＜Symposium IV＞Cerebral amyloid angiopathy and Alzheimer's disease

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Cerebral amyloid angiopathy （CAA） is increasingly recognized as a major contributor of Alzheimer’sdisease（ AD） pathogenesis. To date, vascular deposits and not parenchymal plaques appear more sensitive predictorsof dementia. Amyloid deposition in and around cerebral blood vessels plays a central role in a series of responsemechanisms that lead to changes in the integrity of the blood-brain barrier, extravasations of plasma proteins,edema formation, release of inflammatory mediators and matrix metalloproteases which, in turn, produce partialdegradation of the basal lamina with the potential to develop hemorrhagic complications. The progressive buildupof amyloid deposits in and around blood vessels chronically limits blood supply and causes focal deprivation ofoxygen, triggering a secondary cascade of metabolic events several of which involve the generation of nitrogen andoxygen free radicals with consequent oxidative stress and cell toxicity. Many aspects of CAA in early- and lateonsetAD ‒the special preference of Aβ40 to deposit in the vessel walls, the favored vascular compromise associatedwith many Aβ genetic variants, the puzzling observation that some of these vasculotropic variants solely manifestwith recurrent hemorrhagic episodes while others are mainly associated with dementia‒ await clarifi cation. Non-Aβcerebral amyloidoses reinforce the viewpoint that plaque burden is not indicative of dementia while highlighting therelevance of non-fi brillar lesions and vascular involvement in the disease pathogenesis. The lessons learned from thecomparative study of Aβ and non-Aβ cerebral amyloidosis provide new avenues and alternative models to study therole of amyloid in the molecular basis of neurodegeneration.

＜Symposium IV＞Cerebral amyloid angiopathy and Alzheimer's disease

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