Abstract
Alzheimer’s disease (AD) is the result of the deposition of amyloid β (Aβ) peptide into amyloid fibrils and tau into neurofibrillary tangles. At the present time, there are no possible treatments for the disease. We have recently shown that diets enriched in phytonutrients show protection or limit the extent of damage in a number of neurological disorders. GrandFusion (GF) diets have attenuated the outcomes in animal models of traumatic brain injury, cerebral ischemia, and chronic traumatic encephalopathy. In this study, we investigated the effect of GF diets in a mouse model of AD prior to the development of amyloid plaques to show how this treatment paradigm would alter the accumulation of Aβ peptide and related pathologic changes (i.e., inflammation, cathepsin B, and memory impairment). Administration of GF diets (2–4%) over a period of four months in APP/ΔPS1 double-transgenic mice resulted in attenuation in Aβ peptide levels, reduction of amyloid load, and inflammation, increased cathepsin B expression, and improved spatial orientation. Additionally, treatment with GF diets increased nerve growth factor (NGF) levels in the brain and tempered the memory impairment in the animal model. These data suggest that GF diets may alter the development and progression of the mechanisms associated with the disease process to effectively modify AD pathogenesis.
Highlights
Alzheimer’s disease (AD) impacts more than 5.7 million people in the United States alone and is one of the most common forms of dementia and the rate and numbers are expected to increase due to the aging population [1]
AD is characterized by the presence of aggregated amyloid-β (Aβ) peptides that result in extracellular amyloid plaques and hyperphosphorylated tau protein that accumulates within the neurons as neurofibrillary tangles (NFTs)
These studies demonstrate that the GF diets, when started at the time or before amyloid deposition and continued for four months, in the transgenic mice expressing familial AD (FAD) mutant AβPP and presenilin 1 (PS1) cDNAs (AβPP-PS1), we were able to significantly attenuate amyloid plaque burden, levels of Aβ peptide, cathepsin B levels and increased brain nerve growth factor (NGF) when compared to AβPP-PS1 control mice
Summary
Alzheimer’s disease (AD) impacts more than 5.7 million people in the United States alone and is one of the most common forms of dementia and the rate and numbers are expected to increase due to the aging population [1]. Using the APP/PS1 mouse model that we previously have documented, mice were gavaged daily with the 2 and 4% GF diets enriched with fruits and vegetables and examined the animals for the impact on neurological outcomes (behavior), biochemical changes and amyloid pathology [19] These studies demonstrate that the GF diets, when started at the time or before amyloid deposition and continued for four months, in the transgenic mice expressing familial AD (FAD) mutant AβPP and presenilin 1 (PS1) cDNAs (AβPP-PS1), we were able to significantly attenuate amyloid plaque burden, levels of Aβ peptide, cathepsin B levels (inflammation) and increased brain NGF when compared to AβPP-PS1 control mice. These data suggest that the GF diets may perhaps be beneficial in the slowing of the AD process in man
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