scholarly journals Bushen Huoxue decoction improves cognitive decline in rats with cerebral hypoperfusion

2014 ◽  
Vol 10 (3) ◽  
pp. 1635-1641 ◽  
Author(s):  
SHUIFEN YE ◽  
YONG GU ◽  
YIHUI XU ◽  
WEN FAN ◽  
XIAOTING WANG ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Cerebral Hypoperfusion ◽  
Bushen Huoxue Decoction

The role of high-mobility group box protein 1 in chronic cerebral hypoperfusion-induced vascular cognitive impairment animals

2019 ◽  
Author(s):  
Amelia Nur Vidyanti ◽  
Jia-Yu Hsieh ◽  
Kun-Ju Lin ◽  
Yao-Ching Fang ◽  
Ismail Setyopranoto ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Decline ◽  
High Mobility ◽  
Vascular Cognitive Impairment ◽  
High Mobility Group ◽  
Cerebral Hypoperfusion ◽  
Hippocampal Atrophy ◽  
Amyloid Pet ◽  
Knock Out

Abstract Background: The molecular mechanisms of vascular cognitive impairment (VCI) are diverse and still in puzzle. VCI could be attributed to chronic cerebral hypoperfusion (CCH). CCH may cause a cascade of reactions involved in ischemia and neuro-inflammation which plays important roles in the pathophysiology of VCI. High-mobility group box protein 1 (HMGB1) is a non-histone protein that serves as a damage-associated molecular signal leading to cascades of inflammation. Increased level of HMGB1 has been established in the acute phase of CCH. However, the role of HMGB1 at the chronic phase of CCH remains elucidated. Methods: We performed modified bilateral common carotid artery occlusion (BCCAO) in C57BL/6 mice to induce CCH. We examined the cerebral blood flow (CBF) reduction by laser doppler flowmetry, the protein expression of HMGB1 and its pro-inflammatory cytokines (TNF-a, IL-1b, and IL-6) by western blotting and immunohistochemistry. The brain pathology was assessed by 7T-animal MRI and amyloid-b accumulation was assessed by amyloid-PET scanning. We further evaluated the effect of HMGB1 suppression by injecting CRISPR/Cas9 knock-out plasmid intra-hippocampus bilaterally. Results: There were reduction of CBF up to 50% which persisted three months after CCH. The modified-BCCAO animals developed significant cognitive decline. The 7T-MRI image showed hippocampal atrophy, although the amyloid-PET showed no significant amyloid-beta accumulation. Increased protein levels of HMGB1, TNF-a and IL-1b were found three months after BCCAO. HMGB1 suppression by CRISPR/Cas9 knock-out plasmid restored the CBF, IL-1B, TNF-alpha, IL-6, and attenuated hippocampal atrophy and cognitive decline. Conclusion: HMGB1 plays a pivotal role in the pathophysiology of the animal model of CCH and it might be a candidate as therapeutic targets of VCI.

scholarly journals Role of HMGB1 in an Animal Model of Vascular Cognitive Impairment Induced by Chronic Cerebral Hypoperfusion

2020 ◽  
Vol 21 (6) ◽  
pp. 2176 ◽  
Author(s):  
Amelia Nur Vidyanti ◽  
Jia-Yu Hsieh ◽  
Kun-Ju Lin ◽  
Yao-Ching Fang ◽  
Ismail Setyopranoto ◽  
...  
Keyword(s):  
Animal Model ◽  
Cognitive Impairment ◽  
Cognitive Decline ◽  
Chronic Phase ◽  
Vascular Cognitive Impairment ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Hippocampal Atrophy ◽  
Tnf Α

