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Open AccessReview

The Role of Macrophage Migration Inhibitory Factor in Alzheimer′s Disease: Conventionally Pathogenetic or Unconventionally Protective?

1
Department of Educational Sciences, University of Catania, 95124 Catania, Italy
2
Department of Physiology and Pharmacology, University Sapienza, Piazzale A. Moro, 5, 00185 Roma, Italy
3
IRCCS Neuromed, Località Camerelle, 86077 Pozzilli, Italy
4
Department of Biomedical and Biotechnological Sciences, University of Catania, Via S. Sofia 89, 95123 Catania, Italy
*
Author to whom correspondence should be addressed.
Molecules 2020, 25(2), 291; https://doi.org/10.3390/molecules25020291
Received: 18 December 2019 / Revised: 3 January 2020 / Accepted: 9 January 2020 / Published: 10 January 2020
Recent preclinical and clinical observations have offered relevant insights on the etiopathogenesis of late onset Alzheimer′s disease (AD) and upregulated immunoinflammatory events have been described as underlying mechanisms involved in the development of AD. Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine produced by several cells of the innate and adaptive immune system, as well as non-immune cells. In the present review, we highlight experimental, genetic, and clinical studies on MIF in rodent models of AD and AD patients, and we discuss emerging therapeutic opportunities for tailored modulation of the activity of MIF, that may potentially be applied to AD patients. Dismantling the exact role of MIF and its receptors in AD may offer novel diagnostic and therapeutic opportunities in AD.
Keywords: Alzheimer′s disease; macrophage migration inhibitory factor; neuroinflammation Alzheimer′s disease; macrophage migration inhibitory factor; neuroinflammation
MDPI and ACS Style

Petralia, M.C.; Battaglia, G.; Bruno, V.; Pennisi, M.; Mangano, K.; Lombardo, S.D.; Fagone, P.; Cavalli, E.; Saraceno, A.; Nicoletti, F.; Basile, M.S. The Role of Macrophage Migration Inhibitory Factor in Alzheimer′s Disease: Conventionally Pathogenetic or Unconventionally Protective? Molecules 2020, 25, 291.

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