阿尔茨海默病（AD）是一种全球性的慢性进行性神经退行性疾病。我们旨在研究和比较乙酰-L-肉碱和卡路里限制（CR）对AlCl3诱导的AD的神经保护影响，以探索AD的病理机制和治疗策略。 67只成年雄性Wistar大鼠被分配到对照组，AlCl3组，AlCl3-乙酰-L-肉碱组和AlCl3-CR组。每天用饲胃管给予AlCl3和乙酰-L-肉碱，剂量为每公斤体重100毫克，通过给予控制组日平均热量摄入量的70％来进行CR。大鼠经过开放场测试，Y型迷宫测试，新物体识别测试和被动避免测试的行为评估，测定血清磷酸化tau（pTau），海马匀浆磷酸化腺苷酸激活蛋白激酶，Beclin-1，Bcl-2相关X蛋白和B细胞淋巴瘤2的生化试验（Bcl2），以及海马Ki-67和胶质纤维酸性蛋白免疫组织化学。 AlCl3诱导的认知和行为缺陷与受损的自噬和增强的凋亡相关，这与缺陷的神经发生和缺陷的星形胶质细胞激活有关。 乙酰-L-肉碱和CR部分保护免受AlCl3诱导的行为，认知，生化和组织学变化的影响，乙酰-L-肉碱更具有对海马凋亡标志物的改善作用，CR则在行为和组织学方面有更明显的改善。

Alzheimer's disease (AD) is a worldwide chronic progressive neurodegenerative disease. We aimed to investigate and compare the neuroprotective impact of acetyl-l-carnitine and caloric restriction (CR) on AlCl3-induced AD to explore the pathogenesis and therapeutic strategies of AD. Sixty-seven adult male Wistar rats were allocated into Control, AlCl3, AlCl3-acetyl-l-carnitine, and AlCl3-CR groups. Each of AlCl3 and acetyl-l-carnitine were given by gavage in a daily dose of 100 mg/kg and CR was conducted by giving 70% of the daily average caloric intake of the control group. Rats were subjected to behavioral assessment using open field test, Y maze, novel object recognition test and passive avoidance test, biochemical assay of serum phosphorylated tau (pTau), hippocampal homogenate phosphorylated adenosine monophosphate-activated protein kinase, Beclin-1, Bcl-2-associated X protein, and B cell lymphoma 2 (Bcl2) as well as hippocampal Ki-67 and glial fibrillary acidic protein immunohistochemistry. AlCl3-induced cognitive and behavioral deficits coincident with impaired autophagy and enhanced apoptosis associated with defective neurogenesis and defective astrocyte activation. Acetyl-l-carnitine and CR partially protect against AlCl3-induced behavioral, cognitive, biochemical, and histological changes, with more ameliorative effect of acetyl-l-carnitine on hippocampal apoptotic markers, and more obvious behavioral and histological improvement with CR.