Study: Dab2 can exhibit neuroprotective effects in Alzheimer's by regulating TGF-β1/SMAD signaling

Transforming growth factor-beta (TGF-β) type II receptor (TβRII) levels are extremely low in the brain tissue of patients with Alzheimer's disease. This receptor inhibits TGF-β1/SMAD signaling and thereby aggravates amyolid-beta deposition and neuronal injury. Dab2, a specifc adapter protein, protects TβRII from degradation and ensures the effective conduction of TGF-β1/SMAD signaling. Prof. Jun Liu and team from Norman Bethune First Hospital of Jilin University in China used an adenoviral vector to overexpress Dab2 in the APP/PS1 transgenic mouse model of Alzheimer's disease, and investigated the regulatory effect of Dab2 protein on transforming growth factor-β1/SMAD signaling and brain injury in Alzheimer's disease. They found that after Dab2 expression, hippocampal TβRII and p-SMAD2/3 levels were significantly increased, while amyloid-beta deposition, microglia activation, tumor necrosis factor-β and interleulin-6 levels and neuronal loss were significantly attenuated in APP/PS1 mouse brain tissue. These findings, published in the Neural Regeneration Research (Vol. 9, No. 1, 2014), suggest that Dab2 can exhibit neuroprotective effects in Alzheimer's disease by regulating TGF-β1/SMAD signaling.

Article: " Dab2 attenuates brain injury in APP/PS1 mice via targeting transforming growth factor-beta/SMAD signaling" by Lei Song1, Yue Gu2, Jing Jie2, Xiaoxue Bai2, Ying Yang2, Chaoying Liu2, Qun Liu1 (1 Department of Neurology, Norman Bethune First Hospital of Jilin University, Changchun, Jilin Province, China; 2 Department of Respiratory Medicine, Norman Bethune First Hospital of Jilin University, Changchun, Jilin Province, China)