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Alzheimer's disease (AD) is the most frequent cause of dementia. Misfolded protein pathological hallmarks of AD are brain deposits of amyloid-β (Aβ) plaques and phosphorylated tau neurofibrillary tangles. However, doubts about the role of Aβ in AD pathology have been raised as Aβ is a common component of extracellular brain deposits found, also by  in vivo  imaging, in non-demented aged individuals. It has been suggested that some individuals are more prone to Aβ neurotoxicity and hence more likely to develop AD when aging brains start accumulating Aβ plaques. Here, we applied genome-wide transcriptomic profiling of lymphoblastoid cells lines (LCLs) from healthy individuals and AD patients for identifying genes that predict sensitivity to Aβ. Real-time PCR validation identified 3.78-fold lower expression of  RGS2  (regulator of G-protein signaling 2;  P =0.0085) in LCLs from healthy individuals exhibiting high vs low Aβ sensitivity. Furthermore,  RGS2  showed 3.3-fold lower expression ( P =0.0008) in AD LCLs compared with controls. Notably,  RGS2  expression in AD LCLs correlated with the patients' cognitive function. Lower  RGS2  expression levels were also discovered in published expression data sets from postmortem AD brain tissues as well as in mild cognitive impairment and AD blood samples compared with controls. In conclusion, Aβ sensitivity phenotyping followed by transcriptomic profiling and published patient data mining identified reduced peripheral and brain expression levels of  RGS2 , a key regulator of G-protein-coupled receptor signaling and neuronal plasticity.  RGS2  is suggested as a novel AD biomarker (alongside other genes) toward early AD detection and future disease modifying therapeutics.

RGS2 expression predicts amyloid-β sensitivity, MCI and Alzheimer’s disease: genome-wide transcriptomic profiling and bioinformatics data mining