Effect of cardiac rehabilitation on the renal function in chronic kidney disease - Analysis using serum cystatin-C based glomerular filtration rate

Background: Whether an individually determined appropriate level of cardiac rehabilitation (CR) has a favorable effect on the renal function still remains unclarified. The aim of this study was to confirm the effect of CR on the estimated glomerular filtration rate (eGFR) using cystatin C, which is known to be unaffected by physical exercise. Methods: The study population was comprised of 86 patients (61 males; average age 74 y/o) with a lower-moderate level of chronic kidney disease (CKD) who was admitted to our hospital for treatment of cardiovascular disease (CVD) and who participated in our 3-month CR program. The exercise capacity was assessed by cardiopulmonary exercise testing (CPX) and the eGFR was measured by a formula based on the serum cystatin C concentration (eGFRcys) in each patient both at the beginning and end of the CR. Results: In the CVD patients with CKD, both the peak oxygen uptake (VO2) and peak work rate (WR) improved significantly after CR (15.0 ± 3 to 15.8 ± 3 ml/min/kg, p = 0.002. 65.5 ± 21 to 70.2 ± 25 W, p = 0.001). Regarding the renal function, the eGFRcys improved (45.2 ± 11 to 47.3 ± 13 ml/min/1.73 m2, p = 0.023), however, the eGFR assessed by the serum creatinine (eGFRcr) did not improve after CR (45.1 ± 12 to 44.9 ± 13 ml/min/1.73 m2, p = 0.834). Conclusions: In CVD patients, a novel CR program significantly improved the exercise capacity. Further, CR was shown to have a favorable effect on the renal function when it was estimated by the eGFRcys. Keywords: Cardiac rehabilitation, Chronic kidney disease, Cardiovascular disease, Cystatin C, Estimated glomerular filtration rate, Exercise capacit

Selective butyrylcholinesterase inhibition elevates brain acetylcholine, augments learning and lowers Alzheimer β-amyloid peptide in rodent

Like acetylcholinesterase, butyrylcholinesterase (BChE) inactivates the neurotransmitter acetylcholine (ACh) and is hence a viable therapeutic target in Alzheimer's disease, which is characterized by a cholinergic deficit. Potent, reversible, and brain-targeted BChE inhibitors (cymserine analogs) were developed based on binding domain structures to help elucidate the role of this enzyme in the central nervous system. In rats, cymserine analogs caused long-term inhibition of brain BChE and elevated extracellular ACh levels, without inhibitory effects on acetylcholinesterase. In rat brain slices, selective BChE inhibition augmented long-term potentiation. These compounds also improved the cognitive performance (maze navigation) of aged rats. In cultured human SK-N-SH neuroblastoma cells, intra- and extracellular β-amyloid precursor protein, and secreted β-amyloid peptide levels were reduced without affecting cell viability. Treatment of transgenic mice that overexpressed human mutant amyloid precursor protein also resulted in lower β-amyloid peptide brain levels than controls. Selective, reversible inhibition of brain BChE may represent a treatment for Alzheimer's disease, improving cognition and modulating neuropathological markers of the disease