High blood lipid medications may be resistant to Alzheimer's disease

The team of Yao Yonggang of Kunming Animal Institute of the Chinese Academy of Sciences expounded the molecular mechanism of anti-Alzheimer's disease of the nuclear-subjected peroxidase α (PPARA) astigtors, Gifirozi and Piliniac acid. The results were published in the journal Autophagy.
the pathogenesis of Alzheimer's disease (AD) is very complex, in which abnormal blood lipids are one of the important risk factors for AD. Studies have found that genetic variations in the PPARA gene are associated with AD risk. Autophagy is a common process of cell degradation of its own organocysts and abnormal proteins in the body mediated by lysosomes. Numerous studies have shown that autophagy dysfunction plays an important role in the pathogenesis of AD, so the occurrence of induced autophagy is expected to become a new perspective for the treatment of AD.
Yonggang's team carried out systematic research from molecular, cell and mouse animal models. At the cellular level, the study found that the U.S. Food and Drug Administration (FDA) approved the drug for the treatment of high blood lipids, Giffirozi and Plinic acid, as an agitant for PPARA, which activates autophagy to remove beta A. At the model level of AD mice, Giffirozi and Piliniic acid can effectively induce astrocytes and small glial cells to be active, causing them to gather around A-beta plaques, further significantly enhancing the phagocytic and degradation function of a star-shaped glial cells and small glial cells on A-beta, thereby improving the pathophysiological characteristics of A-beta. And this effect is closely related to the occurrence of autophagy. Ultimately, Giffirozi and Piliniic acid significantly improved the structure and function of damaged neurons in AD mice and significantly improved the learning and memory capabilities of AD model mice.
the study provided the basis for a clinical trial of AD therapy for the FDA-approved drug Gypherozzi for hyperlipidemia. (Source: Science Network) Information on
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