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Amyloid propagation in a sporadic model of Alzheimer disease
15 auth. J. Andreo-Lopez, Francisco Cantero‐Molina, M. Bettinetti-Luque, K. Huynh, Marie Minh Thu Nguyen, A. Cheung, Janine Pham Tran, Celia da Cunha, Laura Trujillo-Estrada, Cristina Nuñez‐Diaz, ...
Most age‐associated neurodegenerative disorders involve the aggregation of specific proteins within the nervous system, as occurs in Alzheimer’s disease (AD). Recent evidence indicates that Aβ can misfold and aggregate into seeds that structurally c…
Most age‐associated neurodegenerative disorders involve the aggregation of specific proteins within the nervous system, as occurs in Alzheimer’s disease (AD). Recent evidence indicates that Aβ can misfold and aggregate into seeds that structurally corrupt native proteins, mimicking a prion‐like process of template protein corruption or seeding. In fact, studies in FAD‐based animal models show that Aβ deposition and cerebral amyloid angiopathy may be induced by intracerebral infusion of brain extracts from AD patients or from aged APP‐transgenic mice. These studies have shown that the characteristic of both the seeding agent and the host influence the pathologic signature of the Aβ seeds. In this regard, the majority of the Aβ‐seeding studies have been done in APP‐transgenic animal models that overproduce APP and/or Aβ. However, it remains to be elucidated whether Aβ deposition can be induced by Aβ seeds in an animal model that does not overexpress APP and produces wild type human Aβ and if these aggregates are similar to the human condition.
Published in
Alzheimer's & Dementia
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0 | 2021 |
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