Brain diseases in changing climate

Abstract

Climate change is one of the biggest and most urgent challenges for the 21st century. Rising average temperatures and ocean levels, altered precipitation patterns and increased occurrence of extreme weather events affect not only the global landscape and ecosystem, but also human health. Multiple environmental factors influence the onset and severity of human diseases and changing climate may have a great impact on these factors. Climate shifts disrupt the quantity and quality of water, increase environmental pollution, change the distribution of pathogens and severely impacts food production - all of which are important regarding public health. This paper focuses on brain health and provides an overview of climate change impacts on risk factors specific to brain diseases and disorders. We also discuss emerging hazards in brain health due to mitigation and adaptation strategies in response to climate changes.

Keywords: Brain disease; Climate change; Environment; Health.

Figure 1.

Direct and indirect consequences of global climate change contribute to increased occurrence of risk factors in brain disease.

Figure 2.

Hypothetical mechanisms of the impact of heat exposure on brain (patho)physiology. Heat exposure results in mitochondrial dysfunction decreased mitochondrial membrane potential (↓Δѱ_m) causing increased electron leakage. The latter is associated with increased superoxide (O₂^·−) generation and further increase in reactive oxygen species (ROS) production resulting in oxidative stress together with decreased antioxidant enzymes activity. Both oxidative stress and heat exposure impair endoplasmic reticulum (ER) functioning ultimately leading to ER stress. Increased cytochrome c (Cyt c) release due to mitochondrial dysfunction induces caspase-3 activation and apoptotic signaling. The latter is aggravated by oxidative and ER stress. Hypothetically, a tight interplay between mitochondrial dysfunction, apoptosis, oxidative stress and ER stress may underlie heat-induced neurodegeneration. The overall effect of heat exposure is also associated with increased brain glutamate levels, although the particular mechanisms are unclear. Elevated glutamate levels induce NMDA receptor signaling causing intracellular Ca²⁺ flux. Taken together with Ca²⁺ release from ER, glutamate-induced Ca²⁺ uptake results in increasing intracellural calcium levels ([Ca²⁺]i) levels, leading to excitotoxicity and seizures. Moreover, increased [Ca²⁺]i levels aggravate apoptotic signaling through caspase-3 activation.