Search Results for "Neuroinflammation"

Neuroinflammation is activation of the brain’s immune system—primarily microglia—which release inflammatory mediators (cytokines and reactive oxygen species) that alter neuronal signaling. In the short term this response is protective, but when microglia remain chronically activated the resulting inflammation disrupts brain circuits and produces symptoms that depend on which regions are affected (e.g., basal ganglia → sudden OCD/tics like PANS/PANDAS; amygdala → severe anxiety; motor cortex/substantia nigra → movement problems or Parkinsonian features). Key inflammatory mediators mentioned include interleukin‑1β, tumor necrosis factor‑α, interleukin‑6 and reactive oxygen species. Persistent neuroinflammation may also drive accumulation of beta‑amyloid and phosphorylated tau—proteins that can impair synapses and contribute to cognitive decline and dementia—and help explain treatment‑resistant mood or anxiety disorders when inflammation is the underlying driver. Systemic inflammatory states (diabetes, obesity, cardiovascular disease, metabolic dysfunction) and peripheral signals can activate microglia, which can act as signal amplifiers, and newer PET/MRI methods can detect microglial activation. Clinically this means evaluating for region‑specific inflammation and addressing underlying inflammatory drivers, because therapies that only target neurotransmitters may provide limited benefit when neuroinflammation is present.

For more information, refer to https://drtalks.com/videos/the-neuroinflammation-map-how-different-brain-regions-drive-symptoms/.