Abstract
Hippocampal T2 signal loss and decreased radial arm maze performance in transgenic murine model for AD
Highlights
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by memory loss and progressive loss of cognitive functions that impede performance of daily activities
The diagnostic hallmarks of AD are the presence of amyloid beta (Aβ) plaques, neurofibrillary tangles from phosphorylated tau proteins, neurodegeneration and synapse loss [1,2] seen in post mortem brain studies
We hypothesize that dysregulation of iron storage stimulates oxidative damage to neurons, which in turn promotes amyloid beta, and neurofibrillary tangles deposits. Both of these proteins are found to have strong affinity iron [15,16,17,18]; there are studies showing strong association of iron with amyloid beta [19], and with neurofibrillary tangles [34, 35]. These iron deposits can be visualized in magnetic resonance platform; we propose an increase in plaques and tangles in transgenic mice vs wild types that would be seen in Magnetic Resonance Imaging (MRI) as well as mouse behavioral tasks
Summary
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by memory loss and progressive loss of cognitive functions that impede performance of daily activities It is mostly seen in the elderly population and is the leading cause of dementia. The diagnostic hallmarks of AD are the presence of amyloid beta (Aβ) plaques, neurofibrillary tangles from phosphorylated tau proteins, neurodegeneration and synapse loss [1,2] seen in post mortem brain studies. Formation of such plaques and tangles precedes, up to a decade or more, any clinical symptoms [3,4]. Advances in methods for treatment and diagnosis, such as Magnetic Resonance Imaging (MRI), are extremely important for the future of patients with AD; MRI in particular, has already become a widely used tool to study AD [9,10]
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