The pathophysiology of vascular cognitive impairment (VCI) is associated with chronic cerebral hypoperfusion (CCH). Increased high-mobility group box protein 1 (HMGB1), a nonhistone protein involved in injury and inflammation, has been established in the acute phase of CCH. However, the role of HMGB1 in the chronic phase of CCH remains unclear. We developed a novel animal model of CCH with a modified bilateral common carotid artery occlusion (BCCAO) in C57BL/6 mice. Cerebral blood flow (CBF) reduction, the expression of HMGB1 and its proinflammatory cytokines (tumor necrosis factor-alpha [TNF-α], interleukin [IL]-1β, and IL-6), and brain pathology were assessed. Furthermore, we evaluated the effect of HMGB1 suppression through bilateral intrahippocampus injection with the CRISPR/Cas9 knockout plasmid. Three months after CCH induction, CBF decreased to 30–50% with significant cognitive decline in BCCAO mice. The 7T-aMRI showed hippocampal atrophy, but amyloid positron imaging tomography showed nonsignificant amyloid-beta accumulation. Increased levels of HMGB1, TNF-α, IL-1β, and IL-6 were observed 3 months after BCCAO. HMGB1 suppression with CRISPR/Cas9 knockout plasmid restored TNF-α, IL-1β, and IL-6 and attenuated hippocampal atrophy and cognitive decline. We believe that HMGB1 plays a pivotal role in CCH-induced VCI pathophysiology and can be a potential therapeutic target of VCI.

Preoperative Cerebral Hypoperfusion in the Left, Not in the Right, Hemisphere Is Associated With Cognitive Decline After Cardiac Surgery

2012 ◽  
Vol 74 (1) ◽  
pp. 73-80 ◽  
Author(s):  
Simone Messerotti Benvenuti ◽  
Paolo Zanatta ◽  
Carolina Longo ◽  
Anna Paola Mazzarolo ◽  
Daniela Palomba
Keyword(s):  
Cardiac Surgery ◽  
Cognitive Decline ◽  
Right Hemisphere ◽  
Cerebral Hypoperfusion ◽  
The Right

scholarly journals Angiogenic and Vasoprotective Effects of Adrenomedullin on Prevention of Cognitive Decline After Chronic Cerebral Hypoperfusion in Mice

Stroke ◽  
2011 ◽  
Vol 42 (4) ◽  
pp. 1122-1128 ◽  
Author(s):  
Takakuni Maki ◽  
Masafumi Ihara ◽  
Youshi Fujita ◽  
Takuo Nambu ◽  
Kazutoshi Miyashita ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion

scholarly journals Cognitive Function and Atrial Fibrillation: From the Strength of Relationship to the Dark Side of Prevention. Is There a Contribution from Sinus Rhythm Restoration and Maintenance?

Medicina ◽  
2019 ◽  
Vol 55 (9) ◽  
pp. 587 ◽  
Author(s):  
Emanuele Gallinoro ◽  
Saverio D’Elia ◽  
Dario Prozzo ◽  
Michele Lioncino ◽  
Francesco Natale ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Cognitive Function ◽  
Sinus Rhythm ◽  
Cognitive Decline ◽  
Cognitive Dysfunction ◽  
Population Aging ◽  
Cerebral Hypoperfusion ◽  
Dark Side ◽  
White Matter Hyperintensity ◽  
The Impact

Atrial fibrillation (AF) is the most common chronic cardiac arrhythmia with an increasing prevalence over time mainly because of population aging. It is well established that the presence of AF increases the risk of stroke, heart failure, sudden death, and cardiovascular morbidity. In the last two decades several reports have shown an association between AF and cognitive function, ranging from impairment to dementia. Ischemic stroke linked to AF is a well-known risk factor and predictor of cognitive decline. In this clinical scenario, the risk of stroke might be reduced by oral anticoagulation. However, recent data suggest that AF may be a predictor of cognitive impairment and dementia also in the absence of stroke. Cerebral hypoperfusion, reduced brain volume, microbleeds, white matter hyperintensity, neuroinflammation, and genetic factors have been considered as potential mechanisms involved in the pathogenesis of AF-related cognitive dysfunction. However, a cause-effect relationship remains still controversial. Consequently, no therapeutic strategies are available to prevent AF-related cognitive decline in stroke-free patients. This review will analyze the potential mechanisms leading to cognitive dysfunction in AF patients and examine the available data on the impact of a sinus rhythm restoration and maintenance strategy in reducing the risk of cognitive decline.

