The presence of amyloid beta plaques, hyperphosphorylated tau, and iron depositions in the retina: a murine model of Alzheimer's disease
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Abstract
Alzheimer’s disease (AD) is a progressive and incurable neurodegenerative disorder. This chronic brain disorder affects specific areas of the brain that control memory, language, and thought processes.1 The pathology of AD can be distinguished by depositions of extracellular senile plaques, primarily mediated by amyloid beta (Aβ), and by the development of intracellular hyperphosphorylated neurofibrillary tau tangles (HP-tau). These plaques and tangles in turn promote degeneration of neuronal synapses, which is progressive, and irreversible.2 In 2020, as many as 5.8 million Americans were living with AD.3 AD is one of the top 10 leading causes of death in the United States.4 Researchers are now beginning to study whether education, diet, and environmental factors play a role in developing AD. Understanding the environmental factors that contribute to AD is essential for prevention, diagnosis and treatment which will extend the lives of millions. The purpose of this experiment was to gain knowledge and data pertaining to the fundamental connection between diet and the amount of Aβ plaques, hyperphosphorylated tau (HP-tau), and iron depositions that are present in the retina of mice in a murine model of AD. The results showed that the AD proteins could be visualized within the retina but were inclusive regarding whether the Western diet was a contributor to the overload of these target proteins. The data results supported the notion that a homocysteine diet (HCY) had a greater effect on the accumulation of iron depositions and HP-tau tangles than a Western diet.
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2024