Peixin Li

TL;DR: The results indicated that early onset of metabolic abnormalities may contribute to the pathology of AD, which is associated with increased inflammation as well as decreased neuronal population and key neuropeptides in the hypothalamus, and a hypothalamic-mediated mechanism where exercise prevents the progression of dementia and of Alzheimer's disease.

TL;DR: There is a need for further research into the specific mechanisms explaining improved body composition, elevated energy expenditure, and reduced lipid content in both liver and adipose tissue in α-Klotho-treated mice.

TL;DR: Investigation of the effects of acute, moderate-intensity exercise on food intake and neuronal activity in the arcuate nucleus (ARC) of the hypothalamus reveals that ARCAgRP/NPY activation is required for acute exercise induced food intake in mice, thus providing insight into the critical role of ARCAGRP/ NPY neurons in maintaining energy homeostasis in cases of exercise-mediated energy deficit.

TL;DR: A prominent role of hypothalamic α-klotho/FGFR1/PI3K signaling in the modulation of NPY/AgRP neuron activity and maintenance of energy homeostasis is indicated, thus providing new insight into the pathophysiology of metabolic disease.

TL;DR: Human CSF data provide the first evidence that impaired central α-klotho function may be involved in the pathophysiology of obesity, and results in mouse models identify ARC POMC neurons and astrocytes as novel molecular effectors of centralα- Klotho.