TRPV1蛋白是一种钙离子通道，允许非选择性阳离子通过并以其疼痛调节途径而闻名。之前的研究发现，一种三重转基因阿尔茨海默病（AD）小鼠模型（3xTg-AD +/+）具有抗AD效果。对3xTg-AD/TRPV1转基因小鼠模型中脑源神经营养因子（BDNF）/环磷酸腺苷（cAMP）反应元件结合蛋白（CREB）信号传导途径中蛋白质的表达进行了研究，以更好地理解TRPV1缺陷对AD的调节效应。结果显示，TRPV1缺陷通过增加BDNF水平和促进酪氨酸受体激酶B（TrkB）、细胞外信号调节激酶（ERK）、蛋白激酶B（Akt）和CREB的磷酸化而导致CREB被激活。此外，TRPV1缺陷诱导的CREB激活增加了抗凋亡因子B细胞淋巴瘤2（Bcl-2）基因，从而下调Bcl-2相关X（Bax）表达，降低了剪切的半胱氨酸蛋白酶-3和剪切的聚（ADP核糖）聚合酶（PARP），防止海马区的细胞凋亡。总之，TRPV1缺陷通过BDNF/CREB信号转导途径中的细胞保护作用而预防了3xTg-AD小鼠海马区的凋亡。

Transient receptor potential vanilloid 1 (TRPV1) protein is a Ca2+-permeable non-selective cation channel known for its pain modulation pathway. In a previous study, it was discovered that a triple-transgenic Alzheimer's disease (AD) mouse model (3xTg-AD+/+) has anti-AD effects. The expression of proteins in the brain-derived neurotrophic factor (BDNF)/cAMP response element binding protein (CREB) pathway in a 3xTg-AD/TRPV1 transgenic mice model was investigated to better understand the AD regulatory effect of TRPV1 deficiency. The results show that TRPV1 deficiency leads to CREB activation by increasing BDNF levels and promoting phosphorylation of tyrosine receptor kinase B (TrkB), extracellular signal-regulated kinase (ERK), protein kinase B (Akt), and CREB in the hippocampus. Additionally, TRPV1 deficiency-induced CREB activation increases the antiapoptotic factor B-cell lymphoma 2 (Bcl-2) gene, which consequently downregulates Bcl-2-associated X (Bax) expression and decreases cleaved caspase-3 and cleaved poly (ADP-ribose) polymerase (PARP), which leads to the prevention of hippocampal apoptosis. In conclusion, TRPV1 deficiency exhibits neuroprotective effects by preventing apoptosis through the BDNF/CREB signal transduction pathway in the hippocampus of 3xTg-AD mice.