Cerebral ischemia is a result of insufficient blood flow to the brain. It leads to limited supply of oxygen and other nutrients to meet metabolic demands. These phenomena lead to brain damage. There are two types of cerebral ischemia: focal and global ischemia. This condition has significant impact on patient’s health and health care system requirements. Animal models such as transient occlusion of the middle cerebral artery and permanent occlusion of extracranial vessels have been established to mimic the conditions of the respective type of cerebral ischemia and to further understand pathophysiological mechanisms of these ischemic conditions. It is important to understand the pathophysiology of cerebral ischemia in order to identify therapeutic strategies for prevention and treatment. Here, we review the neuropathologies that are caused by cerebral ischemia and discuss the mechanisms that occur in cerebral ischemia such as reduction of cerebral blood flow, hippocampal damage, white matter lesions, neuronal cell death, cholinergic dysfunction, excitotoxicity, calcium overload, cytotoxic oedema, a decline in adenosine triphosphate (ATP), malfunctioning of Na+/K+-ATPase, and the blood-brain barrier breakdown. Altogether, the information provided can be used to guide therapeutic strategies for cerebral ischemia.

Objectives Xanthones isolated from the pericarp of Garcinia mangostana has been reported to exhibit neuroprotective effect. Methods In this study, the effect of xanthone-enriched fraction of Garcinia mangostana (XEFGM) and a-mangostin (a-MG) were investigated on cognitive functions of the chronic cerebral hypoperfusion (CCH) rats. Key findings HPLC analysis revealed that XEFGM contained 55.84% of a-MG. Acute oral administration of XEFGM (25, 50 and 100 mg/kg) and a-MG (25 and 50 mg/kg) before locomotor activity and Morris water maze (MWM) tests showed no significant difference between the groups for locomotor activity. Conclusions However, a-MG (50 mg/kg) and XEFGM (100 mg/kg) reversed the cognitive impairment induced by CCH in MWM test. a-MG (50 mg/kg) was further tested upon sub-acute 14-day treatment in CCH rats. Cognitive improvement was shown in MWM test but not in long-term potentiation (LTP). BDNF but not CaMKII was found to be down-regulated in CCH rats; however, both parameters were not affected by a-MG. In conclusion, a-MG ameliorated learning and memory deficits in both acute and sub-acute treatments in CCH rats by improving the spatial learning but not hippocampal LTP. Hence, a-MG may be a promising lead compound for CCH-associated neurodegenerative diseases, including vascular dementia and Alzheimer's disease.

Public interest statement Plants are rich source of chemical diversity and provides the initiation platform for any drug discovery programme. Identifying the potential plants with anti-cholinesterase activity provides a platform to develop more e ective drugs for treatment of AD.

Alzheimer’s disease (AD) is a progressive neurodegenerative disease that is currently affecting 40-50 million people worldwide. It is generally recognized from its main symptom dementia, in which the patient undergoes a progressive decline in their cognitive memory. Recent studies have shown that medicinal plants such as Clitoria ternatea equipped with antioxidant properties has high potential in treating AD. The study was conducted using zebrafish model of AD induced with aluminium chloride for 28 days. The treatment dose of C. ternatea extract (4.34 mg/L) was then given for 14 days. The behaviour of the zebrafish were evaluated through memory testing by using a T-maze test and novel tank diving test. Histological studies were also performed. 50% of the zebrafish tested showed improvement in memory through the T-maze test after treatment with C. ternatea extract. Zebrafish model of AD treated with C. ternatea extract also shows a decrease in anxiety in the novel tank diving test. A significant increase of purkinje cells were also observed from the histological study after treatment with C. ternatea extract. Nucleus elongation of oligodendrocytes from zebrafish model of AD induced with aluminium chloride were improved when treated with the C. ternatea extract. In conclusion, it was found that C. ternatea extract exhibits strong potential for treating zebrafish model of AD induced with aluminium chloride.

No abstract