Published online by Cambridge University Press: 16 May 2024
The COVID-19 pandemic resurfaced and potentially exacerbated the issue of comorbidities in mental health, with anxiety and depression being a prominent example. The co-occurrence of these conditions may exceed 50%, while there is also an overlap in treatment options and challenges in treatment response. This is supported by evidence indicating similarities between mood and anxiety across multiple dimensions, including cognitive, behavioural, neurobiological, and intracellular mechanisms. Cognitive commonalities primarily refer to attentional and recollection biases towards threatening stimuli and negative information. Behavioural inhibition due to avoidance or reduced motivation is another similarity of anxiety and depression. Shared neurobiological mechanisms include amygdala hyper-reactivity and dysregulation of the HPA axis. At a cellular level, mitochondrial dysfunctions might be underlying stress response and the mechanisms responsible for stress adaptation and regulation. Novel therapeutics, such as photobiomodulation (PBM), have been informed by these mechanistic models.
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