Neurodegenerative disorders are typically characterized by progressive and extensive neuronal loss in specific populations of neurons and brain areas which lead to the observed clinical manifestations. Despite the recent advances in molecular neuroscience, the subcellular bases such as Golgi apparatus (GA) for most neurodegenerative diseases are poorly understood. This review gives a brief overview of the contribution of the neuronal GA in the pathogeneses of neurodegeneration, summarizes what is known of the GA machinery in these diseases, and present the relationship between GA fragmentation and the aggregation and accumulation of misfolded or aberrant proteins including mutant SOD1, a-synuclein, tau, which is considered to be a key event in the pathogenic process, and perturbating in calcium homeostasis, regulation of hormones, lipid metabolism are also linkage to the function of the GA thought to underlie neurodegeneration. Although these precise diseases mechanisms remain to be clarified, more research is needed to better understand how GA function for it and to enable physicians to use this knowledge for the benefit of the patients.

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Stroke is a major cause of death and adult disability. However, therapeutic options remain limited. Numerous pathways underlie acute responses of brain tissue to stroke. Early events following ischemic damage include reactive oxygen species (ROS)-mediated oxidative stress and glutamate-induced excitotoxicity, both of which contribute to rapid cell death within the infarct core. A subsequent cascade of inflammatory events escalates damage progression. This review explores potential neuroprotective strategies for targeting key steps in the cascade of ischemia–reperfusion (I/R) injury. NADPH oxidase (NOX) inhibitors and several drugs currently approved by the U.S. Food and Drug Administration including glucose-lowering agents, antibiotics, and immunomodulators, have shown promise in the treatment of stroke in both animal experiments and clinical trials. Ischemic conditioning, a phenomenon by which one or more cycles of a short period of sublethal ischemia to an organ or tissue protects against subsequent ischemic events in another organ, may be another potential neuroprotective strategy for the treatment of stroke by targeting key steps in the I/R injury cascade.

Background/Aims: The goal of this study was to examine the reliability and validity of the Changsha version of the Montreal Cognitive Assessment (MoCA-CS) in ischemic cerebrovascular disease patients of Hunan Province, China, and to explore the optimal cutoff score for detecting vascular cognitive impairment-no dementia (VCI-ND) and vascular dementia (VD). Methods: Three hundred and thirty-eight ischemic cerebrovascular disease patients (131 with normal cognition, 111 with VCI-ND, and 96 with VD) and 132 healthy controls were recruited. All participants accepted examination by the MoCA-CS, Mini-Mental State Examination (MMSE), and other related scales. A detailed neuropsychological battery was used for making a final cognitive diagnosis. SPSS 16.0 statistical software was used for reliability, validity examination, and optimal cutoff score detection. Results: Cronbach’s α of the MoCA-CS was 0.884, and test-retest and interrater reliability of the MoCA-CS were 0.966 and 0.926, respectively. MoCA-CS scores were highly correlated with MMSE scores (r = 0.867) and simplified intelligence quotients (r = 0.822). The results indicate that 1 point should be added for subjects with less than 6 years of education, and that the optimal cutoff score for detecting VCI-ND is 26/27 (sensitivity 96.1%, specificity 75.6%), whereas the optimal cutoff score for detecting VD is 16/17 (sensitivity 92.7%, specificity 96.3%). Conclusion: The MoCA-CS has good reliability and validity, and is a useful cognitive screening instrument for detecting VCI in the Chinese population.

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Ischemic stroke starts a series of pathophysiological processes that cause brain injury. Caveolin-1 (cav-1) is an integrated protein and locates at the caveolar membrane. It has been demonstrated that cav-1 can protect blood–brain barrier (BBB) integrity by inhibiting matrix metalloproteases (MMPs) which degrade tight junction proteins. This article reviews recent developments in understanding the mechanisms underlying BBB dysfunction, neuroinflammation, and oxidative stress after ischemic stroke, and focuses on how cav-1 modulates a series of activities after ischemic stroke. In general, cav-1 reduces BBB permeability mainly by downregulating MMP9, reduces neuroinflammation through influencing cytokines and inflammatory cells, promotes nerve regeneration and angiogenesis via cav-1/VEGF pathway, reduces apoptosis, and reduces the damage mediated by oxidative stress. In addition, we also summarize some experimental results that are contrary to the above and explore possible reasons for these differences.

In patients with spinal chordoma, young age, location in sacral spine, dedifferentiated pathology, and chemotherapy were negative predictors of PFS, while young and old age, bladder or bowel dysfunction at presentation, dedifferentiated pathology, recurrence or progression, and metastases portended a worse OS.

Increasing evidence implicating that the organelle-dependent initiation of cell death merits further research. The evidence also implicates Golgi as a sensor and common downstream-effector of stress signals in cell death pathways, and it undergoes disassembly and fragmentation during apoptosis in several neurological disorders. It has also been reported that during apoptotic cell death, there is a cross talk between ER, mitochondria, and Golgi. Thus, we hypothesized that Golgi might trigger death signals during oxidative stress through its own machinery. The current study found that GOLPH3, an outer membrane protein of the Golgi complex, was significantly upregulated in N2A cells upon oxygen-glucose deprivation and reoxygenation (OGD/R), positioning from the compact perinuclear ribbon to dispersed vesicle-like structures throughout the cytoplasm. Additionally, elevated GOLPH3 promoted a stress-induced conversion of the LC3 subunit I to II and reactive oxygen species (ROS) production in long-term OGD/R groups. The collective data indicated that GOLPH3 not only acted as a sensor of Golgi stress for its prompt upregulation during oxidative stress but also as an initiator that triggered and propagated specific Golgi stress signals to downstream effectors. This affected ROS production and stress-related autophagy and finally controlled the entry into apoptosis. The data also supported the hypothesis that the Golgi apparatus could be an ideal target for stroke, neurodegenerative diseases, or cancer therapy through its own functional proteins.