Angiotensin II-induced hypertension does not exacerbate α-SYNUCLEIN pathology in a mouse model of Parkinson’s disease

Description

Ignacio Silva-Llanes and seven co-authors test whether high blood pressure worsens Parkinson-type brain damage in mice, a plausible fear since vascular disease and inflammation travel as a pair in aging brains. Their model forces mouse brains to make too much alpha-synuclein, the protein that clumps in Parkinson's disease, inside the substantia nigra on one side.

Chronic infusion of angiotensin II produced hypertension, yet neuron loss in the dopamine system matched normotensive animals exactly. Support-cell activation in astrocytes and microglia also refused to budge. The inflammatory gene program switched on by the protein, including the inflammasome machinery that matures inflammatory signals, ran no hotter under hypertension. The pyroptosis executioner protein rose where the protein was made in excess, mainly inside microglia, whatever the blood pressure. The authors conclude that synuclein pathology drives this inflammation, and that hypertension may need aging or other vascular partners to matter.

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Source: https://europepmc.org/article/MED/PMC13651558