Afternoon exercise was associated with greater fat loss than morning exercise in overweight/obese adults: an exploratory study of PER3 rs228697 genotype matching.

Migraine is one of the most prevalent neurological disorders worldwide and a leading cause of disability [, ]. Its pathophysiology is complex and involves multiple phases and symptoms that extend beyond the actual headache, including cutaneous allodynia, photophobia, and negative affective states [, ]. Currently available acute and preventive treatments remain inadequate for many patients, including a substantial subset treated with calcitonin gene-related peptide (CGRP)-targeting therapies [, ]. These observations suggest that migraine reflects distributed dysfunction across multiple neural systems and that important CGRP-sensitive mechanisms remain incompletely understood. Among the factors implicated in migraine, CGRP has emerged as a key signaling molecule. CGRP is expressed in trigeminal ganglion neurons, including afferents that innervate the dura, and acts through a receptor complex composed of calcitonin receptor-like receptor (), receptor activity-modifying protein 1 (), and receptor component protein (). CGRP released from trigeminal afferents can act at the meninges to promote migraine-like responses, and preclinical studies have shown that direct dural application of CGRP produces female-selective hypersensitivity in rodents [, ]. These studies support a critical role for peripheral CGRP signaling but how meningeal CGRP engages central circuits that contribute to the sensory and affective dimensions of migraine-like states remains unknown. Migraine is also associated with hypersensitivity to light and altered emotional processing. Experimental studies have shown that CGRP can induce light-aversive behavior in mice through both peripheral and central mechanisms, supporting the idea that CGRP influences not only nociception, but also aversive and sensory-affective behaviors relevant to migraine [, ]. In parallel, human imaging studies have implicated both brainstem and limbic structures in migraine, including increased activation in the amygdala and dorsolateral pons [, , ]. These findings suggest that migraine-related symptoms may depend on interactions between peripheral trigeminovascular signaling and central circuits involved in salience, threat, and affect.