Reduced brain-derived neurotrophic factor is associated with cognitive dysfunction in patients with chronic heart failure

2017 ◽  
Vol 17 (5) ◽  
pp. 852-854 ◽  
Author(s):  
Hideaki Suzuki ◽  
Yasuharu Matsumoto ◽  
Hideki Ota ◽  
Koichiro Sugimura ◽  
Jun Takahashi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Cognitive Dysfunction ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor

Additive clinical value of serum brain-derived neurotrophic factor for prediction of chronic heart failure outcome

2015 ◽  
Vol 31 (4) ◽  
pp. 535-544 ◽  
Author(s):  
Shinpei Kadowaki ◽  
Tetsuro Shishido ◽  
Yuki Honda ◽  
Taro Narumi ◽  
Yoichiro Otaki ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Clinical Value

Abstract 210: Impaired Brain-Derived Neurotrophic Factor-TrkB Signaling in Nucleus Tractus Solitarius During Chronic Heart Failure Blunts Baroreflex Sensitivity

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Bryan K Becker ◽  
Hanjun Wang ◽  
Irving H Zucker
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Neurotrophic Factor ◽  
Baroreflex Sensitivity ◽  
Nucleus Tractus Solitarius ◽  
Critical Role ◽  
Brain Derived Neurotrophic Factor ◽  
Central Target ◽  
Autonomic Imbalance ◽  
Baroreflex Function

Blunted baroreflex function is a negatively prognostic marker of autonomic imbalance in chronic heart failure (CHF), yet the mechanisms underlying baroreflex blunting in CHF are not fully understood. The nucleus tractus solitarius (NTS) is the primary central target of baroreceptor afferents, and plays a critical role in regulating central baroreflex sensitivity. Brain-derived neurotrophic factor (BDNF) and its receptor, TrkB, are highly expressed in the NTS, but little is known about the role of BDNF signaling in the NTS. We hypothesized that in the NTS, BDNF enhances baroreflex sensitivity, and impaired BDNF-TrkB signaling contributes to the blunted baroreflex function in CHF. To test this hypothesis, 50 nl of BDNF or the selective TrkB antagonist ANA-12 were microinjected bilaterally into the dorso-medial NTS of sham-operated rats and myocardial infarct-induced CHF rats. BDNF evoked a greater decrease in blood pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) in sham vs. CHF rats. Injection of ANA-12 increased MAP, HR, and RSNA to a greater extent in sham vs. CHF rats (Table). Following 125 μM ANA-12, baroreflex sensitivity was blunted in sham rats (3.7 ± 0.3 vs. 1.9 ± 0.1 bpm/mmHg max gain, p < .05 before vs. after, n = 4). CHF rats had blunted baroreflex sensitivity vs. sham (2.3 ± 0.1 bpm/mmHg, p < .05, n = 4), and ANA-12 had little effect on baroreflex sensitivity in CHF (2.0 ± 0.1 bpm/mmHg, n = 4). These data suggest that endogenous BDNF plays an important role in maintaining baroreflex sensitivity in the NTS, and that BDNF-TrkB signaling is impaired in CHF, which may contribute to blunted baroreflex sensitivity and autonomic imbalance.

Forced running exercise mitigates radiation-induced cognitive deficits via regulated DNA hydroxymethylation

Epigenomics ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 385-396 ◽  
Author(s):  
Junjun Zhang ◽  
Junyan Li ◽  
Yiwen Zhu ◽  
Zhigang Miao ◽  
Ye Tian
Keyword(s):  
Cognitive Dysfunction ◽  
Neurotrophic Factor ◽  
Epigenetic Modification ◽  
Brain Derived Neurotrophic Factor ◽  
Hippocampal Neurogenesis ◽  
Mice Model ◽  
Whole Brain Irradiation ◽  
Running Exercise ◽  
Radiation Induced ◽  
Forced Running

Aim: Roles of forced running exercise (FE) in remediation of neurogenesis inhibition and radiation-induced cognitive dysfunction were investigated in a whole-brain irradiation mice model via the regulation of DNA 5-hydroxymethylation modification (5 hmC) and its catalytic enzymes ten–eleven translocation (Tet) proteins. Materials & methods: Hippocampal neurogenesis and cognitive function, DNA 5 hmC level and Tet expression were determined in mice. Results: The expression of DNA 5 hmC and Tet2, brain-derived neurotrophic factor significantly decreased in hippocampus postradiation. FE mitigated radiation-induced neurogenesis deficits and cognitive dysfunction. Furthermore, FE increased 5 hmC and brain-derived neurotrophic factor expression. SC1, a Tet inhibitor, reversed partly such changes. Conclusion: Tet-mediated 5 hmC modification represents a kind of diagnostic biomarkers of radiation-induced cognitive dysfunction. Targeting Tet-related epigenetic modification may be a novel therapeutic strategy for radiation-induced brain injury.

Brain-Derived Neurotrophic Factor Could Regulate Mitochondrial Function in the Skeletal Muscle Through Ampk-Pgc1α Signaling in Heart Failure Mice

2015 ◽  
Vol 21 (10) ◽  
pp. S197
Author(s):  
Takayuki Nakajima ◽  
Shintaro Kinugawa ◽  
Shingo Takada ◽  
Junichi Matsumoto ◽  
Wataru Misushima ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Mitochondrial Function ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor

scholarly journals Brain-Derived Neurotrophic Factor Improves Limited Exercise Capacity in Mice With Heart Failure

Circulation ◽  
2018 ◽  
Vol 138 (18) ◽  
pp. 2064-2066 ◽  
Author(s):  
Junichi Matsumoto ◽  
Shingo Takada ◽  
Shintaro Kinugawa ◽  
Takaaki Furihata ◽  
Hideo Nambu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Exercise Capacity ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor
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