Axon–glial disruption: the link between vascular disease and Alzheimer's disease?

2011 ◽  
Vol 39 (4) ◽  
pp. 881-885 ◽  
Author(s):  
Karen Horsburgh ◽  
Michell M. Reimer ◽  
Philip Holland ◽  
Guiquan Chen ◽  
Gillian Scullion ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
White Matter ◽  
Cognitive Decline ◽  
Vascular Dysfunction ◽  
Critical Role ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Early Event ◽  
Published Data

Vascular risk factors play a critical role in the development of cognitive decline and AD (Alzheimer's disease), during aging, and often result in chronic cerebral hypoperfusion. The neurobiological link between hypoperfusion and cognitive decline is not yet defined, but is proposed to involve damage to the brain's white matter. In a newly developed mouse model, hypoperfusion, in isolation, produces a slowly developing and diffuse damage to myelinated axons, which is widespread in the brain, and is associated with a selective impairment in working memory. Cerebral hypoperfusion, an early event in AD, has also been shown to be associated with white matter damage and notably an accumulation of amyloid. The present review highlights some of the published data linking white matter disruption to aging and AD as a result of vascular dysfunction. A model is proposed by which chronic cerebral hypoperfusion, as a result of vascular factors, results in both the generation and accumulation of amyloid and injury to white matter integrity, resulting in cognitive impairment. The generation of amyloid and accumulation in the vasculature may act to perpetuate further vascular dysfunction and accelerate white matter pathology, and as a consequence grey matter pathology and cognitive decline.

scholarly journals Postural Hypotension and Cognitive Function in Older Adults

2017 ◽  
Vol 3 ◽  
pp. 233372141773321 ◽  
Author(s):  
Kenneth J. McLeod ◽  
Teesta Jain
Keyword(s):  
Cognitive Function ◽  
Cognitive Decline ◽  
Cognitive Performance ◽  
Soleus Muscle ◽  
Postural Hypotension ◽  
Cerebral Hypoperfusion ◽  
Muscle Stimulation ◽  
Cognitive Responses ◽  
Age Related ◽  
Quiet Sitting

Background: Cognitive decline in the elderly is associated with chronic cerebral hypoperfusion. While many forms of exercise can slow or reverse cognitive decline, compliance in unsupervised exercise programs is poor. Objective: We address whether passive exercise, that is, muscle stimulation, is capable of reversing postural hypotension in an older adult population sufficiently to significantly improve cognitive function as measured by executive function tests. Subjects and Methods: In this study, 50- to 80-year-old women underwent cognitive testing, long-duration cardiac hemodynamic recordings during quiet sitting, and 60 min of soleus muscle stimulation with continued hemodynamic recording. Results: Two thirds of our subjects were hypotensive (diastolic blood pressure [DBP] < 70 mmHg) after 30 min of quiet sitting. Cognitive performance was significantly better in individuals with higher DBPs (0.79 s per 1-mmHg increase in DBP). Soleus muscle stimulation resulted in an average increase in DBP of 6.1 mmHg, which could translate into a 30% or greater improvement in cognitive performance. Conclusions: Incongruent Stroop testing provides high statistical power for distinguishing differential cognitive responses to resting DBP levels. These results set the stage to investigate whether regular use of calf muscle pump stimulation could effectively reverse age-related cognitive impairment.

scholarly journals Pažintinių funkcijų sutrikimai po kardiochirurginių operacijų: intraoperacinių veiksnių įtaka

2008 ◽  
Vol 6 (2) ◽  
pp. 0-0 ◽  
Author(s):  
Ieva Norkienė ◽  
Juozas Ivaškevičius
Keyword(s):  
Risk Factors ◽  
Cardiac Surgery ◽  
Cognitive Decline ◽  
Surgical Intervention ◽  
Early Postoperative Period ◽  
Adverse Outcomes ◽  
Cerebral Hypoperfusion ◽  
Neurocognitive Outcomes ◽  
The Impact

