Robert W. Regenhardt

TL;DR: This work shows that hind limb intramuscular injection of αS can induce pathology in the CNS in the human Ala53Thr (M83) and wild-type (M20) αS transgenic mouse models, and is the first evidence that an entire neurodegenerative proteinopathy associated with a robust, lethal motor phenotype can be initiated by peripheral inoculation with a pathogenic protein.

TL;DR: It is demonstrated that intracerebroventricular infusion of either Ang‐(1–7) or an ACE2 activator, diminazine aceturate (DIZE), prior to and following ET‐1‐induced MCAO significantly attenuated the cerebral infarct size and neurological deficits measured 72 h after the insult, and suggests that the mechanism of the Ang‐ (1-7) protective action includes blunting of inducible nitric oxide synthase expression.

TL;DR: Progress has been made in understanding the clinical mechanisms, imaging characteristics, and genetic basis of lacunar strokes, and the investigation of new therapeutic targets, aimed at reversing CSVD processes and promoting neural repair after LS depends upon further understanding these basic mechanisms.

TL;DR: Findings demonstrate an anti-inflammatory action of Ang-(1-7) in the brain, and suggest that the cerebroprotective action of this peptide in ischemic stroke may involve effects on nitric oxide generation by microglia.

TL;DR: The ischemic penumbra, collateral circulation, autoregulation, and imaging assessment of the penumbr are described and an approach for induced hypertension in the acute treatment of patients with LVOs is suggested.