Current osteoporosis reports · 2026
Osteoporosis and Alzheimer's Disease: The Role of Sclerostin.
СтатьяОбзорНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Gagiano Lorelé, Chen Ziming, Blakeney William G, Jones Christopher, Mastaglia Frank, Zheng Minghao, Yuan Jun
Аннотация
PURPOSE OF REVIEW: Little is known about the underlying cause contributing to the association between Osteoporosis (OP) and Alzheimer's disease (AD). This review highlights the emerging role of sclerostin, a protein mainly produced by osteocytes, in the newly discovered crosstalk between bone and brain, with a focus on its potential contribution to the relationship between OP and AD.
RECENT FINDINGS: Circulating sclerostin levels increase with aging and are positively associated with brain amyloid-β burden in older adults. Studies demonstrate that elevated sclerostin can cross the blood-brain barrier, promote amyloid-β peptide deposition, and impair synaptic plasticity by suppressing Wnt/β-catenin signalling, whereas sclerostin inhibition restores neuronal plasticity and attenuates AD pathology. Sclerostin represents a promising target in the bone-brain interaction pathway. Its dual role as a measurable circulating biomarker and a modifiable component offers new opportunities for early risk assessment and therapeutic repurposing. Future longitudinal and interventional studies are essential to confirm the association between sclerostin and risk of AD, and to clarify whether targeting sclerostin can delay the onset of the disease or modify its trajectory.
RECENT FINDINGS: Circulating sclerostin levels increase with aging and are positively associated with brain amyloid-β burden in older adults. Studies demonstrate that elevated sclerostin can cross the blood-brain barrier, promote amyloid-β peptide deposition, and impair synaptic plasticity by suppressing Wnt/β-catenin signalling, whereas sclerostin inhibition restores neuronal plasticity and attenuates AD pathology. Sclerostin represents a promising target in the bone-brain interaction pathway. Its dual role as a measurable circulating biomarker and a modifiable component offers new opportunities for early risk assessment and therapeutic repurposing. Future longitudinal and interventional studies are essential to confirm the association between sclerostin and risk of AD, and to clarify whether targeting sclerostin can delay the onset of the disease or modify its trajectory.