scholarly journals Cognitive Dysfunction after Heart Disease: A Manifestation of the Heart-Brain Axis

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Chengyang Xu ◽  
Xueshu Tao ◽  
Xiaonan Ma ◽  
Rui Zhao ◽  
Zhipeng Cao
Keyword(s):  
Heart Failure ◽  
Heart Disease ◽  
Cognitive Dysfunction ◽  
Brain Function ◽  
Human Life ◽  
Amyloid Β ◽  
Blood Perfusion ◽  
Clinical Applications ◽  
The Brain ◽  
And Oxidative Stress

The functions of the brain and heart, which are the two main supporting organs of human life, are closely linked. Numerous studies have expounded the mechanisms of the brain-heart axis and its related clinical applications. However, the effect of heart disease on brain function, defined as the heart-brain axis, is less studied even though cognitive dysfunction after heart disease is one of its most frequently reported manifestations. Hypoperfusion caused by heart failure appears to be an important risk factor for cognitive decline. Blood perfusion, the immune response, and oxidative stress are the possible main mechanisms of cognitive dysfunction, indicating that the blood-brain barrier, glial cells, and amyloid-β may play active roles in these mechanisms. Clinicians should pay more attention to the cognitive function of patients with heart disease, especially those with heart failure. In addition, further research elucidating the associated mechanisms would help discover new therapeutic targets to intervene in the process of cognitive dysfunction after heart disease. This review discusses cognitive dysfunction in relation to heart disease and its potential mechanisms.

Abstract 1375: Brain Renin Angiotensin Blockade Attenuates Cytokines and Oxidative Stress in the Paraventricular Nucleus of Hypothalamus and Decreases Sympathoexcitation in Heart Failure Rats

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Ying Ma ◽  
Yu-Ming Kang* ◽  
Zhi-Ming Yang ◽  
Joseph Francis*
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Paraventricular Nucleus ◽  
Cross Talk ◽  
Renin Angiotensin System ◽  
Heart Weight ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Brain ◽  
And Oxidative Stress

Introduction: Neurohumoral mechanisms play an important role in the pathophysiology of congestive heart failure (HF). Recent studies suggest that the brain renin angiotensin system (RAS) plays an important role in regulating body fluids and sympathetic drive in HF. In addition, it has been shown that there is cross talk between cytokines and RAS in cardiovascular disease. In this study we determined whether blockade of brain RAS attenuate inflammatory cytokines and oxidative stress in HF rats. Methods and Results: Adult male Sprague-Dawley rats were implanted with intracerebroventricular (ICV) cannulae and subjected to coronary artery ligation to induce HF and confirmed by echocardiography. Rats were treated with an angiotensin type 1 receptors (AT1-R) antagonist losartan (LOS, 20 μg/hr, ICV) or vehicle (VEH) for 4 weeks. At the end of the study, left ventricular (LV) function was measured by echocardiography and rats were sacrificed, and brain and plasma samples were collected for measurements of cytokines and superoxide using immunohistochemistry, Western blot and real time RT-PCR. HF rats induced significant increases in Nuclear Factor-kappaB (NF-κB) p50-positive neurons and activated microglia in the paraventricular nucleus (PVN) of hypothalamus, and TNF-α, IL-1β, IL-6 and NF-κB p50 in hypothalamus when compared with sham rats. These animals also had increased staining for dihydroethidium (DHE) and plasma levels of norepinephrine (NE), an indirect indicator of sympathetic activity. In contrast, ICV treatment with LOS attenuated cytokine expression and oxidative stress in the PVN and hypothalamus when compared with VEH treated HF rats. ICV treatment with LOS also reduced plasma NE levels, and proinflammatory cytokine, heart weight to body weight ratio with decreased LV end-diastolic pressure. Conclusions : These findings suggest the cross talk between the cytokines and renin angiotensin system within the brain contribute to sympatho-excitation in HF.

