The proteinopenia hypothesis: Loss of Aβ42 and the onset of Alzheimer's Disease

Alberto J. Espay; Karl Herrup; Kasper P. Kepp; Timothy Daly

doi:10.1016/j.arr.2023.102112

The proteinopenia hypothesis: Loss of Aβ₄₂ and the onset of Alzheimer's Disease

Alberto J. Espay^*, Karl Herrup, Kasper P. Kepp, Timothy Daly^*

^*Corresponding author for this work

Department of Chemistry

Research output: Contribution to journal › Review › peer-review

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Abstract

The dominant protein-lowering strategy in Alzheimer's Disease (AD) has failed to provide a clinically-meaningful treatment for patients. We hypothesize that the loss of functional, soluble Aβ42 during the process of aggregation into amyloid is more detrimental to the brain than the corresponding accrual of insoluble amyloid.

Original language	English
Article number	102112
Journal	Ageing Research Reviews
Volume	92
Number of pages	5
ISSN	1568-1637
DOIs	https://doi.org/10.1016/j.arr.2023.102112
Publication status	Published - 2023

Keywords

Alzheimer's disease
Amyloid
Aβ42
Loss of function
Soluble protein

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title = "The proteinopenia hypothesis: Loss of Aβ42 and the onset of Alzheimer's Disease",

abstract = "The dominant protein-lowering strategy in Alzheimer's Disease (AD) has failed to provide a clinically-meaningful treatment for patients. We hypothesize that the loss of functional, soluble Aβ42 during the process of aggregation into amyloid is more detrimental to the brain than the corresponding accrual of insoluble amyloid.",

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