Hence, TGF-β1 shows protective effect on neurons, which might be through the PI3K/Akt/Wnt/β-catenin signaling pathway, serving as a potential target in AD pathology.
The ameliorative effects of PLP on AD were predicted to be associated with regulating neural cell apoptosis, inflammatory response, and neurotrophy via various pathways such as PI3K-Akt signaling pathway, MAPK signaling pathway, and neurotrophin signaling pathway.
NBM-DBS starting from 4 months of age for 21 days at a high frequency (100 Hz) has therapeutic effects on AD through activating phosphatidylinositol 3'-kinase (PI3K)/Akt pathway and inhibiting ERK1/2 pathway.
Here, we report that inactivation of the p110δ isoform of phosphoinositide 3-kinase (PI3K) reduces anterograde axonal trafficking of APP in hippocampal neurons and dampens secretion of the inflammatory cytokine tumor necrosis factor-alpha by microglial cells in the familial AD APP<sub>swe</sub>/PS1<sub>ΔE9</sub> (APP/PS1) mouse model.
There is a large amount of evidence demonstrating the neuroprotective effect of Nicotine neurotransmission in AD, mainly through nicotinic acetylcholine receptor (nAChR) activation and antiapoptotic PI3K/Akt/Bcl-2 pathway signaling.
Our study highlights that upregulation of the lncRNA MEG3 improves cognitive impairment, alleviates neuronal damage, and inhibits activation of astrocytes in hippocampus tissues in AD through inhibiting the PI3K/Akt signaling pathway.
Evidence indicates that Schisandrin inhibition of Aβ<sub>1-42</sub> -mediated cellular damage in AD neurons may involve activation of the PI3K/Akt signaling pathway where up-regulation of <i>p</i>-Akt activity consequently leads downstream to decreased activity of <i>p</i>-GSK-3β phosphorylation accompanied by reduced tau protein.
Alzheimer's disease (AD) is one of the most common neurodegenerative diseases in which the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/protein kinase B (PKB or Akt) pathway is deregulated in response to phosphatase and tensin homolog (PTEN) overexpression.
As examples, the role of phosphoinositide 3 kinase/Akt/ mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway in cell cycle re-entry and blocking autophagy are discussed as potential common intracellular components between AD and cancer pathogenesis, with diverse clinical diagnosis.
Genome-wide RNA sequencing analysis reveals that IGF-2 attenuates memory decline, oxidative stress and amyloid plaques in an Alzheimer's disease mouse model (AD) by activating the PI3K/AKT/CREB signaling pathway.
Modules positively correlated with AD and RBM8A-low are significantly involved in the RAP1 signaling pathway, PI3K-AKT signaling pathway, hematopoietic cell lineage, autophagy and APELIN signaling pathway.
Type 2 diabetes (T2D) poses the most important risk factor for developing AD after ageing and dysfunctional IR/PI3K/Akt signalling is a major contributor in both diseases.
Thus, it can be speculated that Exendin-4 may mitigate AD-like manifestations including mitochondrial toxicity perhaps through PI3K/Akt-mediated pathway in the experimental animals.
The putatively pathogenic brain somatic mutations identified in 26.9% (14 of 52) of AD individuals are enriched in PI3K-AKT, MAPK, and AMPK pathway genes known to contribute to hyperphosphorylation of tau.
The effects of dulaglutide on decreasing the hyperphosphorylation of tau and NFs proteins through improving the PI3K/AKT/GSK3β signaling pathway may be related to its protective effects on impairment of AD-like learning and memory.
How impaired insulin-PI3K-Akt signaling in peripheral tissues or in the central nervous system (CNS) affects the development or progression of AD is currently poorly understood.
This study is launched to uncover the inner function of microRNA-196a (miR-196a) on cognitive dysfunction and neuronal damage in Alzheimer's disease (AD) rats through regulating the PI3K/Akt signaling pathway.
Our results demonstrated that KXS could ameliorate AD by regulating neurotransmitter and PI3K/Akt signal pathway as an effective multitarget treatment so that the potential value of this classic prescription could be explored from a novel perspective.
Thus, the present study aimed to investigate the relationship between PI3K/Akt pathway and the activation of ACE2/MasR in the AD model of D-galactose-ovariectomized rats.