Journal
JOURNAL OF ALZHEIMERS DISEASE
Volume 71, Issue 3, Pages 907-920Publisher
IOS PRESS
DOI: 10.3233/JAD-190494
Keywords
Alzheimer's disease; neuroinflammation; NF-kB pathway; stroke; TREM2; Uch-L1
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Funding
- University of Genoa
- Regione Piemonte
- University of Torino
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Neuroinflammation is involved in the pathogenesis of Alzheimer's disease, and the transcription factor NF-kappa B is a player in this event. We found here that the ischemic damage alone or in association with A beta(1-42) activates the NF-kappa B pathway, induces an increase of BACE1 and a parallel inhibition of Uch-L1 and TREM2, both in vitro and in vivo, in Tg 5XFAD and in human brains of sporadic AD. This mechanism creates a synergistic loop that fosters inflammation. We also demonstrated a significant protection exerted by the restoration of Uch-L1 activity. The rescue of the enzyme is able to abolish the decrease of TREM2 and the parameters of neuroinflammation.
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