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Summary   Aims  Recently, histone deacetylase ( HDAC ) inhibitors are considered a possible therapeutic strategy in Alzheimer's disease ( AD ). However,  HDAC i treatments exhibit diverse functions with unfavorable effects in  AD . Thus, the development of selective  HDAC i without side effects is urgently needed.    Methods   HDAC i, namely,  BML 210,  MGCD 0103,  PXD 101, and Droxinostat, were screened in mouse hippocampal primary cultures incubated with oligomeric Aβ 25‐35  (50 μmol/L).  MGCD 0103 was chosen for in vivo tests and was intraperitoneally injected into C57 BL /6J mice (0.5 mg/kg, once per day) for 4 weeks following an intrahippocampal  CA 1 injection of oligomeric Aβ 25‐35 . Brain samples were collected for pathological analyses after the behavioral analyses including open‐ field test ( OFT ), elevated plus maze ( EPM ), Y‐maze, and Morris water maze ( MWM ).    Results  Among the  HDAC i,  MGCD 0103 exhibited significant neuroprotection against the Aβ toxicity in primary cultures.  MGCD 0103 coattenuated cognitive deficits and anxiety against Aβ damage in mice.  MGCD 0103 further ameliorated pathological features such as the levels of acetylated histone 3 at Lys 9 site (H3K9) and α‐tubulin, synaptophysin, Aβ, tau protein phosphorylation, and serotonergic neuron loss against Aβ toxicity. Furthermore, chronic  MGCD 0103 treatment did not show liver or kidney toxicity in mice.    Conclusions  These results reveal  MGCD 0103 could be a potential therapeutic agent against  AD .

MGCD 0103, a selective histone deacetylase inhibitor, coameliorates oligomeric Aβ 25‐35 ‐induced anxiety and cognitive deficits in a mouse model