Centre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Ralph and Patricia Sarich Neuroscience Research Institute, Edith Cowan University, Nedlands, WA, Australia.
Curtin Health Innovation Research Institute, School of Pharmacy and Biomedical Sciences, Curtin University, Bentley WA, Australia.
J Alzheimers Dis. 2020;74(2):441-448. doi: 10.3233/JAD-190948.
Increased amyloid-β (Aβ) accumulation associated with abnormal autophagy-lysosomal activity and nutrient kinase dysregulation are common features in Alzheimer's disease (AD) brain. Recent studies have identified PRKAG2 and TIPRL genes that control nutrient kinase regulated autophagy, and here we determined if their expression is altered in postmortem AD brains. Gene and protein expression of TIPRL were unchanged. However, gene expression of PRKAG2 was increased 3-fold and its protein levels positively correlated with Aβ accumulation in the AD brain. In summary, our findings suggest that increased PRKAG2 is an important contributing factor to Aβ accumulation in the AD brain.
淀粉样蛋白-β（Aβ）积累增加与自噬-溶酶体活性异常和营养激酶失调有关，这是阿尔茨海默病（AD）大脑的共同特征。最近的研究已经确定了控制营养激酶调节自噬的 PRKAG2 和 TIPRL 基因，在这里我们确定它们在 AD 大脑中的表达是否发生改变。TIPRL 的基因和蛋白表达没有改变。然而，PRKAG2 的基因表达增加了 3 倍，其蛋白水平与 AD 大脑中的 Aβ 积累呈正相关。总之，我们的研究结果表明，PRKAG2 的增加是 AD 大脑中 Aβ 积累的一个重要因素。
