A therapeutic approach for promoting neuroprotection and brain functional regeneration after strokes is still lacking. Histone deacetylase 1 (HDAC1), which belongs to the histone deacetylase family, is involved in the transcriptional repression of cell-cycle-modulated genes and DNA damage repair during neurodegeneration. Our previous data showed that the protein level and enzymatic activity of HDAC1 are deregulated in stroke pathogenesis. A novel compound named 5104434 exhibits efficacy to selectively activate HDAC1 enzymatic function in neurodegeneration, but its potential in stroke therapy is still unknown. In this study, we adopted an induced rat model with cerebral ischemia using the vessel dilator endothelin-1 to evaluate the potential of compound 5104434. Our results indicated compound 5104434 selectively restored HDAC1 enzymatic activity after oxygen and glucose deprivation, preserved neurite morphology, and protected neurons from ischemic damage in vitro. In addition, compound 5104434 attenuated the infarct volume, neuronal loss, apoptosis, DNA damage, and DNA breaks in cerebral ischemia rats. It further ameliorated the behavioral outcomes of neuromuscular response, balance, forepaw strength, and functional recovery. Collectively, our data support the efficacy of compound 5104434 in stroke therapy and contend that it can be considered for clinical trial evaluation.

Introduction: Experimental traumatic brain injury (TBI) elicits acute local inflammatory responses, including up-regulation of adhesion molecules and neutrophils in the injured brain. However, in clinical experiences there were at least three types of TBI, which included mild, moderate and severe types, and there would be different neuroinflammatory responses. This study investigated the inflammatory responses after mild TBI in rats. Methods: Adult male Sprague–Dawley rats (n = 40) were group-housed and injured using an impact method. Motor function was assessed 1–4 days after the injury by using a grip test (Grip strength meter; Singa). Blood samples collected from the rats before the injury and after the injury and the Intercellular adhesion molecule-1 (ICAM-1) level were measured. Results: The ICAM-1 expression from pre-injury to post-injury showed a significantly greater gradual elevation in the rats in the mild-injury group than in the moderate-injury group. The neurological function evaluated with grip test showed no deterioration of neurological function in the mild-injury group but gradual deterioration in the moderate-injury group. Conclusion: These findings showed a delayed inflammatory reaction in the mild-injury group without progressive deterioration of neurological function. Therefore, in the moderate-injury group, no progression phase was observed.

Tumors in the pineal region usually present with acute hydrocephalus. Histologic diagnosis is most important, as it greatly influences treatment, because over 17 tumor types occur in this area. Biopsies of these lesions play an important role in further management. Pineocytomas are benign and rare tumors that typically exhibit a slow progression. However, the appropriate treatment for pineocytoma varies. Surgical excision was considered for good long-term outcomes; however, this may not always be possible. Radiotherapy also appears to be effective in patients with residual pineocytomas. We report a case of pineocytoma with hemorrhagic transformation and complicated hydrocephalus. The patient refused to undergo aggressive tumor excision. Thus, the patient only underwent endoscopic biopsy and external ventricular drain (EVD) implantation, but the outcome was acceptable. In addition, we reviewed the current management strategies for pineocytomas in the literature.

Parkinson’s disease (PD) is characterized by progressive dopaminergic neurodegeneration driven by oxidative stress, mitochondrial dysfunction, synaptic loss, and impaired neurotrophic signaling; however, the role of integrin α5β1 in neuronal vulnerability remains unclear. Here, the data show that rotenone-induced stress reduces integrin α5 expression in a dose- and time-dependent manner, leading to increased ROS accumulation, glutathione imbalance, synaptic degeneration, senescence-like β-gal activity, and apoptosis, whereas integrin α5 knockdown further exacerbates these deficits, supporting a protective role of α5β1. In contrast, treatment with the fibronectin-derived α5β1-activating peptide Ac-PHSRN-NH₂ restores integrin signaling by engaging the FAK–PI3K–AKT/ERK cascade and NRF2-mediated antioxidant responses, thereby reducing oxidative stress, suppressing cell death, and improving redox homeostasis. Moreover, PHSRN enhances NGF and BDNF levels, preserves synaptic integrity, and promotes dopaminergic neuronal activity and dopamine release. Consistently, in MPTP-lesioned mice, PHSRN preserves nigral TH-positive neurons, reduces apoptosis, restores neurotrophic support, and improves motor function. Collectively, these findings identify integrin α5β1 as a critical protective axis and support PHSRN as a potential disease-modifying therapeutic strategy for PD.