Neutrophils promote Alzheimer's disease–like pathology and cognitive decline via LFA-1 integrin

By Elena Zenaro, E. Pietronigro, V. Bianca, G. Piacentino, L. Marongiu, S. Budui, Ermanna Turano, Barbara Rossi, Stefano Angiari, Silvia Dusi and 9 more. Nature Medicine, 2015

797 citations recorded by the source corpus.

Subfields: Molecular Biology, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/84ffdaf4c2358156ab35da2921f82a85c956feae

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In Molecular Biology

1. E. Wohleb

In Neurology

1. S. Woodburn
2. J. Bollinger
3. E. Wohleb

Citations in the corpus

• The blood-brain barrier in Alzheimer's disease (2017, neutral): “Thesedata suggestthat A β bindingto fi brin-ogen can also exacerbate cerebrovascular permeability during AD, by modulating VE-cadherin levels in cerebral microvessels (Muradashvili et al., 2014).”
• Functional morphology of the blood-brain barrier in health and disease (2018, neutral): “Neutrophils can also migrate in the brains of AD patients and transgenic animals with AD-like disease [92, 93, 143, 144] (Fig.”
• The semantics of microglia activation: neuroinflammation, homeostasis, and stress (2021, background): “Importantly, depleting neutrophils reduced Aβ42 levels and was associated with better cognitive outcomes, suggesting that neutrophils play a role in AD pathogenesis [66].”