Aim Of The Study: Kyung-Ok-Ko (KOK), a traditional herbal prescription composed of Rehmannia glutinosa var. purpurae, Panax ginseng, Poria cocos, Lycium chinense, Aquillaria agallocha and honey, has been used to treat age-related symptoms, such as amnesia or dementia, and has been shown to ameliorate scopolamine-induced memory impairment in mice. However, the effects of KOK on transient cerebral global ischemia-induced brain damage are unclear.
Materials And Methods: Transient cerebral global ischemia was induced by occluding the bilateral common carotid artery for 5 min followed by reperfusion for 7 days. KOK (0.25, 0.5, 1, or 2 g/kg) was administered orally immediately after reperfusion and once a day over the next 7 days. Y-maze or novel object recognition tasks were to analyze learning and memory capabilities at 4 or 5 days after reperfusion, respectively. Histochemistry and immunohistochemistry were used for evaluation of the effect of KOK on neuronal degeneration.
Results: Histochemical studies showed that KOK increased the number of viable cells detected by Nissl staining and decreased the number of degenerated neuronal cells detected by Fluoro-Jade B staining in the hippocampal CA1 region. In the immunohistochemical study, the sub-chronic KOK administration attenuated the ischemia-induced activation of microglia and astrocytes and the increase of cytokine IL-1β (P<0.05). In addition, KOK administration significantly attenuated the ischemia-induced cognitive impairments observed in the Y-maze and novel object recognition tasks (P<0.05).
Conclusion: These findings suggest that the neuroprotective effects of KOK may be mediated by its anti-inflammatory activities, resulting in the attenuation of memory impairment.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.jep.2011.10.016 | DOI Listing |
Background: Focused ultrasound (FUS)-induced blood-brain barrier opening (BBBO) is a technique for safely, non-invasively, and transiently opening the blood brain barrier in a targeted area of the brain. Pre-clinical and clinical studies have shown that FUS is capable of decreasing amyloid plaque load and stimulating neurogenesis in Alzheimer's Disease (AD) models, in addition to being safe for use in human patients. However, the effect of FUS-BBBO on neurons has not yet been characterized, despite its crucial role in cognition and regulating brain function.
View Article and Find Full Text PDFBackground: Convergent evidence indicates that deficits in the endosomal recycling pathway underlies pathogenesis of Alzheimer's disease (AD). SORL1 encodes the retromer-associated receptor SORLA that plays an essential role in recycling of AD-associated cargos such as the amyloid precursor protein and the glutamatergic AMPA receptor. Importantly, loss of function pathogenic SORL1 variants are associated with AD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Keck School of Medicine at University of Southern California, Los Angeles, CA, USA.
Background: ABCA1-mediated cholesterol transport is a central feature in many lipid- dependent diseases including APOE4-associated Alzheimer's disease and atherosclerosis-CVD. ABCA1 upregulation of RNA transcription by nuclear factors (LXR, RXR) have been associated with liver side-effects because of the common promotor element for ABCA1 and Fatty Acid Synthase. The ABCA1 agonist CS6253, derived from the C-terminal of apoE was designed to stabilize and enhance ABCA1 function, thereby providing a safe alternative to transcriptional upregulation.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Tohoku University, Sendai, Miyagi, Japan.
Background: Loneliness has been linked to cognitive decline and an elevated risk of Alzheimer's disease (AD). Previous studies measured loneliness at a single point time, which may not accurately capture the longitudinal changes of different loneliness types (e.g.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Hinda and Arthur Marcus Institute for Aging Research at Hebrew SeniorLife, Boston, MA, USA.
Background: Alzheimer's disease (AD) affects over 55 million people worldwide and is characterized by abnormal deposition of amyloid-β and tau in the brain causing neuronal damage and disrupting transmission within brain circuits. Episodic memory loss, executive deficits, and depression are common symptoms arising from altered function in spatially distinct brain circuits that greatly contribute to disability. Transcranial electrical stimulation (tES) can target these circuits and has shown promise to relieve specific symptoms.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!