Caffeine improves memory and cognition via modulating neural progenitor cell survival and decreasing oxidative stress in Alzheimer's rat model.

IF 1.8 4区医学 Q3 CLINICAL NEUROLOGY Current Alzheimer research Pub Date : 2023-06-05 DOI:10.2174/1567205020666230605113856

Virendra Tiwari, Akanksha Mishra, Sonu Singh, Shubha Shukla

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引用次数: 1

Abstract

Aims: Caffeine possesses potent antioxidant, anti-inflammatory and anti-apoptotic activities against a variety of neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD). The goal of this study was to investigate the protective role of a psychoactive substance like caffeine on hippocampal neurogenesis and memory functions in streptozotocin (STZ)-induced neurodegeneration in rats.

Background: Caffeine is a natural CNS stimulant, belonging to the methylxanthine class, and is a widely consumed psychoactive substance. It is reported to abate the risk of various abnormalities that are cardiovascular system (CVS) related, cancer related, or due to metabolism dysregulation. Short-term caffeine exposure has been widely evaluated, but its chronic exposure is less explored and pursued. Several studies suggest a devastating role of caffeine in neurodegenerative disorders. However, the protective role of caffeine on neurodegeneration is still unclear.

Objective: Here, we examined the effects of chronic caffeine administration on hippocampal neurogenesis in intracerebroventricular STZ injection induced memory dysfunction in rats. The chronic effect of caffeine on proliferation and neuronal fate determination of hippocampal neurons was evaluated by co-labeling of neurons by thymidine analogue BrdU that labels new born cells, DCX (a marker for immature neurons) and NeuN that labels mature neurons.

Method: STZ (1 mg/kg, 2 μl) was injected stereotaxically into the lateral ventricles (intracerebroventricular injection) once on day 1, followed by chronic treatment with caffeine (10 mg/kg, i.p) and donepezil (5 mg/kg, i.p.). Protective effect of caffeine on cognitive impairment and adult hippocampal neurogenesis was evaluated.

Result: Our findings show decreased oxidative stress burden and amyloid burden following caffeine administration in STZ lesioned SD rats. Further, double immunolabeling with bromodeoxyuridine+/doublecortin+ (BrdU+/DCX+) and bromodeoxyuridine+/ neuronal nuclei+ (BrdU+/NeuN+) has indicated that caffeine improved neuronal stem cell proliferation and long term survival in STZ lesioned rats.

Conclusion: Our findings support the neurogenic potential of caffeine in STZ induced neurodegeneration.

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在阿尔茨海默病大鼠模型中，咖啡因通过调节神经祖细胞存活和降低氧化应激来改善记忆和认知。

目的:咖啡因对多种神经退行性疾病，包括阿尔茨海默病(AD)和帕金森病(PD)具有有效的抗氧化、抗炎和抗凋亡活性。本研究旨在探讨咖啡因等精神活性物质对链脲佐菌素(STZ)诱导的大鼠海马神经发生和记忆功能的保护作用。背景:咖啡因是一种天然的中枢神经系统兴奋剂，属于甲基黄嘌呤类，是一种广泛使用的精神活性物质。据报道，它可以降低心血管系统(CVS)相关、癌症相关或代谢失调引起的各种异常的风险。短期咖啡因暴露已被广泛评估，但其长期暴露较少探索和追求。几项研究表明，咖啡因在神经退行性疾病中起着毁灭性的作用。然而，咖啡因对神经变性的保护作用仍不清楚。目的:观察慢性咖啡因给药对脑室注射STZ诱导记忆功能障碍大鼠海马神经发生的影响。通过胸苷类似物BrdU(新生细胞的标记物)、DCX(未成熟神经元的标记物)和NeuN(成熟神经元的标记物)共同标记神经元，评估咖啡因对海马神经元增殖和神经元命运决定的慢性影响。方法:将STZ (1 mg/kg, 2 μl)于第1天立体定向注射侧脑室(脑室内注射)1次，随后用咖啡因(10 mg/kg, 1次)和多奈哌齐(5 mg/kg, 1次)慢性治疗。评价了咖啡因对认知障碍和成人海马神经发生的保护作用。结果:我们的研究结果表明，在STZ损伤的SD大鼠中，咖啡因可以降低氧化应激负担和淀粉样蛋白负担。此外，溴脱氧尿苷+/双皮质素+ (BrdU+/DCX+)和溴脱氧尿苷+/神经元核+ (BrdU+/NeuN+)的双重免疫标记表明，咖啡因可改善STZ损伤大鼠的神经干细胞增殖和长期存活。结论:我们的研究结果支持咖啡因在STZ诱导的神经变性中的神经源性潜力。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Current Alzheimer research 医学-神经科学

CiteScore

4.00

自引率

4.80%

发文量

审稿时长

4-8 weeks

期刊介绍： Current Alzheimer Research publishes peer-reviewed frontier review, research, drug clinical trial studies and letter articles on all areas of Alzheimer’s disease. This multidisciplinary journal will help in understanding the neurobiology, genetics, pathogenesis, and treatment strategies of Alzheimer’s disease. The journal publishes objective reviews written by experts and leaders actively engaged in research using cellular, molecular, and animal models. The journal also covers original articles on recent research in fast emerging areas of molecular diagnostics, brain imaging, drug development and discovery, and clinical aspects of Alzheimer’s disease. Manuscripts are encouraged that relate to the synergistic mechanism of Alzheimer''s disease with other dementia and neurodegenerative disorders. Book reviews, meeting reports and letters-to-the-editor are also published. The journal is essential reading for researchers, educators and physicians with interest in age-related dementia and Alzheimer’s disease. Current Alzheimer Research provides a comprehensive ''bird''s-eye view'' of the current state of Alzheimer''s research for neuroscientists, clinicians, health science planners, granting, caregivers and families of this devastating disease.