Advanced nanoparticular approaches to combat Alzheimer's disease

2021 ◽  
Vol 09 ◽  
Author(s):  
Rahul Shah ◽  
Sankha Bhattacharya
Keyword(s):  
Alzheimer’S Disease ◽  
Drug Delivery ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Ageing Population ◽  
Disease Therapy ◽  
Cns Penetration ◽  
The Brain ◽  
Improve Patient ◽  
And Oxidative Stress

: Alzheimer's disease (AD) is a neurological disease that affects many of the world's rapidly ageing population. In the etiology of Alzheimer’s disease (AD), the involvement of amyloid β (Aβ) plaque accumulation and oxidative stress in the brain have important roles. Various drugs have been proposed to prevent and treat AD, but delivering these therapeutic agents to the brain is difficult. Over the last decade, nanoparticle-mediated drug delivery represents one promising strategy to increase the CNS penetration of several therapeutic moieties successfully. Different nanocarriers are being investigated to treat and diagnose AD. NTDDS (nanotechnology-based drug delivery systems) can be used in various methods to improve patient compliance and treatment outcomes. However, literature analysis revealed that clinical activities such as NTDDS application in Alzheimer's disease research lag behind despite extensive research. This review gives an account of the BBB and discusses the literature on some drugs which are successfully encapsulated as nanoparticles for a future therapeutic approach. It also emphasizes the current clinical studies for Alzheimer's disease therapy.

Sulforaphane Reverses the Amyloid-β Oligomers Induced Depressive-Like Behavior

2020 ◽  
Vol 78 (1) ◽  
pp. 127-137 ◽  
Author(s):  
Wei Wang ◽  
Cuibai Wei ◽  
Meina Quan ◽  
Tingting Li ◽  
Jianping Jia
Keyword(s):  
Oxidative Stress ◽  
Memory Impairment ◽  
Molecular Mechanisms ◽  
Psychological Symptoms ◽  
Amyloid Β ◽  
Serotonergic System ◽  
Inflammatory Factors ◽  
The Relationship ◽  
The Brain ◽  
And Oxidative Stress

Background: Depression is one of the most common behavioral and psychological symptoms in people with Alzheimer’s disease (AD). To date, however, the molecular mechanisms underlying the clinical association between depression and AD remained elusive. Objective: Here, we study the relationship between memory impairment and depressive-like behavior in AD animal model, and investigate the potential mechanisms. Methods: Male SD rats were administered amyloid-β oligomers (AβOs) by intracerebroventricular injection, and then the depressive-like behavior, neuroinflammation, oxidative stress, and the serotonergic system were measured in the brain. Sulforaphane (SF), a compound with dual capacities of anti-inflammation and anti-oxidative stress, was injected intraperitoneally to evaluate the therapeutic effect. Results: The results showed that AβOs induced both memory impairment and depressive-like behavior in rats, through the mechanisms of inducing neuroinflammation and oxidative stress, and impairing the serotonergic axis. SF could reduce both inflammatory factors and oxidative stress parameters to protect the serotonergic system and alleviate memory impairment and depressive-like behavior in rats. Conclusion: These results provided insights into the biological mechanisms underlying the clinical link between depressive disorder and AD, and offered new drug options for the treatment of depressive symptoms in dementia.

scholarly journals Measures of chronic heart failure as the markers of cognitive dysfunction in patients with coronary heart disease complicated by circulatory failure

Cor et Vasa ◽  
2021 ◽  
Vol 63 (1) ◽  
pp. 20-24
Author(s):  
Natalya S. Akimova ◽  
Oksana V. Bugaeva ◽  
Larisa E. Konshina ◽  
Yury G. Shvarts
Keyword(s):  
Heart Failure ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Chronic Heart Failure ◽  
Cognitive Dysfunction ◽  
Circulatory Failure

scholarly journals 5-Caffeoylquinic Acid Ameliorates Cognitive Decline and Reduces Aβ Deposition by Modulating Aβ Clearance Pathways in APP/PS2 Transgenic Mice

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 494 ◽  
Author(s):  
Keiko Ishida ◽  
Koichi Misawa ◽  
Hitomi Nishimura ◽  
Tomoya Hirata ◽  
Masaki Yamamoto ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Cognitive Dysfunction ◽  
Amyloid Β ◽  
Density Lipoprotein ◽  
Neuronal Loss ◽  
Chronic Administration ◽  
Pathological Feature ◽  
Caffeoylquinic Acid ◽  
Aβ Clearance ◽  
The Brain

