Aging-induced type I interferon response at the choroid plexus negatively affects brain function

I'm sure you want decent cognitive functioning post-stroke. So ask your doctors how they are  blocking type I interferon (IFN-I)–dependent gene expression
http://www.sciencemag.org/content/346/6205/89

1. Kuti Baruch¹,*,
2. Aleksandra Deczkowska¹,*,
3. Eyal David²,
4. Joseph M. Castellano³,
5. Omer Miller¹,
6. Alexander Kertser¹,
7. Tamara Berkutzki¹,
8. Zohar Barnett-Itzhaki²,
9. Dana Bezalel²,
10. Tony Wyss-Coray³,
11. Ido Amit²,†,
12. Michal Schwartz¹,†

+ Author Affiliations

1. ¹Department of Neurobiology, Weizmann Institute of Science, Rehovot 76100, Israel.
2. ²Department of Immunology, Weizmann Institute of Science, Rehovot 76100, Israel.
3. ³Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.

1. ↵†These authors contributed equally to this work and are corresponding authors. E-mail: michal.schwartz@weizmann.ac.il (M.S.); ido.amit@weizmann.ac.il (I.A.)

1. ↵* These authors contributed equally to this work.

• Abstract
• Editor's Summary

Aging-associated cognitive decline is affected by factors produced inside and outside the brain. By using multiorgan genome-wide analysis of aged mice, we found that the choroid plexus, an interface between the brain and the circulation, shows a type I interferon (IFN-I)–dependent gene expression profile that was also found in aged human brains. In aged mice, this response was induced by brain-derived signals, present in the cerebrospinal fluid. Blocking IFN-I signaling within the aged brain partially restored cognitive function and hippocampal neurogenesis and reestablished IFN-II–dependent choroid plexus activity, which is lost in aging. Our data identify a chronic aging-induced IFN-I signature, often associated with antiviral response, at the brain’s choroid plexus and demonstrate its negative influence on brain function, thereby suggesting a target for ameliorating cognitive decline in aging.