Neuroinflammation
Microglial activation, peripheral immune signals and inflammation-targeted therapies.
State of the art
No update yet for Neuroinflammation. An update is a standalone state-of-the-art for the topic — what someone with Parkinson's needs to know about where this approach stands today.
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Exercise and smoking: health rivals revealing shared protective mechanisms in Parkinson’s?
The paper identifies suppression of neuroinflammation (microglial activation and peripheral immune signalling) as one of the shared protective mechanisms activated by both exercise and certain tobacco compounds, positioning it as a key target for future disease-modifying drug development. -
Region-specific cortico-striatal transcriptomic remodeling following early postnatal dopaminergic disturbance
Striatum-specific co-expression modules following early dopaminergic disturbance included immune-related gene clusters: the "darkorange" module was linked to macrophage colony-stimulating factor response and nitric oxide signalling, while the "white" module was associated with leukocyte-mediated immunity. Cell-type enrichment analyses also identified signals in pericytes and vascular leptomeningeal cells, pointing to vascular-immune involvement in the dopamine-depleted striatum — a pattern consistent with neuroinflammatory changes reported in PD. -
Co‐ and Multi‐Pathologies in Parkinson's Disease: An International Parkinson and Movement Disorder Society Scientific Issues Committee Review
The review identifies shared neuroinflammatory mechanisms as a key driver of the synergistic interaction between alpha-synuclein and co-pathologies: oligomeric forms of tau, amyloid-β, and alpha-synuclein each activate microglia and astrocytes, and this shared inflammatory response then feeds back to accelerate aggregate formation across all protein types simultaneously. -
Parkinson : une voie cérébrale protège les neurones féminins - Daily Beirut
The Texas A&M mouse study found that genetically boosting β2-containing nicotinic acetylcholine receptors in dopaminergic neurons reduced apoptotic (cell-death) signalling and ER stress — a cellular stress pathway linked to neuroinflammation — but only in females, suggesting sex-specific differences in how these protective circuits operate at the molecular level. -
'Garbage collectors' of the brain grind to a halt in fatal multiple system atrophy
A post-mortem single-nucleus RNA sequencing study of 117,000+ brain cells found that microglia in MSA patients are exhausted and functionally inactive in late-stage disease — the opposite of the microglial overactivation seen in Parkinson's. The researchers propose that early immune overactivation leads to burnout, leaving the brain unable to clear toxic waste, which may explain MSA's faster progression compared to Parkinson's.