin could improve the learning and memory ability in APP^swe/PS1^dE9 (APP/PS1) transgenic mice. ¹⁸F-FDG PET-CT result showed that metformin could ameliorate the neural dysfunction in APP/PS1 transgenic mice. PCR analysis showed that metformin could effectively improve the mRNA expression level of nerve and synapse-related genes (Syp, Ngf, and Bdnf) in the brain. Metformin decreased oxidative stress (malondialdehyde and superoxide dismutase) and neuroinflammation (IL-1β and IL-6) in APP/PS1 mice. In addition, metformin obviously reduced the Aβ level in the brain of APP/PS1 mice. Metformin did not affect the enzyme activities and mRNA expression levels of Aβ-related secretases (ADAM10, BACE1, and PS1). Meanwhile, metformin also did not affect the mRNA expression levels of Aβ-related transporters (LRP1 and RAGE). Metformin increased the protein levels of p-AMPK and IDE in the brain of APP/PS1 mice, which might be the key mechanism of metformin on AD. In conclusion, the well-known antidiabetic drug, metformin, could be a promising drug for AD treatment.

Background: Glycyrrhizinic acid (GA), a major active ingredient enriched in the roots of licorice, possesses well-confirmed anti-inflammatory effects. Objective: To evaluate the underlying mechanisms of GA against lipopolysaccharide (LPS)-induced chronic neuroinflammation and memory impairment. Design: We explored to investigate the effects of GA on neuroinflammation and memory impairment in an LPS-induced Alzheimer’s mouse model. Results: Data of micro-PET/CT imaging and morris water maze test suggested that GA, when administrated orally, could reverse LPS-induced abnormalized glucose intake and metabolism in the brain and alleviate LPS-induced memory loss and cognitive defects in mice. Histological and immunohistochemical staining results revealed that GA treatment suppressed overexpressions of pro-inflammatory cytokines of IL-1 β and TNF-α in the brain of C57 mice by inhibiting toll-like receptor 4 (TLR4) signaling pathway activation. Conclusion: Our findings suggest that GA may be a therapeutic agent for the treatment of neuroinflammation and cognitive impairment.