The accumulation of amyloid β (Aβ) in the brain is a major pathological feature of Alzheimer’s disease (AD). In our previous study, we demonstrated that coffee polyphenols (CPP) prevent cognitive dysfunction and Aβ deposition in the brain of an APP/PS2 transgenic mouse AD model. The underlying mechanisms, however, remain to be elucidated. Here, we investigated the effects of the chronic administration of 5-caffeoylquinic acid (5-CQA), the most abundant component of CPP, on cognitive dysfunction in APP/PS2 mice to identify the role of CPP in Aβ elimination. Relative to the untreated controls, the mice fed a 5-CQA-supplemented diet showed significant improvements in their cognitive function assessed by Y-maze and novel object recognition tests. Histochemical analysis revealed that 5-CQA substantially reduced Aβ plaque formation and neuronal loss in the hippocampi. Moreover, 5-CQA upregulated the gene encoding low-density lipoprotein receptor-related protein 1, an Aβ efflux receptor, and normalized the perivascular localization of aquaporin 4, which facilitates Aβ clearance along the paravascular pathway. These results suggest that 5-CQA reduces Aβ deposition in the brain by modulating the Aβ clearance pathways and ameliorating cognitive decline and neuronal loss in APP/PS2 mice. Thus, 5-CQA may be effective in preventing cognitive dysfunction in AD.

scholarly journals Exploiting the neuroprotective effects of ɑ-klotho to tackle ageing- and neurodegeneration-related cognitive dysfunction

2021 ◽  
Author(s):  
Kelsey Hanson ◽  
Kate Fisher ◽  
Nigel M Hooper
Keyword(s):  
Cognitive Dysfunction ◽  
Significant Proportion ◽  
Amyloid Β ◽  
Synaptic Function ◽  
Ageing Population ◽  
Neuroprotective Effects ◽  
Anti Oxidant ◽  
Klotho Protein ◽  
The Brain

Cognitive dysfunction is a key symptom of aging and neurodegenerative disorders, such as Alzheimer’s disease. Strategies to enhance cognition would impact the quality of life for a significant proportion of the ageing population. The ɑ-klotho protein may protect against cognitive decline through multiple mechanisms: such as promoting optimal synaptic function via activation of N-methyl-D-aspartate receptor signalling; stimulating the anti-oxidant defence system; reducing inflammation; promoting autophagy; and enhancing clearance of amyloid-β. However, the molecular and cellular pathways by which ɑ-klotho mediates these neuroprotective functions have yet to be fully elucidated. Key questions remain unanswered: which form of ɑ-klotho (transmembrane, soluble or secreted) mediates its cognitive enhancing properties; what is the neuronal receptor for ɑ-klotho and which signalling pathways are activated by ɑ-klotho in the brain to enhance cognition; how does peripherally administered ɑ-klotho mediate neuroprotection; and what is the molecular basis for the beneficial effect of the VS variant of ɑ-klotho? In this review we summarise the recent research on neuronal ɑ-klotho and discuss how the neuroprotective properties of ɑ-klotho could be exploited to tackle age- and neurodegeneration-associated cognitive dysfunction.

The value of the parameters of the severity of chronic heart failure in the assessment of cognitive dysfunction in patients with coronary heart disease

Therapy ◽  
2021 ◽  
Vol 3_2021 ◽  
pp. 20-27
Author(s):  
Akimova N.S. Akimova ◽  
Bugaeva O.V. Bugaeva ◽  
Sokolov I.M. Sokolov ◽  
Schwartz E.Yu. Schwartz ◽  
Kiselev A.R. Kiselev ◽  
...  
Keyword(s):  
Heart Failure ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Chronic Heart Failure ◽  
Cognitive Dysfunction

Protective role of peroxiredoxin-4 in heart failure

2020 ◽  
Vol 134 (1) ◽  
pp. 71-72
Author(s):  
Naseer Ahmed ◽  
Masooma Naseem ◽  
Javeria Farooq
Keyword(s):  
Heart Failure ◽  
Cardiac Fibroblasts ◽  
Protective Role ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Total Antioxidant ◽  
Galectin 3 ◽  
Consequent Increase ◽  
And Oxidative Stress

Abstract Recently, we have read with great interest the article published by Ibarrola et al. (Clin. Sci. (Lond.) (2018) 132, 1471–1485), which used proteomics and immunodetection methods to show that Galectin-3 (Gal-3) down-regulated the antioxidant peroxiredoxin-4 (Prx-4) in cardiac fibroblasts. Authors concluded that ‘antioxidant activity of Prx-4 had been identified as a protein down-regulated by Gal-3. Moreover, Gal-3 induced a decrease in total antioxidant capacity which resulted in a consequent increase in peroxide levels and oxidative stress markers in cardiac fibroblasts.’ We would like to point out some results stated in the article that need further investigation and more detailed discussion to clarify certain factors involved in the protective role of Prx-4 in heart failure.

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