In APP/PS-1 Transgenic Mice and Aβ-Induced P12 Cell Models, ADCYAP1 Inhibits Neuronal Apoptosis and Autophagy, Thereby Alleviating The Pathology of Alzheimer's Disease.

Characterization of the knock-in AppSAA mouse model as a powerful tool for Alzheimer’s disease preclinical research

AppSAA mice recapitulate age-dependent, human-relevant AD phenotypes with defined therapeutic windows for preclinical research and is available without restriction from The Jackson Laboratory.

LncRNA Loc646329 modulates Alzheimer’s disease-related phenotypes through the miR-150/WNT/β-catenin axis in cellular and APP/PS1 mouse models

Findings provide preclinical evidence that the Loc646329/miR-150/WNT signaling axis contributes to neuronal survival and modulates AD-related pathological changes.

The Neuroscience Journal

Gene-Modified Cell-Based Therapy for AD prior to transplantation can be beneficial for increasing cell survival and making them more effective, and adapted cells could be used for the transfer of factors that can ameliorate neurological complaints.

LncRNA DLX6-AS1 Regulates the Pathological Process Related to Alzheimer’s Disease via miR-204-5p

Serum DLX6-AS1 is a potential biomarker for early diagnosis and assessment of AD, and regulates Aβ-induced neuronal damage and tau phosphorylation by targeting miR-204-5p, offering a new mechanism target for AD molecular therapy.

No evidence of major integrative brain clearance impairment in an Alzheimer´s disease model of transgenic APPswe/PS1dE9 mice

The findings indicate that the APPswe/PS1dE9 mouse model does not exhibit evidence of major integrative brain clearance impairment, despite this being a hallmark of sporadic AD in humans and suggest limitations of this model for studying clearance-related mechanisms of late-onset AD should be acknowledged when planning...

miR-584-5p suppresses Aβ1-42-induced apoptosis in Alzheimer's disease cell model via targeting of HDAC1.