Cold exposure induced cognitive impairment: A systematic review

Area of Science:

• Neuroscience
• Environmental Health
• Physiology

Background:

• Extreme cold exposure (CE) poses a significant public health risk to cognitive function in vulnerable populations.
• The precise biological mechanisms driving cold-induced cognitive impairment are not fully understood.
• Populations at risk include military personnel, polar workers, and high-latitude residents.

Purpose of the Study:

• To systematically review the effects of CE on cognitive function.
• To elucidate the interconnected biological mechanisms underlying CE-induced cognitive impairment.
• To propose protective strategies and identify future research directions.

Main Methods:

• Systematic literature review synthesizing existing research on CE and cognitive function.
• Analysis of biological pathways including neuroendocrine, oxidative stress, neuroinflammation, and mitochondrial function.
• Identification of feedback loops and interactions between these pathways.

Main Results:

• CE impairs cognition via neuroendocrine dysregulation (HPA/HPT axes), oxidative stress (ROS, Nrf2 pathway), neuroinflammation (microglia, inflammasomes), and mitochondrial dysfunction.
• These pathways interact synergistically, leading to hippocampal damage, synaptic plasticity collapse, and memory deficits.
• Excessive glucocorticoids, ROS bursts, and pro-inflammatory cytokines are key mediators.

Conclusions:

• Cognitive deficits from CE result from a complex interplay of neuroendocrine, oxidative, inflammatory, and metabolic disruptions.
• Comprehensive protective strategies, including acclimatization and targeted therapies, are proposed.
• Standardized research and further mechanistic validation are needed to protect brain health in extreme environments.