A Review on the Alzheimer Disease Animal Models and Retinal Degeneration

Authors

  • Andrew Wu University of Calgary
  • Kin Chiu LKS Faculty of Medicine University of Hong Kong
  • Raymond Chuen Chung Chang LKS Faculty of Medicine University of Hong Kong

Keywords:

Alzheimer, Retinal Degradation

Abstract

Alzheimer’s disease (AD) is a chronic neurodegen- erative disease, serving as the most common form of dementia among the elderly population. AD targets various neurological processes in humans such as the visual pathway and hence resulting in various forms of visual abnormalities. Several studies have reported the loss of retinal ganglion cells, reduced thickness of nerve fibre layers (NFL) and damage of the optic nerve head and fiber layers. These findings suggest a putative link between AD and visual function deficits.

As genetic defects have been found to be associated with AD, it is possible to experimentally mimic this condition in animal models. AD gene mutations discovered in human amyloid pre- cursor protein (APP), presenilin 1/2 (PS1/PS2) and microtubule- associated tau protein have been used to engineer AD animal models.

In this review, we discuss the underlying molecular mecha- nisms of AD in terms of amyloidogenesis and tauopathies, as well as explain the pathological changes leading to vision loss in AD patients. Subsequently, the biology of the genes/proteins which have a causative link to AD, including APP, PS1 and PS2 will be discussed. Several recent reports of retinal degeneration in AD transgenic mouse models are selected to examine the relationship between AD and visual disturbance. We believe that a well- established method to generate transgenic mice will enhance our understanding of AD pathology and its correlation with retinal degeneration, leading to possible detection and treatment methods for AD.

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2011-10-01

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