Abstract
Regulating amyloidogenesis through the natural triggering receptor expressed in myeloid/microglial cells 2 (TREM2).
Highlights
Amyloidogenesis, the progressive accumulation of amyloid-beta (Aβ) peptides into insoluble, toxic, senile plaque lesions is one of the major defining features of the Alzheimer’s disease (AD) brain
REM2 and amyloidogenesis same end effects on phagocytosis as downregulation of a fully functional triggering receptor expressed in myeloid/microglial cells 2 (TREM2) in sporadic AD; and that (2) modest TREM2 over-expression might be useful in enhancing the scavenging and removal of cellular debris in the central nervous system (CNS), including neurotoxic and self-aggregating Aβ42 peptides
TREM2 signaling has been recently shown to be selectively inducible and manipulated from outside of the cell, suggesting that the modulation of TREM2 expression may be effectively regulated using highly specific targeting via drug-based pharmacological strategies exogenously supplied (Alexandrov et al, 2013; Lukiw, 2013; Zhao et al, 2013)
Summary
Amyloidogenesis, the progressive accumulation of amyloid-beta (Aβ) peptides into insoluble, toxic, senile plaque lesions is one of the major defining features of the Alzheimer’s disease (AD) brain.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
