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Discoidin domain receptor inhibition reduces neuropathology and attenuates inflammation in neurodegeneration models.

Abstract：

:The role of cell surface tyrosine kinase collagen-activated receptors known as discoidin domain receptors (DDRs) is unknown in neurodegenerative diseases. We detect up-regulation in DDRs level in post-mortem Alzheimer and Parkinson brains. Lentiviral shRNA knockdown of DDR1 and DDR2 reduces the levels of α-synuclein, tau, and β-amyloid and prevents cell loss in vivo and in vitro. DDR1 and DDR2 knockdown alters brain immunity and significantly reduces the level of triggering receptor expressed on myeloid cells (TREM)-2 and microglia. These studies suggest that DDR1 and DDR2 inhibition is a potential target to clear neurotoxic proteins and reduce inflammation in neurodegeneration.

journal_name

J Neuroimmunol

journal_title

Journal of neuroimmunology

authors

Hebron M,Peyton M,Liu X,Gao X,Wang R,Lonskaya I,Moussa CE

doi

10.1016/j.jneuroim.2017.07.009

subject

Has Abstract

pub_date

2017-10-15 00:00:00

pages

1-9

eissn

0165-5728

issn

1872-8421

pii

S0165-5728(17)30141-8

journal_volume

311

pub_type

杂志文章

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