Fibril formation by amyloidogenic proteins and peptides is considered the cause of a number of incurable diseases. One of the most known amyloid diseases is Alzheimer’s disease (AD). Traditionally, amyloidogenic beta peptides Aβ40 and Aβ42 (Aβs) are considered as main causes of AD and the foremost targets in AD fight. The main efforts in pharmacology are aimed at reducing Aβs concentration to prevent their accumulation, aggregation, formation of senile plaques, neuronal death, and neurodegeneration. However, a number of publications have demonstrated certain beneficial physiological effects of Aβs. Simultaneously, it is indicated that the effects of Aβs turn into pathological due to the development of certain diseases in the body. The accumulation of C- and N-terminal truncated Aβs under diverse conditions is supposed to play a role in AD development. The significance of transformation of glutamate residue at positions 3 or 11 of Aβs catalyzed by glutaminyl cyclase making them more degradation resistant, hydrophobic, and prone to aggregation, as well as the participation of dipeptidyl peptidase IV in these transformations are discussed. The experimental data presented confirm the maintenance of physiological, nonaggregated state of Aβs by plant preparations. In conclusion, this review suggests that in the fight against AD, instead of removing Aβs, preference should be given to the treatment of common diseases. Glutaminyl cyclase and dipeptidyl peptidase IV can be considered as targets in AD treatment. Flavonoids and plant preparations that possess antiamyloidogenic propensity are proposed as beneficial neuroprotective, anticancer, and antidiabetic food additives.

中文翻译：

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淀粉样β肽作用的多样性

淀粉样蛋白和肽形成的原纤维被认为是许多不治之症的原因。最著名的淀粉样蛋白疾病之一是阿尔茨海默病（AD）。传统上，淀粉样β肽Aβ40和Aβ42 (Aβs)被认为是AD的主要原因，也是AD对抗中最重要的目标。药理学方面的主要努力旨在降低Aβ浓度，以防止其积累、聚集、老年斑形成、神经元死亡和神经变性。然而，许多出版物已经证明了 Aβ 的某些有益的生理作用。同时也表明，由于体内某些疾病的发展，Aβ的作用转变成病理性的。C 端和 N 端截短的 Aβ 在不同条件下的积累被认为在 AD 的发展中发挥着作用。讨论了谷氨酰胺酰环化酶催化的 Aβ 3 或 11 位谷氨酸残基转化的重要性，使它们更具抗降解性、疏水性和易于聚集，以及二肽基肽酶 IV 在这些转化中的参与。所提供的实验数据证实了植物制剂可维持 Aβ 的生理、非聚集状态。总之，本综述建议，在对抗 AD 的过程中，不应去除 Aβ，而应优先治疗常见疾病。谷氨酰胺酰环化酶和二肽基肽酶IV可被视为AD治疗的靶点。具有抗淀粉样蛋白生成倾向的类黄酮和植物制剂被提议作为有益的神经保护、抗癌和抗糖尿病食品添加剂。