ASTAXANTHIN AS A NEUROPROTECTIVE AGENT AGAINST ACUTE STRESS-INDUCED COGNITIVE IMPAIRMENT

The sympathetic-adrenomedullary system and the hypothalamic-pituitary-adrenal (HPA) axis are both activated by acute stress. Although adaptive initially, excessive acute stress causes glucocorticoid overload, oxidative stress, mitochondrial dysfunction, and neuroinflammation. These changes particularly affect the hippocampus and prefrontal cortex, impairing synaptic plasticity, neurogenesis, and cognition, including working memory, spatial learning, attention, and executive function. Oxidative stress and inflammation are now recognised as key mediators linking HPA-axis hyperactivation to cognitive decline. Astaxanthin, a xanthophyll carotenoid derived from microalgae such as Haematococcus pluvialis, yeast, and marine organisms, has drawn attention for its anti-inflammatory, anti-apoptotic, and antioxidant qualities. It is a prospective neuroprotective drug because of its lipophilic nature and capacity to pass the blood–brain barrier. According to preclinical research, astaxanthin improves learning and memory in stress and neurodegenerative models, lowers lipid peroxidation, increases endogenous antioxidants, inhibits inflammatory mediators, and stimulates the Nrf2/HO-1 pathway. Methods: Relevant experimental, preclinical, and clinical studies were identified through systematic searches of major scientific databases focusing on acute stress, cognitive dysfunction, oxidative stress, and astaxanthin-mediated neuroprotection. Results: All of these results point to astaxanthin as a viable multi-target treatment option, but more carefully planned human trials are needed to determine its effectiveness, dosage recommendations, and long-term safety in stress-related cognitive impairment.