TY - JOUR
AU - Lee, Jong Eun
AB - Competitive amyloidogenic pathways play an important role in many neurological diseases such as the onset of various degenerative diseases and ischemic stroke. Overexpression of amyloid precursor protein (APP) and amyloid-beta is modulated via the amyloidogenic pathway, which plays a crucial role in neuroinflammation. During ischemic conditions, the activity of the anti-inflammatory non-amyloidogenic pathway decreases, thus increasing the activity of amyloidogenic pathway. The soluble alpha form of APP (sAPPα), formed via the non-amyloidogenic pathway, exhibits neuroprotective effects against neurological diseases. sAPPα is thought to have a modulatory effect on several cell survival pathways, including its ability to inhibit the phosphoinositide 3-kinases (PI3K) pathway, thereby inhibiting the inflammatory response. The APP derivative, APP96-110, could act as a functional substitute for native sAPPα. Herein, we investigated whether APP96-110 has neuroprotective effects against neuroinflammation and damage following cerebral ischemic stroke. Treatment with diluted APP96-110 (0.005 mg/kg) in mice after 30 min of transient middle cerebral artery occlusion (tMCAO) showed improved motor function and reduced expression of the inflammatory marker CD86. APP96-110 decreased the infarct size and induced an anti-inflammatory response by inhibiting the PI3K pathway. These results suggest that the treatment of APP96-110 is efficacious in reducing neuroinflammation and infarct size in ischemic stroke.
TI - APP96-110 Elicits Neuroprotective Effects Following Ischemic Insult in Animal Models
JF - Neurochemical Research
DO - 10.1007/s11064-023-03928-6
DA - 2023-08-01
UR - https://www.deepdyve.com/lp/springer-journals/app96-110-elicits-neuroprotective-effects-following-ischemic-insult-in-SwbEI0prVs
SP - 2568
EP - 2579
VL - 48
IS - 8
DP - DeepDyve
ER -