Молодежный инновационный вестникМолодежный инновационный вестник2415-7805Федеральное государственное бюджетное образовательное учреждение высшего образования "Воронежский государственный медицинский университет имени Н.Н. Бурденко" Министерства здравоохранения Российской Федерации10872UnclassifiedThe role of tau protein and β-amyloid in Alzheimer's disease, biochemistry of prion proteinsKamaletdinovNurislam Dinarovichnurislam_2005@icloud.comhttps://orcid.org/0009-0006-4238-450XMenshikovaIrina Askhatovna<p>Candidate of Medical Sciences, Associate Professor</p>rafila.kamaletdinova@mail.ruBashkir State Medical University0411202514261641404202512082025Copyright © 2025, Kamaletdinov N.D., Menshikova I.A.2025<p style="text-align: justify;">Alzheimer's disease (AD) remains one of the most acute problems of modern medicine: according to WHO, about 55 million people worldwide live with dementia, with AD accounting for 60-70% of cases. Despite many years of research, there are no effective treatments that can stop or reverse neurodegeneration. Existing drugs, such as acetylcholinesterase inhibitors, only temporarily alleviate the symptoms without affecting the progression of the disease. This highlights the need for an in-depth study of the molecular mechanisms of AD, among which -amyloid (A) and tau protein play a key role. The relevance of studying their interaction is due to the incompleteness of the classical "amyloid hypothesis", which does not explain all aspects of pathogenesis, including the dissociation between the accumulation of amyloid plaques and clinical manifestations. The growing attention to tau pathology as a driver of neurodegeneration requires a revision of the role of A in the context of synergy with tau protein. In addition, the concept of prion-like propagation of pathological proteins, which combines the mechanisms of AD and prion diseases, has been gaining momentum in recent years. The study of prion protein biochemistry (PrP) in the context of AD opens up new horizons for understanding the universal patterns of neurodegeneration. The ability of A and tau proteins to self-replicate aggregation, resembling prion processes, indicates common pathways of proteotoxicity. This creates the basis for the development of innovative therapeutic strategies aimed not only at individual proteins, but also at the mechanisms of their interaction, conformational stability and intercellular transmission.</p> <p> </p>tau proteinβ-amyloidprion proteinsAlzheimer's diseasebiochemistryтау-белокβ -амилоидаприоновые белкиболезнь Альцгеймерабиохимия1.Петрова М.М., Руденко В.А., Тимербаев В.Р. Гиперфосфорилирование тау-белка как триггер синаптической дисфункции при болезни Альцгеймера // Биохимия. – 2020. – Т. 85, № 8. – С. 1120–1135. – DOI: [10.1134/S0006297920080056](https://doi.org/10.1134/S0006297920080056)2.Горбачёва А.Л., Степанова Т.В., Козлов Г.И. Новые подходы к терапии болезни Альцгеймера: таргетинг амилоидного каскада и тау-патологии // Клиническая медицина. – 2021. – Т. 99, № 5. – С. 345–352. – DOI: [10.30629/0023-2149-2021-99-5-345-352](https://doi.org/10.30629/0023-2149-2021-99-5-345-352)3.Анисимов В.Н., Москалев А.А., Попович И.Г. Прионоподобное распространение патологических белков: общие механизмы при болезни Альцгеймера и прионных энцефалопатиях // Успехи современной биологии. – 2021. – Т. 141, № 1. – С. 3–16. – DOI: [10.31857/S0042132421010028](https://doi.org/10.31857/S0042132421010028)4.Смирнов А.В., Лебедев П.А. Механизмы протеотоксичности β-амилоида и тау-белка: сравнительный анализ с прионными белками // Молекулярная биология. – 2023. – Т. 57, № 3. – С. 410–423. – DOI: [10.31857/S0026898423030131](https://doi.org/10.31857/S0026898423030131)5.Кузнецова И.Д., Николаева Н.Ю. Ингибирование агрегации тау-белка и β-амилоида: перспективы малых молекул в терапии болезни Альцгеймера // Acta Naturae. – 2022. – Т. 14, № 4(55). – С. 54–63. – DOI: [10.32607/actanaturae.11814](https://doi.org/10.32607/actanaturae.11814)