Ieva Norkienė, Juozas IvaškevičiusVilniaus universiteto Anesteziologijos ir reanimatologijos klinika,Vilniaus greitosios pagalbos universitetinė ligoninė, Šiltnamių g. 29, LT-04130 VilniusEl paštas: [email protected] Šiuolaikinėje širdies chirurgijoje prioritetu tampa ne tik paciento gyvybės išsaugojimas, bet ir sveikatos grąžinimas. Pooperaciniu laikotarpiu pacientų sveikimą ir grįžimą prie įprastinio gyvenimo ritmo, net jei fizinė savijauta gera, dažnai sunkina rečiau ir sunkiau diagnozuojamos neuropsichologinės komplikacijos. Pažintinių (kognityvinių) funkcijų sutrikimai, arba kognityvinė disfunkcija, įvairių autorių duomenimis, gali būti nustatoma net iki 53% pacientų ankstyvuoju pooperaciniu laikotarpiu, o praėjus keleriems metams išlieka apie 20% gydytų ligonių. Ieškant efektyviausių būdų neurologinėms komplikacijoms išvengti, šiuolaikinėje medicinos literatūroje aktyviai svarstoma, kokią įtaką šiai patologinei būklei rastis turi intraoperaciniai veiksniai. Straipsnyje apžvelgiama dirbtinės kraujo apytakos, embolizacijos, hipoperfuzijos ir anestezijos sąsaja su pažintinių funkcijų pokyčiais po kardiochirurginių operacijų. Pagrindiniai žodžiai: pažintinių funkcijų sutrikimai, kardiochirurgija, rizikos veiksniai Cognitive decline after cardiac surgery: the impact of intraoperative factors Ieva Norkienė, Juozas IvaškevičiusClinic of Anesthesiology and Intensive Care of Vilnius UniversityEmergency Hospital, Šiltnamių 29, LT-04130 Vilnius, LithuaniaE-mail: [email protected] The quality of postoperative life becomes one of the most important aspects in assessing the outcomes of any surgical intervention. Recovery from the immediate effects of cardiac surgery is often complicated by less noticeable and hardly diagnosed neuropsychological complications. According to various authors, cognitive decline occurs in up to 53% of patients in the early postoperative period and persists in 20% of patients for a couple of years after surgery. Recent studies suggest that the incidence of these adverse outcomes may be closely related to intraoperative factors. In the present paper, we discuss the influence of cardiopulmonary bypass, embolisation, cerebral hypoperfusion and anesthesia on neurocognitive outcomes after cardiac surgery. Key words: cognitive decline, cardiac surgery, risk factors

scholarly journals Prevention of Cognitive Decline in Alzheimer’s Disease by Novel Antioxidative Supplements

2020 ◽  
Vol 21 (6) ◽  
pp. 1974 ◽  
Author(s):  
Koh Tadokoro ◽  
Yasuyuki Ohta ◽  
Haruhiko Inufusa ◽  
Alan Foo Nyuk Loon ◽  
Koji Abe
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lipid Peroxidation ◽  
Cognitive Decline ◽  
Antioxidant Defense ◽  
Amyloid Β ◽  
Preclinical Study ◽  
Cerebral Hypoperfusion ◽  
Prodromal Stage

Oxidative stress plays a crucial role in Alzheimer’s disease (AD) from its prodromal stage of mild cognitive impairment. There is an interplay between oxidative stress and the amyloid β (Aβ) cascade via various mechanisms including mitochondrial dysfunction, lipid peroxidation, protein oxidation, glycoxidation, deoxyribonucleotide acid damage, altered antioxidant defense, impaired amyloid clearance, inflammation and chronic cerebral hypoperfusion. Based on findings that indicate that oxidative stress plays a major role in AD, oxidative stress has been considered as a therapeutic target of AD. In spite of favorable preclinical study outcomes, previous antioxidative components, including a single antioxidative supplement such as vitamin C, vitamin E or their mixtures, did not clearly show any therapeutic effect on cognitive decline in AD. However, novel antioxidative supplements can be beneficial for AD patients. In this review, we summarize the interplay between oxidative stress and the Aβ cascade, and introduce novel antioxidative supplements expected to prevent cognitive decline in AD.

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