Hemodynamic Instability in Heart Failure Intensifies Age-Dependent Cognitive Decline

2020 ◽  
Vol 76 (1) ◽  
pp. 63-84
Author(s):  
Jack C. de la Torre
Author(s):  
Christa A. Hammond ◽  
Natalie J. Blades ◽  
Sarwat I. Chaudhry ◽  
John A. Dodson ◽  
W.T. Longstreth ◽  
...  

2017 ◽  
Vol 1863 (10) ◽  
pp. 2680-2691 ◽  
Author(s):  
Dzmitry Matsiukevich ◽  
Giovanna Piraino ◽  
Patrick Lahni ◽  
Paul W. Hake ◽  
Vivian Wolfe ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Zhou Wu ◽  
Janchun Yu ◽  
Aiqin Zhu ◽  
Hiroshi Nakanishi

As the life expectancy continues to increase, the cognitive decline associated with Alzheimer’s disease (AD) becomes a big major issue in the world. After cellular activation upon systemic inflammation, microglia, the resident immune cells in the brain, start to release proinflammatory mediators to trigger neuroinflammation. We have found that chronic systemic inflammatory challenges induce differential age-dependent microglial responses, which are in line with the impairment of learning and memory, even in middle-aged animals. We thus raise the concept of “microglia aging.” This concept is based on the fact that microglia are the key contributor to the acceleration of cognitive decline, which is the major sign of brain aging. On the other hand, inflammation induces oxidative stress and DNA damage, which leads to the overproduction of reactive oxygen species by the numerous types of cells, including macrophages and microglia. Oxidative stress-damaged cells successively produce larger amounts of inflammatory mediators to promote microglia aging. Nutrients are necessary for maintaining general health, including the health of brain. The intake of antioxidant nutrients reduces both systemic inflammation and neuroinflammation and thus reduces cognitive decline during aging. We herein review our microglia aging concept and discuss systemic inflammation and microglia aging. We propose that a nutritional approach to controlling microglia aging will open a new window for healthy brain aging.


2007 ◽  
Vol 28 (9) ◽  
pp. 1421-1435 ◽  
Author(s):  
Christian Freichel ◽  
Manuela Neumann ◽  
Theresa Ballard ◽  
Veronika Müller ◽  
Marie Woolley ◽  
...  

2006 ◽  
Vol 291 (5) ◽  
pp. H2192-H2198 ◽  
Author(s):  
Arun Sridhar ◽  
Spencer J. Dech ◽  
Veronique A. Lacombe ◽  
Terry S. Elton ◽  
Sylvia A. McCune ◽  
...  

Hypertension is a common cause of heart failure, and ventricular arrhythmias are a major cause of death in heart failure. The spontaneous hypertension heart failure (SHHF) rat model was used to study altered ventricular electrophysiology in hypertension and heart failure. We hypothesized that a reduction in the inward rectifier K+ current ( IK1) and expression of pacemaker current ( If) would favor abnormal automaticity in the SHHF ventricle. SHHF ventricular myocytes were isolated at 2 and 8 mo of age and during end-stage heart failure (≥17 mo); myocytes from age-matched rats served as controls. Inward IK1 was significantly reduced at both 8 and ≥17 mo in SHHF rats compared with controls. There was a reduction in inward IK1 due to aging in the controls only at ≥17 mo. We found a significant increase in If at all ages in the SHHF rats, compared with young controls. In controls, there was an age-dependent increase in If. Action potential recordings in the SHHF rats demonstrated abnormal automaticity, which was abolished by the addition of an If blocker (10 μM zatebradine). Increased If during hypertension alone or combined increases in If with reduced IK1 during the progression to hypertensive heart failure contribute to a substrate for arrhythmogenesis.


2017 ◽  
Vol 23 (1) ◽  
pp. 47-55 ◽  
Author(s):  
Jan Bressler ◽  
David S. Knopman ◽  
A. Richey Sharrett ◽  
Rebecca F. Gottesman ◽  
Alan Penman ◽  
...  

2003 ◽  
Vol 17 (2) ◽  
pp. 388-396 ◽  
Author(s):  
Debby Van Dam ◽  
Rudi D'Hooge ◽  
Matthias Staufenbiel ◽  
Chris Van Ginneken ◽  
Frans Van Meir ◽  
...  

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