Local senile amyloidosis in age‐related macular degeneration and Alzheimer's disease

Abstract

AbstractBackgroundThe development of the eye and brain from one germ layer, the community of etiopathogenetic and morphological manifestations of age‐related macular degeneration (AMD) and Alzheimer's disease (AD), the common pathway of β‐amyloid precursor protein (APP) are associated with pathological aggregation of fibrillar β‐amyloid protein (Aβ ) and the development of β‐amyloidopathy in the structural elements of the eye and brain.MethodUsing electron microscopy and selective methods for detecting amyloid and its proteins, 111 eyes with morphological signs of AMD and a brain taken from 56 corpses were examined.ResultOur studies have shown that senile amyloidosis of the eye in combination with senile cerebral amyloidosis occurs in the eighth decade of life, and their frequency increases with age. The cumulative accumulation of β‐amyloid deposits in the structures of the eye and brain was detected in 50.6% of cases. Amyloid‐β deposits were specific for eye druses from AMD and for senile plaques in brain tissue in patients with AD (Fig. 1, 2). In AMD, amyloid deposits are most often found in the Bruch membrane (64.5%) (Fig. 3). Vascular vessels (61.2%) took second place in frequency of occurrence (Fig. 4, 5). The combination of local forms of amyloidosis was characterized by concomitant deposition of β‐amyloid in the vessels of the brain and vessels of the choroid (amyloid angiopathy), as well as in the structural elements of the back of the eye and brain with a typical histochemical characteristic of local forms of senile amyloidosis. Moreover, amyloid angiopathy was more pronounced in the vessels of the brain than in the vessels of the choroid (Fig. 6).ConclusionThe authors demonstrated that changes in the vessels of the brain and the structural elements of the retina and choroid in patients with AMD with AD can be considered as concomitant neurodegenerative processes in these two diseases, which are based on pathological aggregation of β‐amyloid protein. This view of the problem creates the prerequisites for the development of new strategies for the creation of ophthalmogeriatric and neuroprotective drugs that affect pathogenesis and include all stages of Aβ formation and pathological aggregation.