Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
Amyloid beta and tau are associated with the dual effect of neuroinflammation on neurodegeneration.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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.
Povala Guilherme, Bellaver Bruna, Bastiani Marco Antônio De, Ferrari-Souza João Pedro, Aguzzoli Cristiano S, Leffa Douglas T, Ferreira Pamela C L, Lussier Firoza Z, Rocha Andreia, Zalzale Hussein, Soares Carolina, Bauer-Negrini Guilherme, Therriault Joseph, Rahmouni Nesrine, Stevenson Jenna, Servaes Stijn, Tissot Cécile, Zatt Bruno, Karikari Thomas K, Ikonomovic Milos D, Villemagne Victor L, Gauthier Serge, Zimmer Eduardo R, Tudorascu Dana L, Benedet Andrea L, Rosa-Neto Pedro, Pascoal Tharick A
Аннотация
INTRODUCTION: Current literature presents conflicting results regarding the impact of neuroinflammation on Alzheimer's disease (AD)-related neurodegeneration. While some studies suggest that neuroinflammation potentiates neurodegeneration, others indicate a protective effect.
METHODS: We evaluated 145 individuals with positron emission tomography (PET) for amyloid beta (Aβ), tau, and translocator protein (TSPO), a proxy of neuroinflammation, to test the hypothesis that Aβ and tau are associated with the dual effect of neuroinflammation on neurodegeneration across the AD continuum.
RESULTS: The detrimental effects of neuroinflammation on gray matter density occurred in two waves. The first neuroinflammation-related detrimental wave was associated with brain Aβ deposition, while the second was with widespread tau tangle pathology. Furthermore, the concomitant presence of neuroinflammation, Aβ, and tau was associated with faster cognitive decline over 2 years.
CONCLUSIONS: Our results support a model in which Aβ- and tau-associated neuroinflammation are related to two waves of deleterious effects on AD-related neurodegeneration.
HIGHLIGHTS: Two waves of detrimental neuroinflammation effects on brain density associated with Aβ or tau. Aβ associated with deleterious effect of neuroinflammation on brain density in early AD. Tau associated with deleterious effect of neuroinflammation on brain density in late AD. Interactions of Aβ, tau, and neuroinflammation are associated with cognitive decline.
METHODS: We evaluated 145 individuals with positron emission tomography (PET) for amyloid beta (Aβ), tau, and translocator protein (TSPO), a proxy of neuroinflammation, to test the hypothesis that Aβ and tau are associated with the dual effect of neuroinflammation on neurodegeneration across the AD continuum.
RESULTS: The detrimental effects of neuroinflammation on gray matter density occurred in two waves. The first neuroinflammation-related detrimental wave was associated with brain Aβ deposition, while the second was with widespread tau tangle pathology. Furthermore, the concomitant presence of neuroinflammation, Aβ, and tau was associated with faster cognitive decline over 2 years.
CONCLUSIONS: Our results support a model in which Aβ- and tau-associated neuroinflammation are related to two waves of deleterious effects on AD-related neurodegeneration.
HIGHLIGHTS: Two waves of detrimental neuroinflammation effects on brain density associated with Aβ or tau. Aβ associated with deleterious effect of neuroinflammation on brain density in early AD. Tau associated with deleterious effect of neuroinflammation on brain density in late AD. Interactions of Aβ, tau, and neuroinflammation are associated with cognitive decline.