The Dialogue Between Neuroinflammation and Adult Neurogenesis: Mechanisms Involved and Alterations in Neurological Diseases.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic, preclinical, and clinical literature without systematic review methodology.
PubMed 36383328 · doi:10.1007/s12035-022-03102-z
What was done
This narrative review summarizes literature examining the interplay between neuroinflammation and adult neurogenesis in the subgranular and subventricular zones. It describes the regulatory effects of activated glia, cytokines, chemokines, and reactive oxygen species on neurogenesis across neurological disorders (such as Alzheimer's disease, Parkinson's disease, stroke, epilepsy, and traumatic brain injury) and surveys preclinical and clinical therapeutic candidates, including curcumin, ginseng, metformin, and minocycline.
What was found
The abstract provides no quantitative data or pooled statistical outcomes. It qualitatively describes that neuroinflammation regulates every phase of adult neurogenesis—including proliferation, differentiation, migration, newborn neuron survival, maturation, synaptogenesis, and neuritogenesis—acting as either pro- or anti-neurogenic depending on the severity, chronicity, and specific neurological disease state.
Why it matters
The review organizes current concepts on how neuroimmune responses modulate neural regeneration and highlights potential pharmacological targets for neurodegenerative and neuropsychiatric disorders.
Limits
This is a narrative review with no systematic search criteria, quantitative meta-analysis, or formal risk-of-bias assessment. Much of the underlying literature relies on bench and animal models that may not accurately reflect human adult neurogenesis.
Cited by
- supports Elevated levels of systemic inflammation reduce the rate of neurogenesis.