Emerging research suggests that chronic inflammation, rather than neurotransmitter deficiencies alone, may be a major factor behind depression, reshaping traditional views of the condition. This insight links inflammation, both in the body and brain, to depressive symptoms, explaining why some patients don't respond to conventional antidepressants. Studies reveal that stress can trigger immune responses that activate and later damage microglial cells in the brain, worsening depressive symptoms over time.

A recent study found that vitamin D deficiency during childhood accelerates the aging of the thymus, a crucial organ in training immune cells. As the thymus ages, it becomes less effective at filtering out cells that could mistakenly attack the body's own tissues, increasing the risk of autoimmune diseases like type 1 diabetes.

Anti-NMDAR encephalitis, a rare autoimmune disease, can cause extreme psychiatric symptoms such as hallucinations, paranoia, and memory loss, often mimicking bipolar disorder or schizophrenia. This condition, often affecting women in their 20s to 30s, results from antibodies attacking brain receptors essential for cognition and memory.

New research reveals that immune responses play a crucial role in the formation of Lewy bodies, protein aggregates that mark Parkinson's disease and other neurological conditions. Using human stem cells, scientists recreated Lewy bodies in dopaminergic neurons by combining alpha-synuclein protein buildup with immune stimulation.

A new study reveals that inflammation and immune system activation are closely linked to major depressive disorder (MDD), particularly in those resistant to standard antidepressants. Researchers analyzed gene expression in people with depression, finding increased immune-related gene activity, especially in those with higher inflammation.