Background and Purpose: We performed this multicenter study to explore the full spectrum of the clinical characteristics and neuroimaging findings of cerebellar infarction, including patients with mild to severe illnesses.Methods: We studied 293 consecutive patients with cerebellar infarction diagnosed by computed tomography and/or magnetic resonance imaging who were admitted to 36 hospitals during 5 years.Results: Cerebellar infarcts constituted 2.3% of the total patients with acute brain infarction. The backgrounds and risk factors were similar to those in patients with infarctions of the cerebral hemispheres. At least 24% were embolic, and the diagnosis of embolism could not be ruled out in 27%. Infarcts involving the superior cerebellar artery (SCA) region (52%) and the posterior inferior cerebellar artery (PICA) region (49%) were far more frequent than those involving the anterior inferior cerebellar artery (AICA) region (20%o). Patients with SCA infarcts exhibited obtunded consciousness and ataxia more frequently than those with PICA infarcts (P<.05). Infarcts in the PICA regions were associated with abnormalities of the PICA (64%) or the vertebral arteries (57%), whereas infarcts in the SCA and AICA

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With increased histone deacetylase (HDAC) activity and histone hypoacetylation being implicated in neurodegeneration, HDAC inhibitors have been reported to have considerable therapeutic potential. Yet, existing inhibitors lack specificity and may show substantial adverse effect. In this study, we identified a novel HDAC1/2 isoform-specific inhibitor, K560, with protective effects against 1-methyl-4-phenylpyridinium (MPP(+))- and/or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neuronal death in both in vitro and in vivo Parkinson's disease model. K560 attenuated cell death induced by MPP(+) in differentiated SH-SY5Y cells through the sustained expression of an antiapoptotic protein, X-linked inhibitor of apoptosis (XIAP). Inhibition of XIAP expression by locked nucleic acid antisense oligonucleotides abolished the protective effect of K560. Inactivation of mitogen-activated protein kinase cascades, reduced p53 phosphorylation, and down-regulation of p53-upregulated modulator of apoptosis on K560 treatment were also observed. Furthermore, pre- and post-oral administration of K560 to mice prevented MPTP-induced loss of dopaminergic neurons in substantia nigra, suggesting that selective inhibition of HDAC1 and HDAC2 by K560 may pave the way to new strategies for Parkinson's disease treatment.

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