Question

increased inflammation is associated with improvement in anxiety and depression, particularly in older persons.
- true - false

Answer 1

Answer

The statement given is true.

depression is associated with a chronic, low-grade inflammatory response and activation of cell-mediated immunity, as well as activation of the compensatory anti-inflammatory reflex system. It is similarly accompanied by increased oxidative and nitrosative stress (O&NS), which contribute to neuroprogression in the disorder.

Inflammation is increased in patients with mood and anxiety-related disorders due to environmental challenges such as diet and lifestyle factors, medical illness, and psychosocial stress. Immune activation involves intracellular signal transduction pathways and the inflammasome, which can respond to a variety of environmental stressors beyond pathogens including psychosocial stress, to produce the release of inflammatory cytokines. Increased inflammatory cytokines are in turn associated with increased oxidative stress and generation of reactive oxygen and reactive nitrogen species (ROS and RNS). Increased ROS and RNS contribute to the oxidation of tetrahydrobiopterin (BH4), a cofactor required for the enzymatic synthesis of monoamines via phenylalanine hydroxylase (PAH), tryptophan hydroxylase (TPH) and tyrosine hydroxylase (TH), thus disrupting the synthesis of serotonin (5-HT), dopamine (DA) and norepinephrine (NE) through effects on the availability of monoamine precursors such as tryptophan and tyrosine. Inflammation and the release of cytokines also stimulate enzyme pathways such as indoleamine 2,3 dioxygenase (IDO), which can then lead to the release of neurotoxic metabolites of kynurenine that affect glutamate (Glu) including quinolinic acid. In the brain, inflammation causes the release of Glu from microglia and reduced uptake by astrocytes. These actions of inflammatory cytokines ultimately contribute to alterations in neurocircuits in the brain including those related to basal ganglia to prefrontal reward and motor circuits, as well as fear and anxiety-related amygdala, prefrontal and insular circuitry, which may contribute to symptoms of depression and anxiety.