Degeneration and RepairHistone deacetylase-6 modulates amyloid beta-induced cognitive dysfunction rats by regulating PTK2B.Liu, Zhen; Hao, Kai-Min; Wang, Hao-Yu; Qi, Wen-XiuAuthor Information Department of Physiology, Fenyang College of Shanxi Medical University, Fenyang, China Received 16 February 2020 Accepted 12 March 2020 Correspondence to Prof. Wen-Xiu, MD, Department of Physiology, Fenyang College of Shanxi Medical University, Fenyang 032200, China, Tel/fax: 0358-2892014; e-mail: email@example.com NeuroReport: July 10, 2020 - Volume 31 - Issue 10 - p 754-761 doi: 10.1097/WNR.0000000000001481 Buy Metrics Abstract The aim of this study was to investigate the effects of histone deacetylase-6 (HDAC6) on the functional and pathological changes of the amyloid beta (Aβ)-induced cognitive dysfunction rats by regulating protein tyrosine kinase 2 beta (PTK2B). Ninety Sprague Dawley rats were randomly divided into nine groups, consisting of five experimental groups and four control groups. In five experimental groups, Aβ1–42 was infused intracerebroventricularly and 3 days later, rats in each group were infused intracerebroventricularly with tubastatin A hydrochloride (TSA), the HDAC6-specific inhibitor (Aβ + TSA group), theophylline, the HDACs agonist (Aβ + Theo group), PF431396 (PF), the PTK2B inhibitor (Aβ + PF group), the combination of PF and theophylline (Aβ + PF + Theo group), and normal saline (Aβ + normal saline group), respectively. Rats in four control groups took normal saline that was equivalent to the volume of Aβ1–42, and 3 days later, TSA (TSA group), theophylline (Theo group), (PF group, or normal saline group) was given at a volume of 5 µL for rats in each group. Our results showed that HDAC6 may not only lead to the deterioration of learning and memory abilities but also elevate the levels of Aβo and Tau phosphorylation in Aβ-induced cognitive dysfunction rats via upregulating PTK2B. Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.