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Alzheimer's disease (AD) is the most common proteinopathy, which is accompanied by a steady decrease in the patient's cognitive functions with a simultaneous accumulation of amyloid plaques in brain tissues. Amyloid plaques are extracellular aggregates of amyloid β (Aβ) and are associated with neuroinflammation and neurodegeneration. Unlike humans and all other mammals, rats and mice do not reproduce AD-like pathology because there are three amino acid substitutions in their Aβ. Amyloid plaques form in the brains of transgenic mice with overexpression of human Aβ, and such mice are therefore possible to use in biomedicine to model the key features of AD. The transgenic mouse line APPswe/PS1dE9 is widely used as an animal model to study the molecular mechanisms of AD. A study was made to characterize the APPswe/PS1dE9/Blg subline, which was obtained by crossing APPswe/PS1dE9 mice on a CH3 genetic background with C57Bl6/Chg mice. No difference in offspring's survival and fertility was observed in the subline compared to wild-type control mice. Histological analysis of the brain in the APPswe/PS1dE9/Blg line confirmed the main neuromorphological features of AD and showed that amyloid plaques progressively increase in number and size during aging. The APPswe/PS1dE9/Blg line was assumed to provide a convenient model for developing therapeutic strategies to slow down AD progression.

Aim: To investigate clinical and morphological features of amyloidogenesis in age-related macular degeneration (AMD), which is thought to be associated with proteinopathy, namely beta-amyloidopathy., Material and Methods: A total of 111 eyes with morphological signs of AMD as well as brain samples from 56 cadavers (aged at death 60 and over) were assessed with selective methods of amyloid detection., Results: Amyloid deposits were present in 39% of eyes with dry AMD and 80% of eyes with wet AMD. Combined accumulation of amyloid (that is both in eyes and the brain) was found in 50.6% of cases., Conclusion: The results allow to suggest that common etiopathogenetic and morphological features of AMD and Alzheimer's disease (AD) are due to the same metabolic pathway of the transmembrane amyloid precursor protein (APP) responsible for aggregation of beta-amyloid (Aβ), an abnormal fibrillar protein, and the development of beta-amyloidopathy in eyes and brains. It has been demonstrated that beta-amyloidopathy is the keynote of both AMD and AD pathogenesis leading to cytotoxicity, neurodegeneration and pathological apoptosis. Such views on the problem may promote the development of neuroprotective and ophthalmic geriatric medications effective at all stages of pathogenesis, including beta-amyloid formation and aggregation.