Alzheimer ' s Disease as Innate Autoimmunity

The failure of amyloid-β clearance via immunotherapy to produce benefits in Alzheimer's disease patients has spurred a great deal of theorizing, attempts to find a new way forward. Most researchers, from a survey of the field, continue to believe that amyloid-β aggregation is an important contributing factor in at least the early development of Alzheimer's. However, an increasing emphasis on immune dysfunction and chronic inflammation is creeping into modified versions of the amyloid cascade hypothesis, alongside different interpretations of the role of amyloid-β in this process, based on its participation in the innate immune response as an anti-microbial peptide. The role of amyloid-β (Aβ) in Alzheimer's disease (AD) is debated: some argue Aβ takes center stage as the principal actor; others contend it is merely a spectator in the pageant of pathologies that typify AD. Nonetheless, a diversity of data (including in vitro neurotoxicity studies and genetic linkage analyses) do compellingly link Aβ to AD's pathology. Accordingly, rather than unconditionally rejecting the role of Aβ (or any other proposed specific disease mechanism), the need for an innovative broadly encompassing model of AD, which harmonizes multiple divergent theories into a single unified comprehensive explanation, emerges as a much-needed milestone on the road to a cure. Herein, such a broad new molecular-level model of AD is proposed: "Alzheimer's disease as an autoimmune disease" ...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs