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Therapeutic strategies that enhance antioxidant capacity (e.g., hyperbaric oxygen[74]), modulate metabolism and inflammation (e.g., adenosine[75]), or reduce cardiac workload (e.g., atenolol[72]) have shown protective potential, highlighting the importance of targeting metabolic instability and oxidative damage

Reduced synaptic transmission and intrinsic excitability of a subtype of pyramidal neurons in the medial prefrontal cortex in a mouse model of Alzheimers disease

Despite the above-mentioned discrepancy, it appears that GHRs are central to the regulation of the quinone redox state, likely preventing toxicity of quinones, either naturally present or found as environmental pollutants

These findings pertain to the internal mechanisms underlying neuroprotection and reduction of oxidative stress

More research is also needed to determine the long-term efficacy and possible side effects of the treatment

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