Alzheimer’s disease (AD), the most common neurodegenerative disease, is characterized by progressive cognitive impairment. The deposition of amyloid beta (Aβ) and hyperphosphorylated tau is considered the hallmark of AD pathology. Many therapeutic approaches such as Food and Drug Administration-approved cholinesterase inhibitors and N–methyl–D–aspartate receptor antagonists have been used to intervene in AD pathology. However, current therapies only provide limited symptomatic relief and are ineffective in preventing AD progression. Cannabidiol (CBD), a phytocannabinoid devoid of psychoactive responses, provides neuroprotective effects through both cannabinoid and noncannabinoid receptors. Recent studies using an AD mouse model have suggested that CBD can reverse cognitive deficits along with Aβ-induced neuroinflammatory, oxidative responses, and neuronal death. Furthermore, CBD can reduce the accumulation of Aβ and hyperphosphorylation of tau, suggesting the possibility of delaying AD progression. Particularly, the noncannabinoid receptor, peroxisome proliferator-activated receptor gamma, has been suggested to be involved in multiple functions of CBD. Therefore, understanding the underlying mechanisms of CBD is necessary for intervening in AD pathology in depth and for the translation of preclinical studies into clinical settings. In this review, we summarize recent studies on the effect of CBD in AD and suggest problems to be overcome for the therapeutic use of CBD.

中文翻译：

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了解大麻二酚对阿尔茨海默病的调节作用

阿尔茨海默病 (AD) 是最常见的神经退行性疾病，其特征是进行性认知障碍。淀粉样蛋白 β (Aβ) 和过度磷酸化 tau 的沉积被认为是 AD 病理学的标志。许多治疗方法，如食品和药物管理局批准的胆碱酯酶抑制剂和N-甲基-D-天冬氨酸受体拮抗剂已被用于干预 AD 病理。然而，目前的疗法仅提供有限的症状缓解并且在预防 AD 进展方面无效。大麻二酚 (CBD) 是一种没有精神活性反应的植物大麻素，通过大麻素和非大麻素受体提供神经保护作用。最近使用 AD 小鼠模型的研究表明，CBD 可以逆转认知缺陷以及 Aβ 诱导的神经炎症、氧化反应和神经元死亡。此外，CBD 可以减少 Aβ 的积累和 tau 的过度磷酸化，表明延缓 AD 进展的可能性。特别是，非大麻素受体、过氧化物酶体增殖物激活受体 γ 已被认为与 CBD 的多种功能有关。所以，了解 CBD 的潜在机制对于深入干预 AD 病理学以及将临床前研究转化为临床环境是必要的。在这篇综述中，我们总结了最近关于 CBD 对 AD 影响的研究，并提出了 CBD 治疗应用需要克服的问题。