Open AccessThe Aβ Hypothesis: Leading Us to Rationally‐Designed Therapeutic Strategies for the Treatment or Prevention of Alzheimer Disease
Author(s) -
Golde Todd E.
Publication year - 2005
Publication title -
brain pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.986
H-Index - 132
eISSN - 1750-3639
pISSN - 1015-6305
DOI - 10.1111/j.1750-3639.2005.tb00104.x
Subject(s) - neurodegeneration , disease , neuroscience , alzheimer's disease , amyloid β , amyloid (mycology) , medicine , pathological , biochemistry of alzheimer's disease , psychology , amyloid precursor protein , pathology
In recent years the amyloid cascade hypothesis of Alzheimer disease (AD) has been increasingly referred to as the amyloid β protein (Aβ) cascade hypothesis. This subtle rephrasing reflects the acknowledgment that there is debate within the field as to whether Aβ aggregates other than Aβ deposited as classic amyloid fibrils could trigger the pathological cascade that results in neuronal dysfunction and neurodegeneration. Despite this semantic shift, which highlights one enigmatic aspects of AD, the evidence supporting the Aβ hypothesis of AD is extensive. More importantly the Aβ hypothesis of AD has led and will continue to lead to the development of rationale therapeutic strategies that are likely to either prevent or treat this devastating disease. In this review, the evidence supporting the Aβ hypothesis and the recent advances in anti‐Aβ therapy are discussed.